https://osm.bio/index.php?action=history&feed=atom&title=%E9%85%B6%E8%81%94%E5%8F%97%E4%BD%93%E5%8F%8A%E5%85%B6%E4%BF%A1%E5%8F%B7%E8%BD%AC%E5%AF%BC 2026-05-14T14:56:22Z 本wiki上该页面的版本历史 MediaWiki 1.45.1 https://osm.bio/index.php?title=%E9%85%B6%E8%81%94%E5%8F%97%E4%BD%93%E5%8F%8A%E5%85%B6%E4%BF%A1%E5%8F%B7%E8%BD%AC%E5%AF%BC&diff=10334&oldid=prev 2025-07-19T09:12:29Z

<p><span class="autocomment">受体酪氨酸激酶与Ras/MAPK信号通路</span></p> <table style="background-color: #fff; color: #202122;" data-mw="interface"> <col class="diff-marker" /> <col class="diff-content" /> <col class="diff-marker" /> <col class="diff-content" /> <tr class="diff-title" lang="zh-Hans-CN"> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">←上一版本</td> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">2025年7月19日 (六) 17:12的版本</td> </tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l1">第1行：</td> <td colspan="2" class="diff-lineno">第1行：</td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">= 前言 =</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">本篇是信号转导系列的第二篇——酶联受体及其信号转导。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">: ''前篇：[[G蛋白偶联受体及其信号转导]]''</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">: ''后篇：[[其他受体及其信号转导]]''</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>= 受体酪氨酸激酶与Ras/MAPK信号通路 =</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>= 受体酪氨酸激酶与Ras/MAPK信号通路 =</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>MAPK/ERK通路（也称为Ras-Raf-MEK-ERK通路）是一条细胞内蛋白级联信号通路，能够将细胞表面受体接收到的信号传递至细胞核内的DNA。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>MAPK/ERK通路（也称为Ras-Raf-MEK-ERK通路）是一条细胞内蛋白级联信号通路，能够将细胞表面受体接收到的信号传递至细胞核内的DNA。</div></td></tr> </table>

Kotodama https://osm.bio/index.php?title=%E9%85%B6%E8%81%94%E5%8F%97%E4%BD%93%E5%8F%8A%E5%85%B6%E4%BF%A1%E5%8F%B7%E8%BD%AC%E5%AF%BC&diff=10333&oldid=prev 2025-07-19T09:05:25Z

<p><span class="autocomment">mTOR</span></p> <table style="background-color: #fff; color: #202122;" data-mw="interface"> <col class="diff-marker" /> <col class="diff-content" /> <col class="diff-marker" /> <col class="diff-content" /> <tr class="diff-title" lang="zh-Hans-CN"> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">←上一版本</td> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">2025年7月19日 (六) 17:05的版本</td> </tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l232">第232行：</td> <td colspan="2" class="diff-lineno">第232行：</td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>: &#039;&#039;另请参见：[[MTOR的性质|mTOR的性质]]&#039;&#039;</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>: &#039;&#039;另请参见：[[MTOR的性质|mTOR的性质]]&#039;&#039;</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>哺乳动物雷帕霉素靶蛋白(mTOR)也称为雷帕霉素机制靶蛋白，是一种由人类MTOR基因编码的激酶。mTOR 是蛋白激酶磷脂酰肌醇-3-激酶相关激酶家族的成员。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>哺乳动物雷帕霉素靶蛋白(mTOR)也称为雷帕霉素机制靶蛋白，是一种由人类MTOR基因编码的激酶。mTOR 是蛋白激酶磷脂酰肌醇-3-激酶相关激酶家族的成员。</div></td></tr> <tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><del style="font-weight: bold; text-decoration: none;">=== mTORC1 ===</del></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>参与调节mTORC1活性的最重要蛋白质是结节性硬化症复合物（TSC,Tuberous Sclerosis Complex）。TSC会抑制位于溶酶体膜上的Rheb，Rheb是Ras家族的成员，它将激活mTORC1。活化的AKT会抑制TSC从而激活mTORC1，同时激活的mTORC1会反馈抑制insulin和IGF代表的PI3K-Akt途径</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>参与调节mTORC1活性的最重要蛋白质是结节性硬化症复合物（TSC,Tuberous Sclerosis Complex）。TSC会抑制位于溶酶体膜上的Rheb，Rheb是Ras家族的成员，它将激活mTORC1。活化的AKT会抑制TSC从而激活mTORC1，同时激活的mTORC1会反馈抑制insulin和IGF代表的PI3K-Akt途径</div></td></tr> <tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><del style="font-weight: bold; text-decoration: none;">=== mTORC2 ===</del></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>mTORC2借助PH结构域被PI3K合成的PIP3招募到细胞膜上，同时它可以激活Akt。Akt同时对mTORC2有作用，它会磷酸化mSin1从而使mTORC2激活。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>mTORC2借助PH结构域被PI3K合成的PIP3招募到细胞膜上，同时它可以激活Akt。Akt同时对mTORC2有作用，它会磷酸化mSin1从而使mTORC2激活。</div></td></tr> </table>

Kotodama https://osm.bio/index.php?title=%E9%85%B6%E8%81%94%E5%8F%97%E4%BD%93%E5%8F%8A%E5%85%B6%E4%BF%A1%E5%8F%B7%E8%BD%AC%E5%AF%BC&diff=10331&oldid=prev 2025-07-19T08:35:45Z

<p><span class="autocomment">PI3K/AKT/mTOR信号通路</span></p> <table style="background-color: #fff; color: #202122;" data-mw="interface"> <col class="diff-marker" /> <col class="diff-content" /> <col class="diff-marker" /> <col class="diff-content" /> <tr class="diff-title" lang="zh-Hans-CN"> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">←上一版本</td> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">2025年7月19日 (六) 16:35的版本</td> </tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l196">第196行：</td> <td colspan="2" class="diff-lineno">第196行：</td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>p85调节亚基含有SH2和SH3结构域。SH2结构域优先结合氨基酸序列中含有Y-X-X-M磷酸化酪氨酸残基。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>p85调节亚基含有SH2和SH3结构域。SH2结构域优先结合氨基酸序列中含有Y-X-X-M磷酸化酪氨酸残基。</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>=== 激活 ===</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>=== 激活 ===</div></td></tr> <tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><del style="font-weight: bold; text-decoration: none;">当细胞表面的受体（如生长因子受体或胰岛素受体）被配体激活后，PI3K被招募至细胞膜并被激活。激活后的PI3K可将磷脂酰肌醇</del>(4,5)二磷酸（PtdIns(4,5)P2）磷酸化，生成磷脂酰肌醇(3,4,5)三磷酸（PtdIns(3,4,5)P3）。</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">该信号通路可被多种信号激活，包括激素、生长因子和细胞外基质（ECM）成分。其激活过程通常始于胞外配体与质膜上的受体酪氨酸激酶（RTK）结合，导致受体二聚化，并在胞内区酪氨酸残基发生交互磷酸化。调节亚基p85通过其Src同源2（SH2）结构域结合至激活受体上的磷酸化酪氨酸残基，随后招募催化亚基p110，形成具有完全活性的PI3K酶。另一种激活方式是接头分子Grb2结合RTK的磷酸化YXN基序，并通过Grb2相关结合（GAB）支架蛋白招募p85。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">p110亚基也可在无p85的情况下被招募。例如，Grb2还能结合Ras-GEF Sos1，激活Ras。Ras-GTP随后激活PI3K的p110亚基。其他接头分子，如胰岛素受体底物（IRS），也可激活p110。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">此外，PI3K还可被G蛋白偶联受体（GPCR）激活，方式为G蛋白βγ二聚体或Ras直接结合PI3K。此外，Gα亚基能激活Src依赖性整合素信号通路，进而激活PI3K。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">激活后的PI3K可将磷脂酰肌醇</ins>(4,5)二磷酸（PtdIns(4,5)P2）磷酸化，生成磷脂酰肌醇(3,4,5)三磷酸（PtdIns(3,4,5)P3）。</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== PKB（AKT）==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== PKB（AKT）==</div></td></tr> <tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l222">第222行：</td> <td colspan="2" class="diff-lineno">第228行：</td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==== 蛋白磷酸酶 ====</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==== 蛋白磷酸酶 ====</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>PHLPP家族（PHLPP1和PHLPP2）磷酸酶能直接去磷酸化并失活特定Akt同工酶。PHLPP2去磷酸化Akt1和Akt3，PHLPP1则特异去磷酸化Akt2和Akt3。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>PHLPP家族（PHLPP1和PHLPP2）磷酸酶能直接去磷酸化并失活特定Akt同工酶。PHLPP2去磷酸化Akt1和Akt3，PHLPP1则特异去磷酸化Akt2和Akt3。</div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">== mTOR ==</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">: ''另请参见：[[MTOR的性质|mTOR的性质]]''</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">哺乳动物雷帕霉素靶蛋白(mTOR)也称为雷帕霉素机制靶蛋白，是一种由人类MTOR基因编码的激酶。mTOR 是蛋白激酶磷脂酰肌醇-3-激酶相关激酶家族的成员。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">=== mTORC1 ===</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">参与调节mTORC1活性的最重要蛋白质是结节性硬化症复合物（TSC,Tuberous Sclerosis Complex）。TSC会抑制位于溶酶体膜上的Rheb，Rheb是Ras家族的成员，它将激活mTORC1。活化的AKT会抑制TSC从而激活mTORC1，同时激活的mTORC1会反馈抑制insulin和IGF代表的PI3K-Akt途径</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">=== mTORC2 ===</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">mTORC2借助PH结构域被PI3K合成的PIP3招募到细胞膜上，同时它可以激活Akt。Akt同时对mTORC2有作用，它会磷酸化mSin1从而使mTORC2激活。</ins></div></td></tr> </table>

Kotodama https://osm.bio/index.php?title=%E9%85%B6%E8%81%94%E5%8F%97%E4%BD%93%E5%8F%8A%E5%85%B6%E4%BF%A1%E5%8F%B7%E8%BD%AC%E5%AF%BC&diff=10329&oldid=prev 2025-07-19T08:22:08Z

<p><span class="autocomment">磷酸化修饰</span></p> <table style="background-color: #fff; color: #202122;" data-mw="interface"> <col class="diff-marker" /> <col class="diff-content" /> <col class="diff-marker" /> <col class="diff-content" /> <tr class="diff-title" lang="zh-Hans-CN"> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">←上一版本</td> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">2025年7月19日 (六) 16:22的版本</td> </tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l206">第206行：</td> <td colspan="2" class="diff-lineno">第206行：</td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==== 磷酸化修饰 ====</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==== 磷酸化修饰 ====</div></td></tr> <tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Akt定位于细胞膜后，通过与PIP3结合，可被其激活性激酶磷酸化：依赖磷脂酰肌醇的激酶-<del style="font-weight: bold; text-decoration: none;">1（PDPK1，Akt1</del>-T308和Akt2-T309位磷酸化）以及雷帕霉素靶蛋白复合物2（mTORC2，Akt1-S473和Akt2-<del style="font-weight: bold; text-decoration: none;">S474位磷酸化）。在营养充足状态下，mTORC2活性较高，且通常首先由mTORC2磷酸化。mTORC2因此功能上被认为是长期寻找的PDK2分子，尽管包括整合素连接激酶（ILK）和丝裂原活化蛋白激酶激活蛋白激酶</del>-<del style="font-weight: bold; text-decoration: none;">2（MAPKAPK2）等也可作为PDK2。mTORC2的磷酸化作用促进PDPK1对Akt同工酶的进一步磷酸化。</del></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Akt定位于细胞膜后，通过与PIP3结合，可被其激活性激酶磷酸化：依赖磷脂酰肌醇的激酶-<ins style="font-weight: bold; text-decoration: none;">1（PDK1，Akt1</ins>-T308和Akt2-T309位磷酸化）以及雷帕霉素靶蛋白复合物2（mTORC2，Akt1-S473和Akt2-<ins style="font-weight: bold; text-decoration: none;">S474位磷酸化）。在营养充足状态下，mTORC2活性较高，且通常首先由mTORC2磷酸化。mTORC2对Akt丝氨酸残基 的磷酸化会刺激PDK1对Akt苏氨酸残基的磷酸化，从而导致Akt完全激活。mTORC2因此功能上被认为是长期寻找的PDK2分子，尽管包括整合素连接激酶（ILK）和丝裂原活化蛋白激酶激活蛋白激酶</ins>-<ins style="font-weight: bold; text-decoration: none;">2（MAPKAPK2）等也可作为PDK2。</ins></div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>活化后的Akt同工酶可通过其激酶活性激活或抑制多种下游底物（如mTOR）。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>活化后的Akt同工酶可通过其激酶活性激活或抑制多种下游底物（如mTOR）。</div></td></tr> </table>

Kotodama https://osm.bio/index.php?title=%E9%85%B6%E8%81%94%E5%8F%97%E4%BD%93%E5%8F%8A%E5%85%B6%E4%BF%A1%E5%8F%B7%E8%BD%AC%E5%AF%BC&diff=10326&oldid=prev 2025-07-19T08:09:32Z

<p><span class="autocomment">PI3K/AKT/mTOR信号通路</span></p> <table style="background-color: #fff; color: #202122;" data-mw="interface"> <col class="diff-marker" /> <col class="diff-content" /> <col class="diff-marker" /> <col class="diff-content" /> <tr class="diff-title" lang="zh-Hans-CN"> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">←上一版本</td> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">2025年7月19日 (六) 16:09的版本</td> </tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l177">第177行：</td> <td colspan="2" class="diff-lineno">第177行：</td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>= PI3K/AKT/mTOR信号通路 =</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>= PI3K/AKT/mTOR信号通路 =</div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">PI3K/AKT/mTOR通路是一条调节细胞周期的重要细胞内信号通路。它与细胞静止、增殖、癌症及寿命密切相关。PI3K的激活会磷酸化并激活AKT，使其定位于质膜。AKT可产生多种下游效应，如激活CREB、抑制p27、使FOXO定位于细胞质、激活PtdIns-3ps以及激活mTOR，进而影响p70或4EBP1的转录。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">已知有多种因素能够增强PI3K/AKT通路的活性，包括表皮生长因子（EGF）、Sonic Hedgehog（shh）、胰岛素样生长因子1（IGF-1）、胰岛素以及钙调蛋白（calmodulin）。瘦素（leptin）和胰岛素都通过募集PI3K信号参与代谢调节。该通路可以被多种因素拮抗，包括PTEN、GSK3B和HB9。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">在许多癌症中，该通路异常活跃，从而降低细胞凋亡，促进细胞增殖。然而，这一通路对于促进生长和增殖、抑制成体干细胞（尤其是神经干细胞）分化是必需的。如何平衡细胞的增殖与分化，是研究人员在开发各种治疗方法时亟需解决的问题。此外，研究还发现，该通路也是神经元长时程增强（LTP）所必需的关键组成部分。</ins></div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== PI3K ==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== PI3K ==</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:PI3kinase.png|thumb|PIK-93 抑制剂（黄色）与 PI3K 110γ 亚基结合。]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:PI3kinase.png|thumb|PIK-93 抑制剂（黄色）与 PI3K 110γ 亚基结合。]]</div></td></tr> <tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l192">第192行：</td> <td colspan="2" class="diff-lineno">第197行：</td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>=== 激活 ===</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>=== 激活 ===</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>当细胞表面的受体（如生长因子受体或胰岛素受体）被配体激活后，PI3K被招募至细胞膜并被激活。激活后的PI3K可将磷脂酰肌醇(4,5)二磷酸（PtdIns(4,5)P2）磷酸化，生成磷脂酰肌醇(3,4,5)三磷酸（PtdIns(3,4,5)P3）。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>当细胞表面的受体（如生长因子受体或胰岛素受体）被配体激活后，PI3K被招募至细胞膜并被激活。激活后的PI3K可将磷脂酰肌醇(4,5)二磷酸（PtdIns(4,5)P2）磷酸化，生成磷脂酰肌醇(3,4,5)三磷酸（PtdIns(3,4,5)P3）。</div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== PKB（AKT）==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== PKB（AKT）==</div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">蛋白激酶B（PKB），又称Akt，是一组丝氨酸/苏氨酸特异性蛋白激酶的统称，在多种细胞过程如葡萄糖代谢、细胞凋亡、细胞增殖、转录及细胞迁移中发挥关键作用。PKB家族有三种不同的基因编码三种同工酶，分别为AKT1、AKT2和AKT3。Akt1主要调控细胞存活和生长，抑制凋亡并促进细胞迁移，是多种癌症的致病因子；Akt2则主要参与胰岛素信号和葡萄糖代谢，其缺失导致糖尿病表型；Akt3主要在脑中表达，缺失会导致小脑表型。三种同工酶在多种人类肿瘤中常见过度表达和基因扩增。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">=== 调控 ===</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">==== 结合磷脂 ====</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Akt蛋白含有一种称为PH结构域（pleckstrin同源结构域）的蛋白结构域。该结构域能高亲和力结合磷脂酰肌醇。对于Akt蛋白的PH结构域来说，它可以结合PIP3（磷脂酰肌醇-3,4,5-三磷酸，PtdIns-3,4,5-P3）。这种结合方式对细胞信号调控极为重要，因为二磷酸化的磷脂酰肌醇PIP2只会在细胞接收到生长信号后，被磷脂酰肌醇3-激酶（PI3K）催化磷酸化生成PIP3。例如，PI3K可以被G蛋白偶联受体或酪氨酸激酶受体（如胰岛素受体）激活。一旦激活，PI3K将PIP2磷酸化为PIP3。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">==== 磷酸化修饰 ====</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Akt定位于细胞膜后，通过与PIP3结合，可被其激活性激酶磷酸化：依赖磷脂酰肌醇的激酶-1（PDPK1，Akt1-T308和Akt2-T309位磷酸化）以及雷帕霉素靶蛋白复合物2（mTORC2，Akt1-S473和Akt2-S474位磷酸化）。在营养充足状态下，mTORC2活性较高，且通常首先由mTORC2磷酸化。mTORC2因此功能上被认为是长期寻找的PDK2分子，尽管包括整合素连接激酶（ILK）和丝裂原活化蛋白激酶激活蛋白激酶-2（MAPKAPK2）等也可作为PDK2。mTORC2的磷酸化作用促进PDPK1对Akt同工酶的进一步磷酸化。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">活化后的Akt同工酶可通过其激酶活性激活或抑制多种下游底物（如mTOR）。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">除作为PI3K的下游效应分子外，Akt同工酶也可通过PI3K非依赖性途径激活。例如，非受体型酪氨酸激酶ACK1（或TNK2）可在Akt的酪氨酸176位点磷酸化Akt，实现PI3K非依赖性激活。有研究表明，升高cAMP的因子在胰岛素存在下可通过蛋白激酶A（PKA）激活Akt。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">==== 泛素化 ====</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Akt1在翻译过程中通常于T450位点（turn motif）被磷酸化。如果该位点未被磷酸化，Akt1折叠异常，随后被泛素化并由蛋白酶体降解。Akt1在IGF-1刺激下会于T308和S473位点被磷酸化，随后多磷酸化的Akt部分被E3泛素连接酶NEDD4泛素化。大部分泛素化-磷酸化Akt1被蛋白酶体降解，少量则以泛素化依赖方式转移到细胞核，磷酸化其底物。癌症相关的Akt1突变体（如E17K）比野生型更易泛素化和磷酸化，且更易转移到细胞核，这一机制可能促进E17K-Akt1相关的人类癌症发生。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">==== 脂质磷酸酶与PIP3 ====</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">PI3K依赖的Akt1激活可通过肿瘤抑制因子PTEN调控，PTEN的作用与PI3K相反。PTEN作为磷酸酶可将PIP3去磷酸化还原为PIP2，去除Akt信号通路中的膜定位因子。缺乏该定位，Akt1激活速率及其下游通路活性均明显下降。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">PIP3还可被肌醇磷酸酶SHIP家族（SHIP1和SHIP2）在“5”位去磷酸化，生成PIP2。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">==== 蛋白磷酸酶 ====</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">PHLPP家族（PHLPP1和PHLPP2）磷酸酶能直接去磷酸化并失活特定Akt同工酶。PHLPP2去磷酸化Akt1和Akt3，PHLPP1则特异去磷酸化Akt2和Akt3。</ins></div></td></tr> </table>

Kotodama https://osm.bio/index.php?title=%E9%85%B6%E8%81%94%E5%8F%97%E4%BD%93%E5%8F%8A%E5%85%B6%E4%BF%A1%E5%8F%B7%E8%BD%AC%E5%AF%BC&diff=10322&oldid=prev 2025-07-19T07:41:14Z

<p><span class="autocomment">JAK/STAT信号通路</span></p> <table style="background-color: #fff; color: #202122;" data-mw="interface"> <col class="diff-marker" /> <col class="diff-content" /> <col class="diff-marker" /> <col class="diff-content" /> <tr class="diff-title" lang="zh-Hans-CN"> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">←上一版本</td> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">2025年7月19日 (六) 15:41的版本</td> </tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l175">第175行：</td> <td colspan="2" class="diff-lineno">第175行：</td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>一个典型的JAK-STAT信号与其他通路整合的例子是T细胞中的白细胞介素-2（IL-2）受体信号。IL-2受体含有γ链，与JAK3结合后使受体尾部的关键酪氨酸磷酸化，进而募集适配蛋白Shc，激活MAPK/ERK通路，从而促进STAT5介导的基因调控。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>一个典型的JAK-STAT信号与其他通路整合的例子是T细胞中的白细胞介素-2（IL-2）受体信号。IL-2受体含有γ链，与JAK3结合后使受体尾部的关键酪氨酸磷酸化，进而募集适配蛋白Shc，激活MAPK/ERK通路，从而促进STAT5介导的基因调控。</div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">= PI3K/AKT/mTOR信号通路 =</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">== PI3K ==</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">[[Image:PI3kinase.png|thumb|PIK-93 抑制剂（黄色）与 PI3K 110γ 亚基结合。]]</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">磷脂酰肌醇3-激酶（PI3Ks），又称磷脂酰肌醇-3-激酶，是一类参与细胞生长、增殖、分化、运动、生存及细胞内运输等多种细胞功能的酶家族，这些过程又与癌症的发生发展密切相关。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">PI3K是一类相关的细胞内信号转导酶，能够催化磷脂酰肌醇（PtdIns）肌醇环3位羟基的磷酸化反应。该信号通路与癌基因PIK3CA和抑癌基因PTEN有关，并影响肿瘤对胰岛素和胰岛素样生长因子1（IGF1）的敏感性，以及与热量限制的作用机制有关。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">=== 结构 ===</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">参与PI3K/AKT信号通路的PI3Ks为I类PI3K，其能够在体内催化磷脂酰肌醇-4,5-二磷酸（PI-4,5-P₂）转化为磷脂酰肌醇-3,4,5-三磷酸（PI-3,4,5-P₃）。I类PI3K可由G蛋白偶联受体和酪氨酸激酶受体激活。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">I类PI3K为异源二聚体分子，由调节亚基和催化亚基组成。根据序列相似性，可进一步分为IA和IB两个亚群。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">I类A（IA）PI3K由一个p110催化亚基与一个较短的调节亚基（通常为p85）组成。调节亚基有五种变体，催化亚基有三种变体。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">I类B（IB）PI3K由调节亚基p101和催化亚基p110γ组成，两者各由单一基因编码。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">p85调节亚基含有SH2和SH3结构域。SH2结构域优先结合氨基酸序列中含有Y-X-X-M磷酸化酪氨酸残基。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">=== 激活 ===</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">当细胞表面的受体（如生长因子受体或胰岛素受体）被配体激活后，PI3K被招募至细胞膜并被激活。激活后的PI3K可将磷脂酰肌醇(4,5)二磷酸（PtdIns(4,5)P2）磷酸化，生成磷脂酰肌醇(3,4,5)三磷酸（PtdIns(3,4,5)P3）。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">== PKB（AKT）==</ins></div></td></tr> </table>

Kotodama https://osm.bio/index.php?title=%E9%85%B6%E8%81%94%E5%8F%97%E4%BD%93%E5%8F%8A%E5%85%B6%E4%BF%A1%E5%8F%B7%E8%BD%AC%E5%AF%BC&diff=10071&oldid=prev 2025-07-14T08:31:23Z

<p><span class="autocomment">细胞因子受体与JAK/STAT信号通路</span></p> <table style="background-color: #fff; color: #202122;" data-mw="interface"> <col class="diff-marker" /> <col class="diff-content" /> <col class="diff-marker" /> <col class="diff-content" /> <tr class="diff-title" lang="zh-Hans-CN"> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">←上一版本</td> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">2025年7月14日 (一) 16:31的版本</td> </tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l125">第125行：</td> <td colspan="2" class="diff-lineno">第125行：</td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>= 细胞因子受体与JAK/STAT信号通路 =</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>= 细胞因子受体与JAK/STAT信号通路 =</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>JAK-STAT信号通路是细胞内蛋白之间一系列相互作用的链式反应，参与免疫调节、细胞分裂、细胞凋亡以及肿瘤形成等多种生物过程。该通路能够将细胞外的化学信号传递到细胞核，并通过转录过程激活相关基因。JAK-STAT信号通路的三个关键组成部分包括：Janus激酶（JAKs）、信号转导及转录激活因子（STATs）和受体（负责结合化学信号）。[1] JAK-STAT信号的异常可导致多种疾病，如皮肤病、癌症及影响免疫系统的疾病。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>JAK-STAT信号通路是细胞内蛋白之间一系列相互作用的链式反应，参与免疫调节、细胞分裂、细胞凋亡以及肿瘤形成等多种生物过程。该通路能够将细胞外的化学信号传递到细胞核，并通过转录过程激活相关基因。JAK-STAT信号通路的三个关键组成部分包括：Janus激酶（JAKs）、信号转导及转录激活因子（STATs）和受体（负责结合化学信号）。[1] JAK-STAT信号的异常可导致多种疾病，如皮肤病、癌症及影响免疫系统的疾病。</div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">'''其具体过程概述如下：细胞因子→I/II型细胞因子受体→受体二聚化→JAKs交叉磷酸化→JAK磷酸化受体的Tyr残基→SH2结构域形成→STAT通过SH2连接→JAK磷酸化激活STAT→STAT脱离并二聚化→STAT二聚体被转运如细胞核→作为转录因子激活转录'''</ins></div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== 细胞因子与细胞因子受体 ==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== 细胞因子与细胞因子受体 ==</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==== I型细胞因子受体（Type I cytokine receptors）====</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==== I型细胞因子受体（Type I cytokine receptors）====</div></td></tr> </table>

Kotodama https://osm.bio/index.php?title=%E9%85%B6%E8%81%94%E5%8F%97%E4%BD%93%E5%8F%8A%E5%85%B6%E4%BF%A1%E5%8F%B7%E8%BD%AC%E5%AF%BC&diff=10070&oldid=prev 2025-07-14T08:27:01Z

<p><span class="autocomment">受体酪氨酸激酶与Ras/MAPK信号通路</span></p> <table style="background-color: #fff; color: #202122;" data-mw="interface"> <col class="diff-marker" /> <col class="diff-content" /> <col class="diff-marker" /> <col class="diff-content" /> <tr class="diff-title" lang="zh-Hans-CN"> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">←上一版本</td> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">2025年7月14日 (一) 16:27的版本</td> </tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l1">第1行：</td> <td colspan="2" class="diff-lineno">第1行：</td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>= 受体酪氨酸激酶与Ras/MAPK信号通路 =</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>= 受体酪氨酸激酶与Ras/MAPK信号通路 =</div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">MAPK/ERK通路（也称为Ras-Raf-MEK-ERK通路）是一条细胞内蛋白级联信号通路，能够将细胞表面受体接收到的信号传递至细胞核内的DNA。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">这一信号通路的启动始于信号分子与细胞表面受体的结合，终止于细胞核内DNA表达蛋白，进而引发细胞变化，如细胞分裂。该通路包含多种蛋白质，如有丝分裂原活化蛋白激酶（MAPKs），最初称为细胞外信号调节激酶（ERKs），它们通过将磷酸基团添加到相邻蛋白上（即磷酸化），实现彼此间的信号传递，从而像“开关”一样调节下游蛋白的活性。</ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr> <tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">'''其过程概述如下：配体结合→RTK二聚化活化→招募接头蛋白Grb2→结合Sos、Ras→Ras结合GTP激活→激活Raf（MAP3K）→磷酸化激活Mek（MAP2K）→磷酸化激活Erk（MAPK）→磷酸化下游蛋白'''</ins></div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== 受体酪氨酸激酶 ==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== 受体酪氨酸激酶 ==</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>=== 结构 ===</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>=== 结构 ===</div></td></tr> </table>

Kotodama https://osm.bio/index.php?title=%E9%85%B6%E8%81%94%E5%8F%97%E4%BD%93%E5%8F%8A%E5%85%B6%E4%BF%A1%E5%8F%B7%E8%BD%AC%E5%AF%BC&diff=10069&oldid=prev 2025-07-14T08:18:03Z

<p><span class="autocomment">细胞因子与细胞因子受体</span></p> <table style="background-color: #fff; color: #202122;" data-mw="interface"> <col class="diff-marker" /> <col class="diff-content" /> <col class="diff-marker" /> <col class="diff-content" /> <tr class="diff-title" lang="zh-Hans-CN"> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">←上一版本</td> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">2025年7月14日 (一) 16:18的版本</td> </tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l121">第121行：</td> <td colspan="2" class="diff-lineno">第121行：</td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>JAK-STAT信号通路是细胞内蛋白之间一系列相互作用的链式反应，参与免疫调节、细胞分裂、细胞凋亡以及肿瘤形成等多种生物过程。该通路能够将细胞外的化学信号传递到细胞核，并通过转录过程激活相关基因。JAK-STAT信号通路的三个关键组成部分包括：Janus激酶（JAKs）、信号转导及转录激活因子（STATs）和受体（负责结合化学信号）。[1] JAK-STAT信号的异常可导致多种疾病，如皮肤病、癌症及影响免疫系统的疾病。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>JAK-STAT信号通路是细胞内蛋白之间一系列相互作用的链式反应，参与免疫调节、细胞分裂、细胞凋亡以及肿瘤形成等多种生物过程。该通路能够将细胞外的化学信号传递到细胞核，并通过转录过程激活相关基因。JAK-STAT信号通路的三个关键组成部分包括：Janus激酶（JAKs）、信号转导及转录激活因子（STATs）和受体（负责结合化学信号）。[1] JAK-STAT信号的异常可导致多种疾病，如皮肤病、癌症及影响免疫系统的疾病。</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== 细胞因子与细胞因子受体 ==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== 细胞因子与细胞因子受体 ==</div></td></tr> <tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>=== I型细胞因子受体（Type I cytokine receptors）===</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">=</ins>=== I型细胞因子受体（Type I cytokine receptors）<ins style="font-weight: bold; text-decoration: none;">=</ins>===</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>典型配体： 白细胞介素-2（IL-2）、IL-4、IL-6、IL-7、IL-9、IL-11、IL-12、IL-15、IL-21、粒细胞-巨噬细胞集落刺激因子（GM-CSF）、促红细胞生成素（EPO）、生长激素（GH）、促乳素（PRL）等。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>典型配体： 白细胞介素-2（IL-2）、IL-4、IL-6、IL-7、IL-9、IL-11、IL-12、IL-15、IL-21、粒细胞-巨噬细胞集落刺激因子（GM-CSF）、促红细胞生成素（EPO）、生长激素（GH）、促乳素（PRL）等。</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>结构特征： 跨膜区外有保守的WSXWS基序，通常含有多个受体亚基。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>结构特征： 跨膜区外有保守的WSXWS基序，通常含有多个受体亚基。</div></td></tr> <tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>=== II型细胞因子受体（Type II cytokine receptors）===</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">=</ins>=== II型细胞因子受体（Type II cytokine receptors）<ins style="font-weight: bold; text-decoration: none;">=</ins>===</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>典型配体： 干扰素（IFN-α、IFN-β、IFN-γ）、白细胞介素-10（IL-10）等。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>典型配体： 干扰素（IFN-α、IFN-β、IFN-γ）、白细胞介素-10（IL-10）等。</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>结构特征： 不含WSXWS基序，这些受体主要通过其胞外部分的序列相似性而相互关联，这些部分由串联的免疫球蛋白样结构域组成，通常为异二聚体或多聚体。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>结构特征： 不含WSXWS基序，这些受体主要通过其胞外部分的序列相似性而相互关联，这些部分由串联的免疫球蛋白样结构域组成，通常为异二聚体或多聚体。</div></td></tr> </table>

Kotodama https://osm.bio/index.php?title=%E9%85%B6%E8%81%94%E5%8F%97%E4%BD%93%E5%8F%8A%E5%85%B6%E4%BF%A1%E5%8F%B7%E8%BD%AC%E5%AF%BC&diff=10068&oldid=prev 2025-07-14T07:59:48Z

<p><span class="autocomment">JAK/STAT信号通路</span></p> <table style="background-color: #fff; color: #202122;" data-mw="interface"> <col class="diff-marker" /> <col class="diff-content" /> <col class="diff-marker" /> <col class="diff-content" /> <tr class="diff-title" lang="zh-Hans-CN"> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">←上一版本</td> <td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">2025年7月14日 (一) 15:59的版本</td> </tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l144">第144行：</td> <td colspan="2" class="diff-lineno">第144行：</td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== JAK/STAT信号通路 ==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== JAK/STAT信号通路 ==</div></td></tr> <tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>[[Image:Jakstat pathway.svg|thumb|250px|JAK-STAT系统由三大主要组成部分构成：(1) 受体（绿色），穿过细胞膜；(2) Janus激酶（JAK，黄色），与受体结合；(3) 信号转导及转录激活因子（STAT，蓝色），负责将信号传递到细胞核并作用于DNA。红色小点代表磷酸基团。当细胞因子与受体结合后，JAK会在受体上添加磷酸基团（即磷酸化）。这吸引STAT蛋白结合，STAT蛋白也被磷酸化并相互结合，形成二聚体。二聚体进入细胞核，与DNA结合，启动靶基因的转录。能够添加磷酸基团的酶称为蛋白激酶。]</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>[[Image:Jakstat pathway.svg|thumb|250px|JAK-STAT系统由三大主要组成部分构成：(1) 受体（绿色），穿过细胞膜；(2) Janus激酶（JAK，黄色），与受体结合；(3) 信号转导及转录激活因子（STAT，蓝色），负责将信号传递到细胞核并作用于DNA。红色小点代表磷酸基团。当细胞因子与受体结合后，JAK会在受体上添加磷酸基团（即磷酸化）。这吸引STAT蛋白结合，STAT蛋白也被磷酸化并相互结合，形成二聚体。二聚体进入细胞核，与DNA结合，启动靶基因的转录。能够添加磷酸基团的酶称为蛋白激酶。<ins style="font-weight: bold; text-decoration: none;">]</ins>]</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>I型和II型细胞因子受体家族的成员本身不具备激酶活性，它们依赖于JAK（Janus激酶）家族的酪氨酸激酶来介导下游信号转导。此类受体通常以成对多肽链形式存在，拥有两个胞内信号转导结构域。JAK分别与每个胞内结构域中、紧邻细胞膜的富脯氨酸区（即box1/box2结构域）结合。当受体与细胞因子或生长因子等配体结合后，受体发生二聚化，导致与其结合的JAKs彼此靠近，并通过“反式磷酸化”在对方激活环区域的酪氨酸残基上进行相互磷酸化，从而增强JAK激酶活性。</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>I型和II型细胞因子受体家族的成员本身不具备激酶活性，它们依赖于JAK（Janus激酶）家族的酪氨酸激酶来介导下游信号转导。此类受体通常以成对多肽链形式存在，拥有两个胞内信号转导结构域。JAK分别与每个胞内结构域中、紧邻细胞膜的富脯氨酸区（即box1/box2结构域）结合。当受体与细胞因子或生长因子等配体结合后，受体发生二聚化，导致与其结合的JAKs彼此靠近，并通过“反式磷酸化”在对方激活环区域的酪氨酸残基上进行相互磷酸化，从而增强JAK激酶活性。</div></td></tr> <tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br></td></tr> </table>

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