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【科学前ѝ基d院刘恭^教授在signal transduction and targeted therapy上发表最新研I成?/p>
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来源Q基d?
2020-12-31 10:20:19
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<p style="text-indent: 32px; text-align: justify; line-height: 2em;"><span style="font-family: 宋体; color: black; letter-spacing: 1px; font-size: 16px;"><br></span></p>
<p style="text-indent: 32px; text-align: justify; line-height: 2em;"><span style="font-family: 宋体; color: black; letter-spacing: 1px; font-size: 16px;">12?6日， </span><span style="font-family: 宋体; color: black; letter-spacing: 1px; font-size: 16px; text-decoration: none;">signal transduction and targeted therapy</span><span style="font-family: 宋体; color: black; letter-spacing: 1px; font-size: 16px;">Q媄响因?3.493Q在U刊发了基础d院病理生理学pd恭^教授团队研究成果QSTAT3 ameliorates cognitive deficits by positively regulating the expression of NMDARs in a mouse model of FTDP-17.</span></p>
<p style="text-indent: 32px; text-align: justify; line-height: 2em;"><span style="font-family: 宋体; color: black; letter-spacing: 1px; font-size: 16px;">tau病（如阿茨默氏症、额颞痴呆、皮质基底部变性等Q中Tau蛋白异常聚集与学习记忆损伤成正相养I但其分子机制q不清楚。刘恭^教授团队在过表达人突变tauQP301L-hTauQ细胞及整体中，发现q表达P301L-hTau可转录因子STAT3酸化水q_高，但核内蛋白水q降低、活性下降；q一步研I发玎ͼP301L-hTau通过乙酰化{录因子STAT1Q增加STAT1与STAT3在胞内的结合，从而抑制STAT3核{位?月龄鼠CA3区感染P301L-hTau病毒后，抑制STAT3zL及H触相关蛋白NMDARs的{录与表达Q突触可塑性下降，学习记忆受损Q条件性敲除STAT3可以模拟q种模型鼠中以上表型的变化Q过表达STAT3可以逆{P301L-hTau引v的突触损伤和学习记忆障碍。染色质免疫共沉淀l果发现STAT3可以直接l合NMDARs的启动子Q荧光素报告基因发现STAT3对NMDARs有{录激zM用?/span></p>
<p style="text-align: center; line-height: 2em; text-indent: 0em;"><br></p>
<p style="text-align: center"><img src="/__local/1/7C/01/3B2E37A6DCABC47AEEBF07E9C8B_0188735D_3E0ED.png" width="500" vsbhref="vurl" vurl="/_vsl/17C013B2E37A6DCABC47AEEBF07E9C8B/0188735D/3E0ED" vheight="" vwidth="500" orisrc="/__local/1/7C/01/3B2E37A6DCABC47AEEBF07E9C8B_0188735D_3E0ED.png" class="img_vsb_content"></p>
<p style="text-align: center; line-height: 2em; text-indent: 0em;"><span style="font-family: 宋体; color: black; letter-spacing: 1px; font-size: 16px;"></span><br></p>
<p style="text-align: justify; text-indent: 32px; line-height: 2em;"><span style="font-family: 宋体; color: black; letter-spacing: 1px; font-size: 16px;">l合以前发表的文章（EMBO Rep. 2019 Jun;20(6):e47202Q发玎ͼSTAT1与STAT3在调控NMDARs表达斚wh相反的作用，STAT1抑制NMDARs的表达，而STAT3促进NMDARs的表达。Tau蛋白聚积通过ȀzSTAT1、抑制STAT3从而抑制NMDARs的表达，DH触损伤和行为学障碍Q该研究l果揭示了tau病中H触损伤的共同机Ӟ可望为其药物开发提供新的靶标?/span></p>
<p style="margin-bottom: 0px; text-align: justify; text-indent: 34px; line-height: 2em;"><span style="color: black; letter-spacing: 1px; font-size: 16px;">该研I由我校博士研究生洪月、万华丽{共同完成。杨l飞教授Q深圛_疄预防控制中心Q、刘恭^教授为共同通讯作者，华中U技大学为第一发表单位。该N受到国家自然U学基金面上目、科技部国安点研发计划慢病专V深圛_三名工程{项目资助?/span></p>
<p style="margin-bottom:0;text-align:justify;text-justify: inter-ideograph;text-indent:28px;line-height:26px"><br></p>
<p style="margin-bottom: 0px; text-align: justify; text-indent: 28px; line-height: 2em;"><span style="color: black; letter-spacing: 1px; font-size: 16px;">文章在线链接Q?span style="font-size: 16px; color: rgb(51, 51, 51); letter-spacing: 1px; text-align: justify;">https://www.nature.com/articles/s41392-020-00290-9#Ack1</span></span></p>
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