本文選題：HIV-Tat蛋白 + 細胞自噬　； 參考：《病毒學(xué)報》2017年02期

【摘要】：HIV-Tat蛋白是由HIV-1病毒感染細胞后分泌的反式轉(zhuǎn)錄激活因子,在HIV感染神經(jīng)損害中發(fā)揮重要作用,是引起艾滋病相關(guān)腦病的重要致病因子。自噬即自我吞噬,主要作用是供給機體營養(yǎng),但異常自噬則引起細胞死亡。HIV-Tat蛋白可以誘導(dǎo)神經(jīng)細胞自噬,從而使細胞死亡,但引起自噬的機制及信號轉(zhuǎn)導(dǎo)通路不清楚。本文主要從HIV-Tat蛋白誘導(dǎo)神經(jīng)細胞自噬的機制、信號轉(zhuǎn)導(dǎo)通路等方面進行綜述,旨在為進一步研究HIV-Tat蛋白與細胞自噬的關(guān)系及尋找新的治療藥物靶點提供參考。
[Abstract]:HIV-Tat protein is a transcriptional activator secreted by HIV-1 infected cells, which plays an important role in the neuronal damage of HIV infection and is an important pathogenic factor of AIDS-related encephalopathy. Autophagy is self-phagocytosis, its main function is to provide nutrition, but abnormal autophagy can induce neuronal autophagy and then make cells die, but the mechanism and signal transduction pathway of autophagy are not clear. This article reviews the mechanism and signal transduction pathway of neuronal autophagy induced by HIV-Tat protein in order to provide reference for the further study of the relationship between HIV-Tat protein and autophagy and the search for new therapeutic drug targets.
【作者單位】： 中國醫(yī)學(xué)科學(xué)院/北京協(xié)和醫(yī)學(xué)院醫(yī)學(xué)生物學(xué)研究所云南省重大傳染病疫苗研發(fā)重點實驗室;昆明醫(yī)科大學(xué)法醫(yī)學(xué)院;
【基金】：國家科技支撐計劃項目(2014BA101B01),題目:實驗用樹，

本文編號：2103198