自噬简介
XIBAOZISHI(autophagy or autophagocytosis):YOUCHENGWEIⅡXINGXIBAOSIWANG,SHIXIBAOZAIZISHIXIANGGUANJIYIN(autophagy related gene,Atg) DEDIAOKONGXIALIYONGRONGMEITIJIANGJIEZISHENSHOUSUNDEXIBAOQIHEDAFENZIWUZHIDEGUOCHENG。
MUQIANGENJUFASHENGGUOCHENGFENWEISANLEI:Macroautophagy,MicroautophagyHEChaperone-mediated autophagy CMA)。
● DAZISHI(Macroautophagy):JIWOMENSHUODEZISHI(autophagy);
● WEIZISHI(Microautophagy):SHIZHIRONGMEITIZHUDONG、ZHIJIETUNSHIBAOJIANGCHENGFENDEYIZHONGFANGSHI;
● FENZIBANLVJIEDAODEZISHI (Chaperone-mediated autophagy,CMA):YIXIEFENZIBANLV,RUhsp70,NENGBANGZHUWEIZHEDIEDANBAIZHUANWEIRURONGMEITI。TONGCHANGSHUODEZISHIFANZHIMacroautophagy.
自噬的过程
1):细胞接受自噬诱导信号后,在胞浆的某处形成一个小的类似“脂质体”样的膜结构,然后不断扩张,被称为Phagophore。
2):Phagophore不断延伸,将胞浆中的任何成分,全部揽入,然后“收口”,成为密闭的球状的autophagosome,即“自噬体”。
3):自噬体形成后,可与细胞内吞的吞噬泡、吞饮泡和内体融合(这种情况不是必然要发生的)。
4):自噬体与溶酶体融合形成autolysosome,期间自噬体的内膜被溶酶体酶降解,2者的内容物合为一体,自噬体中的“货物”也被降解,产物(氨基酸、脂肪酸等)被输送到胞浆中供细胞重新利用,而残渣或被排出细胞外或滞留在胞浆中。
TU1. ZISHIDEGUOCHENGTU
最有效的在体自噬流检测工具:AAV-mRFP-GFP-LC3
HANHENGSHENGWUJISHUGONGCHENGSHIGOUJIANRFP-GFP-LC3SHUANGBIAODEXIANXIANGGUANBINGDU(AAV)ZAITI,BAOZHUANGCHENGSHUANGBIAODEXIANXIANGGUANBINGDU,KEZAITIGUANCHAZISHI,SHISHIJIANCEZISHILIUDEQIANGRUO,GENGJIAZHUNQUE、QINGXI、ZHIGUAN!MIBULELC3ZISHISHUANGBIAOXIANBINGDUZAITIZHUANRANDEQUEXIAN,BINGQIEKEGENJUZUZHIQIGUANDEQINHEXING,XUANZEBUTONGDEAAVXUEQINGXING,SHIZUIYOUXIAODEZAITIZISHILIUJIANCEGONGJU!
TU2. AAV-mRFP-GFP-LC3ZHISHIZAITINAOZUZHIZISHILIU
(Cell Death Dis.2013 Nov 14;4:e917)
AAV载体不同血清型
YANJIUFAXIAN AAV JUYOUDUOZHONGXUEQINGXING,GEZHONGBUTONGXUEQINGXINGDE AAV ZAITIDEZHUYAOQUBIESHIYIQIAODANBAIBUTONG,YINCIDUIBUTONGDEZUZHIHEXIBAODEZHUANRANXIAOLVCUNZAICHAYI。MUQIANHANHENGSHENGWUZAIBAOZHUANGXIANXIANGGUANBINGDUSHIYOU12 ZHONGBUTONGDE AAV XUEQINGXINGKEGONGKEHUXUANZE,JIANYIKEHUZHENDUIBUTONGZUZHIQIGUANXUANZEXIANGYINGXUEQINGXINGDE AAV BINGDU,JIANBIAO 1。
BIAO1.12ZHONGBUTONGXUEQINGXINGAAVDUIGEZUZHIQIGUANXIBAODEQINHEXING
部分客户发表文献节选
● The immunoproteasome catalytic ?5i subunit regulates cardiac hypertrophy by targeting the autophagy protein ATG5 for degradation
(ZAZHI:SCIENCE ADVANCES,IF=12.804,DALIANYIKEDAXUEFUSHUDIYIYIYUAN)
● Endoplasmic reticulum stress induced by tunicamycin and thapsigargin protects against transient ischemic brain injury: Involvement of PARK2-dependent mitophagy
(ZAZHI:Autophagy,IF=11.059,ZHEJIANGDAXUE)
● BNIP3L/NIX-mediated mitophagy protects against ischemic brain injury independent of PARK2
(ZAZHI:Autophagy,IF=11.059,ZHEJIANGDAXUE)
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