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作 者:Shulin Li Rui Yan Jialu Xu Shiqun Zhao Xinyu Ma Qiming Sun Min Zhang Ying Li Jun-Jie Gogo Liu Liangyi Chen Sai Li Ke Xu Liang Ge
机构地区:[1]State Key Laboratory of Membrane Biology,Beijing,China [2]Tsinghua-Peking Center for Life Sciences,Beijing,China [3]School of Life Sciences,Tsinghua University,Beijing,China [4]Department of Chemistry,University of California,Berkeley,CA,USA [5]Beijing Advanced Innovation Center for Structural Biology,Beijing,China [6]Beijing Key Laboratory of Cardiometabolic Molecular Medicine,Institute of Molecular Medicine,Peking University,Beijing,China [7]National Center for Nanoscience and Technology,Beijing,China [8]Department of Biochemistry,Department of Cardiology of Second Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou,Zhejiang,China
出 处:《Cell Research》2022年第2期119-138,共20页细胞研究(英文版)
基 金:The work is funded by National Key R&D Program of China(2019YFA0508602);the National Natural Science Foundation of China(91854114,32061143009,31872832,31872826);Beijing Natural Science Foundation(JQ20028);Tsinghua Independent Research Program(2019Z06QCX02);Tsinghua University COVID-19 Emergency Aid Fund(2020Z99CFZ024),and Tsinghua-Peking Center for Life Sciences.
摘 要:Under stress,the endomembrane system undergoes reorganization to support autophagosome biogenesis,which is a central step in autophagy.How the endomembrane system remodels has been poorly understood.Here we identify a new type of membrane contact formed between the ER-Golgi intermediate compartment(ERGIC)and the ER-exit site(ERES)in the ER-Golgi system,which is essential for promoting autophagosome biogenesis induced by different stress stimuli.The ERGIC-ERES contact is established by the interaction between TMED9 and SEC12 which generates a short distance opposition(as close as 2-5 nm)between the two compartments.The tight membrane contact allows the ERES-located SEC12 to transactivate COPII assembly on the ERGIC.In addition,a portion of SEC12 also relocates to the ERGIC.Through both mechanisms,the ERGIC-ERES contact promotes formation of the ERGIC-derived COPII vesicle,a membrane precursor of the autophagosome.The ERGIC-ERES contact is physically and functionally different from the TFG-mediated ERGIC-ERES adjunction involved in secretory protein transport,and therefore defines a unique endomembrane structure generated upon stress conditions for autophagic membrane formation.
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