regulation of atg4b stability by rnf5 limits basal levels of autophagy and influences susceptibility to bacterial infection监管rnf5 atg4b稳定的基底的自噬水平限制和影响对细菌感染的易感性.pdfVIP

regulation of atg4b stability by rnf5 limits basal levels of autophagy and influences susceptibility to bacterial infection监管rnf5 atg4b稳定的基底的自噬水平限制和影响对细菌感染的易感性.pdf

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regulation of atg4b stability by rnf5 limits basal levels of autophagy and influences susceptibility to bacterial infection监管rnf5 atg4b稳定的基底的自噬水平限制和影响对细菌感染的易感性

Regulation of ATG4B Stability by RNF5 Limits Basal Levels of Autophagy and Influences Susceptibility to Bacterial Infection Ersheng Kuang1,2, Cheryl Y. M. Okumura3., Sharon Sheffy-Levin4., Tal Varsano 1, Vincent Chih-Wen Shu 1, 1 5,6 7 ´ ´ 8 7 1 Jianfei Qi , Ingrid R. Niesman , Huei-Jiun Yang , Carlos Lopez-Otın , Wei Yuan Yang , John C. Reed , Limor Broday4*, Victor Nizet3*, Ze’ev A. Ronai 1* 1 Signal Transduction and Cell Death Programs, Sanford-Burnham Medical Research Institute, La Jolla, California, United States of America, 2 Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China, 3 Department of Pediatrics, School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego, La Jolla, California, United States of America, 4 Department of Cell and Developmental Biology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel, 5 Department of Anesthesiology, University of California San Diego, La Jolla, California, United States of America, 6 Veterans Administration San Diego Healthcare System, San Diego, California, United States of America, 7 Institute of Biological Chemistry, Academia Sinica, Taipei, ´ ´ Taiwan, 8 Departamento de Bioquımica y Biologıa Molecular, Universidad de Oviedo, Oviedo, Spain Abstract Autophagy is the mechanism by which cytoplasmic components and organelles are degraded by the lysosomal machinery in response to diverse stimuli including nutrient deprivation, intracellular pathogens, and multiple forms of cellular stress. Here, we show that the membrane-associated E3 ligase RNF5 r

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