a knockout of the tsg101 gene leads to decreased expression of erbb receptor tyrosine kinases and induction of autophagy prior to cell deathtsg101基因的敲除会导致减少erbb受体酪氨酸激酶的表达和诱导自噬在细胞死亡.pdfVIP

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2017-09-07 发布于上海
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a knockout of the tsg101 gene leads to decreased expression of erbb receptor tyrosine kinases and induction of autophagy prior to cell deathtsg101基因的敲除会导致减少erbb受体酪氨酸激酶的表达和诱导自噬在细胞死亡.pdf

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a knockout of the tsg101 gene leads to decreased expression of erbb receptor tyrosine kinases and induction of autophagy prior to cell deathtsg101基因的敲除会导致减少erbb受体酪氨酸激酶的表达和诱导自噬在细胞死亡

A Knockout of the Tsg101 Gene Leads to Decreased Expression of ErbB Receptor Tyrosine Kinases and Induction of Autophagy Prior to Cell Death 1. 1. 1 1¤ 1,2 Chantey R. Morris , Marissa J. Stanton , Karoline C. Manthey , Keon Bong Oh , Kay-Uwe Wagner * 1 Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska, United States of America, 2 Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, United States of America Abstract The Tumor Susceptibility Gene 101 (Tsg101) encodes a multi-domain protein that mediates a variety of molecular and biological processes including the trafficking and lysosomal degradation of cell surface receptors. Conventional and conditional knockout models have demonstrated an essential requirement of this gene for cell cycle progression and cell viability, but the consequences of a complete ablation of Tsg101 on intracellular processes have not been examined to date. In this study, we employed mouse embryonic fibroblasts that carry two Tsg101 conditional knockout alleles to investigate the expression of ErbB receptor tyrosine kinases as well as stress-induced intracellular processes that are known to be associated with a defect in growth and cell survival. The conditional deletion of the Tsg101 gene in this well-controlled experimental model resulted in a significant reduction in the steady-state levels of the EGFR and ErbB2 but a stress-induced elevation in the phosphorylation of mitogen activated protein (MAP) kinases independent of growth factor stimulation. As