生物
自噬
帕西林
细胞生物学
自噬体
焦点粘着
黑腹果蝇
神经退行性变
袋3
遗传学
基因
磷酸化
疾病
医学
病理
细胞凋亡
作者
Guang‐Chao Chen,Janice Y. Lee,Hong-Wen Tang,Jayanta Debnath,Sheila Μ. Thomas,Jeffrey Settleman
出处
期刊:Autophagy
[Taylor & Francis]
日期:2008-01-01
卷期号:4 (1): 37-45
被引量:60
摘要
Autophagy is a conserved cellular process of macromolecule recycling that involves vesicle-mediated degradation of cytoplasmic components. Autophagy plays essential roles in normal cell homeostasis and development, the response to stresses such as nutrient starvation, and contributes to disease processes including cancer and neurodegeneration. Although many of the autophagy components identified from genetic screens in yeast are well conserved in higher organisms, the mechanisms by which this process is regulated in any species are just beginning to be elucidated. In a genetic screen in Drosophila melanogaster, we have identified a link between the focal adhesion protein paxillin and the Atg1 kinase, which has been previously implicated in autophagy. In mammalian cells, we find that paxillin is redistributed from focal adhesions during nutrient deprivation, and paxillin-deficient cells exhibit defects in autophagosome formation. Together, these findings reveal a novel evolutionarily conserved role for paxillin in autophagy.
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