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14-3-3ζ 结合 III 类磷酸肌醇 3-激酶并抑制自噬。

14-3-3ζ binds class III phosphatidylinositol-3-kinase and inhibits autophagy.

机构信息

Centro Andaluz de Biología Molecular y Medicina Regenerativa, Consejo Superior de Investigaciones Científicas, Sevilla, Spain.

出版信息

Autophagy. 2011 Feb;7(2):240-2. doi: 10.4161/auto.7.2.14286. Epub 2011 Feb 1.

Abstract

Autophagy is an evolutionarily conserved pathway involved in a great variety of physiological roles such as starvation adaptation, elimination of microorganisms, and intracellular protein and organelle clearance. It seems clear that autophagy is strictly controlled because of the multiplicity of its functions and thus, autophagy components are finely regulated. Here, 14-3-3ζ protein has been shown as negative regulator of autophagy by association and inactivation of the vesicle nucleation component vacuolar protein sorting 34 (hVps34), the class III phosphatidylinositol-3- kinase (PI3KC3).

摘要

自噬是一种进化上保守的途径,参与多种生理作用,如饥饿适应、微生物清除和细胞内蛋白质和细胞器清除。由于其功能的多样性,自噬似乎受到严格的控制,因此自噬成分受到精细的调节。在这里,通过与液泡分选 34 号蛋白(hVps34),即 III 类磷酸肌醇 3-激酶(PI3KC3)的结合和失活,14-3-3ζ 蛋白已被证明是自噬的负调控因子。

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