PTEN 激活伴侣介导的自噬，从而调节新陈代谢。

IF 14.6 1区生物学 Q1 CELL BIOLOGY

Autophagy Pub Date : 2024-01-01 Epub Date: 2023-09-08 DOI:10.1080/15548627.2023.2255966

S Joseph Endicott, Richard A Miller

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引用次数: 0

摘要

PTEN 是 INS-PI3K-AKT 通路的负调节因子，是新陈代谢和细胞生长的重要调节因子。PTEN 是癌症中最常见的突变肿瘤抑制因子之一。然而，PTEN 的过表达可延长雌雄小鼠的寿命。我们最近发现，在小鼠肝脏和培养细胞中，PTEN 是激活伴侣介导的自噬（CMA）的必要和充分条件。当 PTEN 过表达时，通过 CMA 选择性地降解蛋白质是抑制糖酵解和脂肪酸合成所必需的。因此，激活 PTEN 下游的 CMA 可能会通过选择性降解关键代谢酶来调节健康和新陈代谢。

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PTEN activates chaperone-mediated autophagy to regulate metabolism.

PTEN is a negative modulator of the INS-PI3K-AKT pathway and is an essential regulator of metabolism and cell growth. PTEN is one of the most commonly mutated tumor suppressors in cancer. However, PTEN overexpression extends the lifespan of both sexes of mice. We recently showed that PTEN is necessary and sufficient to activate chaperone-mediated autophagy (CMA) in the mouse liver and cultured cells. Selective protein degradation via CMA is required to suppress glycolysis and fatty acid synthesis when PTEN is overexpressed. Thus, activation of CMA downstream of PTEN might modulate health and metabolism through selective degradation of key metabolic enzymes.

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来源期刊

Autophagy 生物-细胞生物学

CiteScore

21.30

自引率

2.30%

发文量

277

审稿时长

1 months

期刊介绍： Autophagy is a peer-reviewed journal that publishes research on autophagic processes, including the lysosome/vacuole dependent degradation of intracellular material. It aims to be the premier journal in the field and covers various connections between autophagy and human health and disease, such as cancer, neurodegeneration, aging, diabetes, myopathies, and heart disease. Autophagy is interested in all experimental systems, from yeast to human. Suggestions for specialized topics are welcome. The journal accepts the following types of articles: Original research, Reviews, Technical papers, Brief Reports, Addenda, Letters to the Editor, Commentaries and Views, and Articles on science and art. Autophagy is abstracted/indexed in Adis International Ltd (Reactions Weekly), EBSCOhost (Biological Abstracts), Elsevier BV (EMBASE and Scopus), PubMed, Biological Abstracts, Science Citation Index Expanded, Web of Science, and MEDLINE.