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Autophagy: Are Amino Acid Signals Dependent on the mTORC1 Pathway or Independent?
Jin, Chenglong; Zhu, Min; Ye, Jinling; Song, Zhiwen; Zheng, Chuntian; Chen, Wei.
Afiliação
  • Jin C; State Key Laboratory of Swine and Poultry Breeding Industry, Guangzhou 510640, China.
  • Zhu M; Institute of Animal Science, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, China.
  • Ye J; Key Laboratory of Animal Nutrition and Feed Science in South China, Ministry of Agriculture and Rural Affairs, Guangzhou 510640, China.
  • Song Z; Guangdong Provincial Key Laboratory of Animal Breeding and Nutrition, Guangzhou 510640, China.
  • Zheng C; Key Laboratory of Animal Genetics, Breeding and Reproduction in the Plateau Mountainous Region, Ministry of Education, College of Animal Science, Guizhou University, Guiyang 550025, China.
  • Chen W; State Key Laboratory of Swine and Poultry Breeding Industry, Guangzhou 510640, China.
Curr Issues Mol Biol ; 46(8): 8780-8793, 2024 Aug 13.
Article em En | MEDLINE | ID: mdl-39194736
ABSTRACT
Autophagy is a kind of "self-eating" phenomenon that is ubiquitous in eukaryotic cells. It mainly manifests in the damaged proteins or organelles in the cell being wrapped and transported by the autophagosome to the lysosome for degradation. Many factors cause autophagy in cells, and the mechanism of nutrient-deficiency-induced autophagy has been a research focus. It has been reported that amino-acid-deficiency-induced cellular autophagy is mainly mediated through the mammalian rapamycin target protein complex 1 (mTORC1) signaling pathway. In addition, some researchers also found that non-mTORC1 signaling pathways also regulate autophagy, and the mechanism of autophagy occurrence induced by the deficiency of different amino acids is not precisely the same. Therefore, this review aims to summarize the process of various amino acids regulating cell autophagy and provide a narrative review on the molecular mechanism of amino acids regulating autophagy.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article