| Literature DB >> 33467535 |
Junfang Yan1,2,3,4,5, Yi Xie1,2,3,4, Jing Si1,2,3,4, Lu Gan1,2,3,4, Hongyan Li1,2,3,4, Chao Sun1,2,3,4, Cuixia Di1,2,3,4, Jinhua Zhang1,2,3,4,5, Guomin Huang1,2,3,4,5, Xuetian Zhang1,2,3,4,5, Hong Zhang1,2,3,4.
Abstract
Cell can integrate the caspase family and mammalian target of rapamycin (mTOR) signaling in response to cellular stress triggered by environment. It is necessary here to elucidate the direct response and interaction mechanism between the two signaling pathways in regulating cell survival and determining cell fate under cellular stress. Members of the caspase family are crucial regulators of inflammation, endoplasmic reticulum stress response and apoptosis. mTOR signaling is known to mediate cell growth, nutrition and metabolism. For instance, over-nutrition can cause the hyperactivation of mTOR signaling, which is associated with diabetes. Nutrition deprivation can inhibit mTOR signaling via SH3 domain-binding protein 4. It is striking that Ras GTPase-activating protein 1 is found to mediate cell survival in a caspase-dependent manner against increasing cellular stress, which describes a new model of apoptosis. The components of mTOR signaling-raptor can be cleaved by caspases to control cell growth. In addition, mTOR is identified to coordinate the defense process of the immune system by suppressing the vitality of caspase-1 or regulating other interferon regulatory factors. The present review discusses the roles of the caspase family or mTOR pathway against cellular stress and generalizes their interplay mechanism in cell fate determination.Entities:
Keywords: cell fate; interplay; mTOR signaling; the caspase family
Mesh:
Substances:
Year: 2021 PMID: 33467535 PMCID: PMC7830632 DOI: 10.3390/ijms22020817
Source DB: PubMed Journal: Int J Mol Sci ISSN: 1422-0067 Impact factor: 5.923