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Furthermore, enhanced glutamine metabolism has been shown to significantly increase -KG production, which, in turn, activates the mTOR1 signaling pathway and further inhibits the autophagy-promoting kinase (APCK) of the ULK1 complex by mediating site-specific phosphorylation of ULK1 (Ser637 and Ser757) and Atg13 (Ser258) activity, thereby promoting cancer cell proliferation [27]

In aggressive breast tumor subtypes such as triple-negative breast cancer, ChaC1 exhibits significant upregulation (151)

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Lauded for its potential as a tumor suppressor, p53 appears to primarily function to halt the division of cells that have undergone DNA damage

Invasion of Herpes Simplex Virus 1 Into Murine Dermis: Role of Nectin-1 and Herpesvirus Entry Mediator as Cellular Receptors During Aging