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Using a recently developed creatine kinase inhibitor (CKi), we explored the role of this inhibitor on GBM biology in vitro

CD82 exerts a protective effect through the upregulation of TFAF2, which activates mTORC1 through K63-linked ubiquitylation and intracellular repositioning of Raptor 39

Macrophages might be the main reason for the increased expression of CD38 and decrease of NAD related to aging in aging tissues

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These pathways activate SYK and PI3K, which in turn promote phagocytosis, proliferation, and microglial survival [448, 449]