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p53 hotspot mutants attenuate CTL-mediated tumor cell killing through a novel ALKBH5-YTHDF3-PD-L1 pathway
Abstract TP53 is a well-documented tumor suppressor gene frequently mutated in malignancies. It has been demonstrated that the gain-of-function (GOF) mutation of p53 promotes the development and progression of cancers; however, its extrinsic oncogenic mechanisms are still poorly understood. Herein, we found that the oncogenic effect of mutant p53 in vivo is dependent on the tumor immune microenvironment.
Loss of the m6A methyltransferase METTL3 in monocyte-derived macrophages ameliorates Alzheimer’s disease pathology in mice
DNMT3A transcriptionally regulates the expression of ATAT1 As an epigenetic modifier, DNMT3A usually binds directly to the gene promoter to regulate transcription [38]. Accordingly, DNMT3A was found to directly bind to both the proximal promoters and distal promoters of Atat1 in BMDMs by chromatin-immunoprecipitation (ChIP) assay (Fig 5A).
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