Abstract
Multiple human polyomaviruses (HPyVs) can infect the skin, but only Merkel Cell Polyomavirus (MCPyV) has been implicated in the development of a cancer, Merkel Cell Carcinoma (MCC). While expression of HPyV6, HPyV7, and MCPyV small T antigens (ST) all induced a senescence associated secretory phenotype (SASP), MCPyV ST uniquely activated non-canonical NF-κB (ncNF-κB), instead of canonical NF-κB signaling to evade senescence. MCPyV activated NFKB2 and RELB transcription through H3K4 trimethylation and promoted the post-translational stability and processing of NFKB2 by inhibiting FBXW7.
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