The downstream transcriptional program of non-canonical NF-κB signaling is driven by a heterodimer of RELB and p52 (NFKB2), both of which are highly significant in the same cluster as transcription factors such as TOX, EOMES, and NFATC1.
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Multiomic profiling of chronically activated CD4+ T cells identifies drivers of exhaustion and metabolic reprogramming.
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