MYC family oncoproteins regulate the expression of a large number of genes and broadly stimulate elongation by RNA polymerase II (RNAPII). While the factors that control the chromatin association of MYC proteins are well understood, much less is known about how interacting proteins mediate MYC's effects on transcription. Here, we show that TFIIIC, an architectural protein complex that controls the three-dimensional chromatin organisation at its target sites, binds directly to the amino-terminal transcriptional regulatory domain of MYCN.
View Article and Find Full Text PDFCachexia is a major cause of morbidity and mortality in individuals with cancer and is characterized by weight loss due to adipose and muscle tissue wasting. Hallmarks of white adipose tissue (WAT) remodeling, which often precedes weight loss, are impaired lipid storage, inflammation and eventually fibrosis. Tissue wasting occurs in response to tumor-secreted factors.
View Article and Find Full Text PDFMYC oncoproteins are key drivers of tumorigenesis. As transcription factors, MYC proteins regulate transcription by all three nuclear polymerases and gene expression. Accumulating evidence shows that MYC proteins are also crucial for enhancing the stress resilience of transcription.
View Article and Find Full Text PDFOncoproteins of the MYC family drive the development of numerous human tumours. In unperturbed cells, MYC proteins bind to nearly all active promoters and control transcription by RNA polymerase II. MYC proteins can also coordinate transcription with DNA replication and promote the repair of transcription-associated DNA damage, but how they exert these mechanistically diverse functions is unknown.
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