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10.1038/bjc.2014.84

http://scihub22266oqcxt.onion/10.1038/bjc.2014.84
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C4453743!4453743!25233399
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suck abstract from ncbi


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pmid25233399      Br+J+Cancer 2014 ; 111 (9): 1688-92
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  • Novel functions of chromatin-bound I?B? in oncogenic transformation #MMPMID25233399
  • Espinosa L; Bigas A; Mulero MC
  • Br J Cancer 2014[Oct]; 111 (9): 1688-92 PMID25233399show ga
  • The nuclear factor-?B (NF-?B) signalling pathway participates in a multitude of biological processes, which imply the requirement of a complex and precise regulation. I?B (for Inhibitor of kappaB) proteins, which bind and retain NF-?B dimers in the cytoplasm, are the main contributors to negative regulation of NF-?B under non-stimulation conditions. Nevertheless, increasing evidences indicate that I?B proteins exert specific nuclear roles that directly contribute to the control of gene transcription. In particular, hypophosphorylated I?B? can bind the promoter region of TNF? leading to persistent gene transcription in macrophages and contributing to the regulation of the inflammatory response. Recently, we demonstrated that phosphorylated and SUMOylated I?B? reside in the nucleus of the cells where it binds to chromatin leading to specific transcriptional repression. Mechanistically, I?B? associates and regulates Polycomb Repressor Complex activity, a function that is evolutionary conserved from flies to mammals, as indicate the homeotic phenotype of Drosophila mutants. Here we discuss the implications of chromatin-bound I?B? function in the context of tumorigenesis.
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