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- W2108596959 abstract "The proto-oncogene c-myb is essential for a controlled balance between cell growth and differentiation. Aberrant c-Myb activity has been reported for numerous human cancers, and enforced c-Myb transcription can transform cells of lymphoid origin by stimulating cellular proliferation and inhibiting apoptotic pathways. Here we demonstrate that activation of the NF-κB pathway by the HTLV-1 Tax protein leads to transcriptional inactivation of c-Myb. This conclusion was supported by the fact that Tax mutants unable to stimulate the NF-κB pathway could not inhibit c-Myb transactivating functions. In addition, inhibition of Tax-mediated NF-κB activation by coexpression of IκBα restored c-Myb transcription, and Tax was unable to block c-Myb transcription in a NEMO knockout cell line. Importantly, physiological stimuli, such as signaling with the cellular cytokines tumor necrosis factor alpha, interleukin 1 beta (IL-1β), and lipopolysaccharide, also inhibited c-Myb transcription. These results uncover a new link between extracellular signaling and c-Myb-dependent transcription. The mechanism underlying NF-κB-mediated repression was identified as sequestration of the coactivators CBP/p300 by RelA. Interestingly, an amino-terminal deletion form of p300 lacking the C/H1 and KIX domains and unable to bind RelA retained the ability to stimulate c-Myb transcription and prevented NF-κB-mediated repression." @default.
- W2108596959 created "2016-06-24" @default.
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- W2108596959 date "2001-11-01" @default.
- W2108596959 modified "2023-09-26" @default.
- W2108596959 title "Human T-Cell Lymphotropic Virus Type 1 Tax Represses c-Myb-Dependent Transcription through Activation of the NF-κB Pathway and Modulation of Coactivator Usage" @default.
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- W2108596959 doi "https://doi.org/10.1128/mcb.21.21.7391-7402.2001" @default.
- W2108596959 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/99912" @default.
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- W2108596959 hasPublicationYear "2001" @default.
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