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• W2073559097 abstract "NF-κB is an inducible transcription factor activated in many different cell types by inflammatory and stress signals. The transcription of a wide variety of NF-κB genes is regulated by the coordinated action of transcription co-activators and co-repressors. Previously we identified Myb binding protein 1a (MYBBP1a) as an interaction partner of the transcription activation domain of RelA/p65. MYBBP1a has been shown by others to regulate various transcription factors, through largely unknown mechanisms. Here we present evidence that MYBBP1a is a novel co-repressor of NF-κB. MYBBP1a interacted directly with RelA/p65 and expression of MYBBP1a in cells repressed NF-κB dependent reporter expression but did affect neither RelA/p65 nuclear translocation nor its DNA binding activity. In vitro, MYBBP1a inhibited transcription from chromatinized templates at a step before pre-initiation complex formation. MYBBP1a was found to compete with the histone acetyl transferase co-activator, p300, for interaction with the transcription activation domain of RelA/p65. Expression levels of MYBBP1a are dependent on the cell type, and are particularly high in Jurkat T cells. These results indicate that MYBBP1a is a novel NF-κB co-repressor of transcription that competes with p300 and may function to regulate cell type specific genes." @default.
• W2073559097 created "2016-06-24" @default.
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• W2073559097 date "2007-02-01" @default.
• W2073559097 modified "2023-09-24" @default.
• W2073559097 title "MYBBP1a is a Novel Repressor of NF-κB" @default.
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• W2073559097 doi "https://doi.org/10.1016/j.jmb.2006.11.099" @default.
• W2073559097 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17196614" @default.
• W2073559097 hasPublicationYear "2007" @default.
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