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SAFB regulated the activity of NF-kappaB signaling in CRC by targeting TAK1 This novel mechanism provides a comprehensive understanding of both SAFB and the NF-kappaB signaling pathway in the progression of CRC and indicates that the SAFB-TAK1-NF-kappaB axis is a potential target for early therapeutic intervention in CRC progression
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Depletion of SAFB1 reduced FUS's localization to chromatin-bound fraction and splicing activity, suggesting SAFB1 could tether FUS to chromatin compartment thorough N-terminal DNA-binding motif. Moreover, FUS interacts with another nuclear matrix-associated protein, Matrin3.
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Data suggest that ERH interacts directly in nucleus with C-terminal Arg-Gly-rich region of SAFB1/SAFB2 and this multimer co-localizes in insoluble nuclear fraction; binding of ERH reverses inhibition exerted by SAFB1/SAFB2 on SRPK1. (ERH = enhancer of rudimentary homolog protein; SAFB = scaffold attachment factor B; SRPK1 = splicing kinase SR protein kinase-1)
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The expression of coding and non-coding genes with SAFB1 cross-link sites was altered by SAFB1 knockdown. The isoform-specific expression of neural cell adhesion molecule (NCAM1) and ASTN2 was influenced by SAFB1.
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Single depletion of either SAFB1 or SAFB2 leads to an increase in expression of the other SAFB protein.
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reveals an unexpected role of SUMO-1 and SAFB in the stimulatory coupling of promoter binding, transcription initiation and RNA processing
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SAFB1 formed a complex with the histone methyltransferase EZH2.
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Data indicate that scaffold attachment factor SAFB1 is transiently recruited to DNA breaks in a poly(ADP-ribose)-polymerase 1- and poly(ADP-ribose)-dependent manner.
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Results indicate that SAFB1 and SAFB2 are crucial repressors for ERalpha dynamics in association with the nuclear matrix and that their synergistic regulation of ERalpha mobility is sufficient for inhibiting ERalpha function.
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transcriptional repressor SAFB1 is modified by both SUMO1 and SUMO2/3, and this modification is necessary for its full repressive activity.
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Data show that binding of p53 to SAFB1 had a significant functional outcome, since SAFB1 was shown to suppress p53-mediated reporter gene expression.
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This study shows that low SAFB protein levels predict poor prognosis of breast cancer patients, suggesting critical functions of SAFB1 and SAFB2 in breast cancer cells.
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Study confirms the primary role of SAFB1/SAFB2 as corepressors and also uncovers a previously unknown role for SAFB1 in the regulation of immune genes and in estrogen-mediated repression of genes.
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HSP27 is a nuclear speckle component in unstressed cells in tissue culture. It is also associated with the nucleolar compartment.
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REVIEW: possibility that SAFB1 and SAFB2 are novel breast tumor suppressor genes, and how they might function in this role, are discussed
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HSP27 expression may have useful diagnostic use for the prognosis of mouth squamous cell carcinoma.
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SAFB1 represses ERalpha activity via indirect association with histone deacetylation and interaction with the basal transcription machinery
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SAFB1 was shown to interact directly with the nuclear receptor corepressor N-CoR.
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SAFB1 interacts in pull-down assays not only with PPARgamma but also with all nuclear receptors tested
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PP2A-mediated dephosphorylation of HSP27 and tau correlated with PP2A-induced preservation of endothelial cell cytoskeleton
