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BCL6 inhibits BCL6. 20 / 22
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"Recent studies suggest that the transcriptional co-activator p300 acetylates BCL-6 and, in doing so, disrupts the ability of BCL-6 to recruit HDACs, thereby compromising its ability to repress transcription and induce cell transformation."
| PMC

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"Accordingly, the expression of Bcl6 and T-bet, lineage defining transcription factors for Tfh and Th1 cells, respectively, revealed a mild but significant trend toward increased Tbet and decreased Bcl6 in response to strong stimulation (XREF_FIG)."

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"IL-4 also triggers a negative autoregulatory mechanism of Bcl6 expression in GC B cells, although it initially enhances Bcl6 in naive B cells to facilitate the generation of GC (51)."

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"Moreover, ABC DLBCLs downmodulate BCL6 expression, likely as a result of their partial plasmacytic differentiation, thereby limiting the action of BCL6."

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"Bcl6 , another transcription factor that has been implicated in memory T cell function ( Ichii et al., 2002 ), was also expressed at 2-fold higher amounts in Blimp-1-deficient cells ( Figure 5 ), a fi[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Cells that express no to low levels of BCL6 enhance BCL6 expression in response to IL-4 signaling, while those that have high levels of BCL6, like GC B cells, downregulate BCL6 in response to IL-4."

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"Importantly, Bcl-6 can be coexpressed with Foxp3 as it seems Foxp3 expression is not inhibited by Bcl-6."

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"Together, these observations identified that loss of BCL6 directly relieves repression and potentiates PPARdelta mediated transactivation to restore fasting liver gene expression in Ppara -/-; Bcl6 LKO mice."

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"Strikingly, a bifurcation between Tfh and effector Th cells was measurable by the second cell division of CD4 + T cells, at day 2 after an acute viral infection : IL2Ralpha int cells expressed Bcl6 and CXCR5 (Tfh cell program), whereas IL2Ralpha hi cells exhibited strong Blimp1 expression that repressed Bcl6 (effector Th cell program)."

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"Recently, it was reported that the acetylation of the proto-oncogene BCL6, which is a zinc finger transcription repressor, inactivates BCL6 [35]."

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"Third, overexpression of BCL6 in immortalized mouse mammary EpH4 cells blocked cellular differentiation and promoted proliferation, supporting a differentiation-suppressive role of BCL6 in mammary epithelial cells."

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"These data suggest that an interaction between Bcl6 and Prkd2 leads to Bcl6 phosphorylation, either directly by Prkd2 or via a Prkd2 kinase dependent event, thereby limiting Bcl6 access to the nucleus."

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"Together, these data support the hypothesis that T-bet is required to inhibit the modest amounts of Bcl-6 expressed in effector T H 1 cells to prevent Bcl-6 from dominantly repressing the expression of glycolysis pathway genes and that this activity is functionally important for promoting glycolysis in effector T H 1 cells."

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"Stat5 suppressed BCL6 expression in B-cell lymphomas, adipocytes and hepatocytes, but stimulated BCL6 in B lymphocytes and in insulin producing beta-cells during pregnancy."

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"Acetylation of BCL6 inhibits the ability of BCL6 to recruit HDAC containing SMRT co-repressor complexes [XREF_BIBR]."

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"As a consequence of the mutations, CREBBP and EP300 lose their ability to acetylate BCL-6 and p53, a post-translational modification that inactivates BCL-6 by disrupting the recruitment of histone deacetylases (HDACs) and thus hindering its capacity to repress transcription, while representing an essential requirement for p53 activation XREF_BIBR - XREF_BIBR."

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"T cell-specific loss of Bcl6 prevented accumulation of Tfh cells and reduced accumulation of Tph cells in pristane-treated mice, indicating a role for Bcl6 in the survival and expansion of both populations."

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"These results collectively suggest that etoposide transactivates BCL6 primarily through the interferon/STAT1 signaling pathway.To elucidate the regulatory link of STAT1 on BCL6, we silenced STAT1 and found that STAT1 knockdown led to a marked decrease in BCL6 protein expression (Figure 4L), while STAT1 overexpression apparently increased BCL6 protein abundance (Figure 4M), implying that STAT1 may be upstream of BCL6."

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"Bcl-6 protein inhibition of the Bcl6 gene instead depends on CtBP xref ( xref )."

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"For example, LITAF could transcriptionally repress Bcl6 expression and mediate a protein-protein interaction with Bcl6 in human B cells, which led to the activation of the intrinsic mitochondrial apop[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"