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Expression data from primary bone marrow-derived wild-type C57BL/6 and bcl6 knockout macrophages

ABSTRACT: We used microarrays to compare gene expression changes in macrophages caused by deletion of bcl6. Keywords: BCL6 deletion compared to wild-type

ORGANISM(S): Mus musculus

PROVIDER: GSE16527 | GEO | 2012/06/08

SECONDARY ACCESSION(S): PRJNA116093

REPOSITORIES: GEO

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Expression data from primary bone marrow-derived wild-type C57BL/6 and bcl6 knockout macrophages

Project description:We used microarrays to compare gene expression changes in macrophages caused by deletion of bcl6. Keywords: BCL6 deletion compared to wild-type Primary bone marrow-derived macrophages were isolated from C57BL/6 mice transplanted and reconstituted with wild type or bcl6 knockout bone marrow.

2012-06-07 | E-GEOD-16527 | biostudies-arrayexpress

Genome-wide location analysis of SMRT and NCoR in wild-type and Bcl6 knockout macrophages

Project description:Using ChIP-seq, we reveal the SMRT and NCoR co-repressor cistromes, which each consist of over 30,000 half-shared binding sites. Moreover, we identify Bcl6-bound sub-cistromes for each co-repressor, which are strongly concentrated on NF-κB-driven inflammatory and tissue remodeling genes. These results reveal a critical role for Bcl6 and its corepressors SMRT and NCoR in the prevention of atherosclerosis and chronic inflammation. Identification of SMRT and NCoR binding sites in wild-type and Bcl6 knockout primary bone-marrow derived macrophages

2012-03-29 | E-GEOD-27033 | biostudies-arrayexpress

Genome-wide location analysis of SMRT and NCoR in wild-type and Bcl6 knockout macrophages

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Gene expression data of BCR-ABL1 transformed B cell precursors from BCL6 wild-type and BCL6 knockout mice

2010-05-10 | GSE20987 | GEO

Gene expression data of BCR-ABL1 transformed B cell precursors from BCL6 wild-type and BCL6 knockout mice

Project description:To elucidate the mechanism of BCL6-mediated pre-B cell survival signaling, we investigated the gene expression pattern in BCR-ABL1-transformed BCL6+/+ and BCL6-/- B cell precursors. Pharmacological inhibition of BCR-ABL1 was performed with the BCR-ABL1 kinase inhibitor STI571 (Imatinib). BCR-ABL1 transformed B cell precursors of BCL6 wildtype and BCL6 knockout mice were either treated with 10ÂµM STI571 (Imatinib) for 16 hours or cultured in absence of STI571. Three samples for each condition were processed.

2010-05-27 | E-GEOD-20987 | biostudies-arrayexpress

Conditional deletion of Bcl6 in naive B cells

Project description:Bcl6 germline deletion causes a prominent inflammatory disease, owing to over-expression of Th2 cytokines, and affects the properties of B cells prior to immunization. Therefore we established the B cell-specific Bcl6 deletion mice and analyze the gene expression of naive B cells under physiological conditions. Total RNAs of splenic follicular and marginal zone B cells from Bcl6(flox/flox), Bcl6(+/flox) or Bcl6(+/+) mice heterozygous for mb1-cre were extracted and analysed on Affymetrix microarrays.

2012-09-21 | E-GEOD-28737 | biostudies-arrayexpress

Gene expression data of BCR-ABL1 transformed myeloid cells from BCL6 wild-type and BCL6 knockout mice treated with and without Imatinib and RI-BPI

2011-08-24 | GSE24813 | GEO

Gene expression data of BCR-ABL1 transformed myeloid cells from BCL6 wild-type and BCL6 knockout mice treated with and without Imatinib and RI-BPI

Project description:To identify differences in the gene regulation between BCL6+/+ and BCL6-/- CML cells a gene expression analysis has been performed. We investigated the gene expression pattern in BCL6+/+ cells in the presence or absence of Imatinib and a combination of Imatinib and RI-BPI (a novel retro-inverso BCL6 peptide inhibitor). In BCL6-/- CML cells, we investigated the gene expression pattern in the presence or absence of Imatinib. BCR-ABL1 transformed myeloid cells from BCL6+/+ mice were cultured in the presence or absence of 10µM Imatinib or 10µM Imatinib and 20µM RI-BPI for 16 hours. BCR-ABL1 transformed myeloid cells from BCL6-/- mice were cultured in the presence or absence of 10µM Imatinib. Two samples for each condition were processed.

2011-08-23 | E-GEOD-24813 | biostudies-arrayexpress

Conditional deletion of Bcl6 in naive B cells

2012-09-21 | GSE28737 | GEO

Small molecule-induced polymerization triggers degradation of BCL6

Project description:Most small-molecule protein degraders act as interface stabilizers ‘molecular glues’ between E3 ubiquitin ligases and target proteins to induce ternary complex formation and ubiquitin-dependent target protein degradation. Here we report polymerization as a novel mechanism for small molecule-induced degradation. Using functional screens in combination with molecular and biochemical assays, we found that BI-3802, which binds to the BTB domain of the oncogenic transcription factor BCL6, induces polymerization of BCL6 into regular helical structures in vitro and foci in vivo. Polymerization precedes degradation by the SIAH1 E3 ubiquitin ligase. Hereby, a VxP amino acid motif on BCL6, distal from the drug-binding BTB domain, is required for SIAH1 binding, ubiquitination and BI-3802-induced degradation. Our findings propose that small molecule-induced polymerization is not only a new modality for targeted protein degradation, but also provides synthetic biology with a tool for tunable protein polymerization and opens new avenues for future drug design.

2020-11-20 | PXD016185 | Pride

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