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Hepatic BCL6 and plasma triglycerides regulate sexual dimorphism in tissue tolerance [set 3]

ABSTRACT: Here, we investigated the role of BCL6 in hepatic response to E.Coli infection. Bcl6 F/F and Bcl6 F/F, Alb-Cre male and female mice were infected with E.Coli and livers were collected 24h after infection for RNAseq analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE138392 | GEO | 2022/10/21

REPOSITORIES: GEO

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Hepatic BCL6 and plasma triglycerides regulate sexual dimorphism in tissue tolerance [set 5]

Project description:Tissue tolerance is a sexually dimorphic trait. Here, we investigated the role of BCL6 in establishing hepatic chromatin landscape promoting sexually dimorphic tissue tolerance during E.Coli infection.

2022-10-21 | GSE138395 | GEO

Hepatic BCL6 and plasma triglycerides regulate sexual dimorphism in tissue tolerance [set 2]

Project description:Hepatic gene expression shows sexual dimorphism. Here, we investigated the role of BCL6 in establishing sexual dimorphism in hepatic gene expression and created Bcl6Flox/Flox,Alb-Cre mice and performed RNAseq from livers of 4- and 8-week-old male and female Ctrl and BCL6 liver knock-out mice.

2022-10-21 | GSE138391 | GEO

Hepatic BCL6 and plasma triglycerides regulate sexual dimorphism in tissue tolerance [set 4]

Project description:Hepatic gene expression shows sexual dimorphism. Here, we investigated the role of BCL6 in establishing sexually dimorphic chromatin state and performed H3K27ac ChIP-seq from livers of female and male Ctrl and BCL6 liver knock-out mice.

2022-10-21 | GSE138393 | GEO

Hepatic BCL6 and plasma trigylecrides regulate sexual dimorphism in tissue tolerance [set6_GDX]

Project description:Aim of the experiment was to study the role of gonadectomy and testosterone treatment on liver gene expression of male mice. Gonadectomized male mice received infusion of testosterone or vehicle, and liver was used to perform RNAseq analysis.

2022-10-21 | GSE147609 | 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

BCL6 orchestrates Tfh differentiation via multiple distinct mechanisms

Project description:Tfh cells are required for T cell help to B cells, and BCL6 is the defining transcription factor of Tfh cells. However, the functions of Bcl6 in Tfh have largely remained unclear. Here we defined the BCL6 cistrome in primary human germinal center Tfh cells to assess mechanisms of BCL6 regulation of CD4 T cells, comparing and contrasting BCL6 function in T and B cells. BCL6 primarily acts as a repressor in Tfh cells, and BCL6 binding was associated with control of Tfh cell migration and repression of alternative cell fates. Interestingly, although some BCL6 bound genes possessed BCL6 DNA binding motifs, many BCL6-bound loci were instead characterized by the presence of DNA motifs for AP1 or STAT. AP1 complexes are key positive downstream mediators of TCR signaling and external stimuli. We show that BCL6 can directly bind AP1, and BCL6 depends on AP1 for recruitment to BCL6 binding sites with AP1 motifs, suggesting that BCL6 subverts AP1 activity. These findings reveal that BCL6 has broad and multifaceted effects on Tfh biology, and provide insight into how this master regulator mediates distinct cell-context dependent phenotypes. Sorted naM-CM-/ve tonsil cells were activated with anti-CD3+CD28 Ab coated beads and transduced with BCL6 or control lentiviral vectors as described. RNA was isolated at day 5 following LV infection and microarrays performed as discussed herein. RNA was isolated with the RNeasy Micro Kit (QIAGEN). The quantity and quality of the RNA were confirmed with a NanoDrop 2000c (Thermo Fisher Scientific) and an Experion Electrophoresis System (Bio-Rad). Samples (20 ng) were amplified with Illumina MessageAmp II aRNA Amplification Kits (Ambion), hybridized to HumanHT-12_V4 BeadChips (Illumina), and quantified with Genome Studio (Illumina). Normalized data (heatmap of blood cells) or raw data (heatmap of tonsil cells and Volcano plot) were analyzed with the GenePattern software suite.

2015-03-01 | E-GEOD-66373 | biostudies-arrayexpress

BCL6 modulates tissue neutrophil survival and exacerbates pulmonary inflammation following influenza infection

Project description:Epidemics of influenza virus are of great challenges to the public concern. The lung inflammation and injury caused by excessive inflammatory cell infiltration into the lungs and overproduction of inflammatory mediators are major consequences during influenza virus infection. Neutrophils are vital for anti-microbial defense. However, the roles of neutrophils during viral infections are less clear. Furthermore, the molecular regulation of neutrophil fate and function at the viral infected sites is largely elusive. We found that BCL6 deficiency in neutrophils, but not in monocytes nor lung macrophages, attenuated host inflammation and morbidity following influenza infection. Mechanistically, BCL6 bound to the neutrophil gene loci involved in cellular apoptosis specifically at the site of infection. As such, BCL6 disruption resulted in increased expression of apoptotic genes in neutrophils in the respiratory tract, but not in the circulation nor bone marrow. Consequently, BCL6 deficiency promoted tissue neutrophil apoptosis. Our results have revealed a previously unappreciated role of BCL6 in modulating neutrophil apoptosis at the site of infection for the regulation of host disease development following viral infection.

2019-06-24 | GSE126622 | GEO

Population gene expression of anti-viral CD4 T cells in Bcl6 and Blimp1 deficient conditions

Project description:Population gene expression of effector CD4+ T cells WT, Bcl6-deficient , Blimp1-deficient or Bcl6 Blimp1-deficient was determined by RNAseq after LCMV Armstrong infection

2021-11-05 | GSE149597 | GEO

Single-cell gene expression of anti-viral CD4 T cells in Bcl6 and Blimp1 deficient conditions

Project description:Single-cell gene expression of effector CD4+ T cells WT, Bcl6-deficient , Blimp1-deficient or Bcl6 Blimp1-deficient was determined by scRNAseq after LCMV Armstrong infection

2021-11-05 | GSE149912 | GEO

Immediate adaption – Quantitative Proteomics of BCL6 silencing and EGFR TK inhibition

Project description:We aimed to identify the response mechanism to EGFR tyrosine kinase inhibition. A431 cells were transfected with mock siRNA or BCL6 siRNA. Cells were then treated with gefitinib. Harvesting was done at 0h, at 24h and at 48h. Two TMT10plex sets were organized as follows: TMT set1: mock 0h (3x, channels 126, 127N and 127C), mock 24h (3x, 128N, 128C and 129N), mock 48h (3x, 129C, 130N, 130C) and internal pooled standard (131) composed from equal aliquots of all samples (mock siRNA and BCL6 siRNA). TMT set2: siBCL6 0h (3x, channels 126, 127N and 127C), siBCL6 24h (3x, 128N, 128C and 129N), siBCL6 48h (3x, 129C, 130N, 130C) and the same internal pooled standard (131) as for set 1.

2020-12-09 | PXD016605 | Pride

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