Ask about this productRelated genes to: BCL6B antibody
- Gene:
- BCL6B NIH gene
- Name:
- BCL6B transcription repressor
- Previous symbol:
- ZNF62
- Synonyms:
- ZBTB28, BAZF
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-20
- Date modifiied:
- 2019-01-25
Related products to: BCL6B antibody
Related articles to: BCL6B antibody
- Chronic stress is known to cause immune system dysfunction, which can contribute to the development of various highly prevalent diseases. Nevertheless, the mechanisms underlying immune dysregulation during chronic stress remain poorly understood. In this study, we examined the effects of 35-day chronic unpredictable mild stress (CUMS) on behavioral patterns, lymphocyte subpopulation ratios, serum cytokine levels, and the peripheral blood leukocyte transcriptome in 20 male Sprague-Dawley rats. After 35 days of CUMS exposure, the rats exhibited established features of chronic unpredictable mild stress, including increased anxiety-like behavior and depression-like behavior. We found a significant increase in the proportion of Th2 cells among lymphocytes, leading to a Th1/Th2 imbalance. Additionally, serum levels of the pro-inflammatory cytokines IL-1α, IL-1β, IFN-γ, and GM-CSF were significantly decreased, whereas the concentration of IL-2 was markedly elevated. Transcriptomic profiling revealed broad alterations in gene expression after CUMS, particularly in pathways related to immune system function. Our findings indicate that chronic stress induces immune dysregulation through a Th1/Th2 imbalance and associated changes in key immune-related genes (including Maf, Irf4, Gfi1, and Bcl6b), suggesting a potential mechanism for stress-induced immune dysfunction. - Source: PubMed
Publication date: 2025/11/06
Luo ZejuHuang YihengTang LuhanGao QikangHou GonglinShao JianzhongShen Yunyun - Hematopoiesis occurs in three consecutive overlapping waves in mammals, regulated by transcription factors. We investigated the role of three relatively poorly studied transcription factors in early embryonic hematopoietic development at single-cell resolution: Atf3, Zfp711 and Bcl6b. These transcription factors are upregulated early in development, when hematopoietic and endothelial lineages separate from cardiac and other mesodermal lineages. We combined multiplexed single-cell RNA sequencing and flow cytometric analysis with knockouts in in vitro differentiating mouse embryonic stem cells to dissect the function of these transcription factors in lineage specification. ΔAtf3 cells showed increased mesodermal differentiation but decreased endothelial cells and erythro-myeloid progenitors, accompanied by aberrant interferon signaling. Mechanistically, loss of Atf3 disrupted key hematopoietic regulatory genes (Runx1, Egr1, Jun, Fos, Mafb and Batf3) required for the formation of erythro-myeloid progenitors. ΔZfp711 cells exhibited increased blood progenitors and erythroid cells, but decreased endothelial cells, with a striking shift from Hoxa+ mesoderm (allantois and limb mesoderm) to Hoxb+ mesoderm (mesenchyme and epicardium). Notably, Zfp711 binds the Atf3 promoter, suggesting a hierarchical regulation. In contrast, ΔBcl6b had no observable effects on early hematopoiesis, despite specific expression in hemato-endothelial progenitors. - Source: PubMed
Publication date: 2025/12/08
Cetin RidvanPicco Giuliavan Staalduinen JenteBindels EricHoogenboezem Remcovan Beek GregorySanders Mathijs AFidan YarenKorkmaz AhmetGribnau Joostvan Haren JeffreyHuylebroeck DannyMulugeta EskeatnafGrosveld Frank - Glioma is a highly malignant tumor of the central nervous system characterized by high morbidity, substantial drug resistance, and poor prognosis. Therapeutic challenges stem from the invasive growth of tumor cells, limited drug penetration through the blood-brain barrier (BBB), and widespread drug resistance induced by the tumor microenvironment. In recent years, biotherapeutic strategies based on the biological characteristics of circular RNAs (circRNAs) have emerged as promising avenues for glioma management. circNEFM functions as a competitive endogenous RNA (ceRNA) by sponging miR-1248 and miR-1236, thereby upregulating the expression of BCL6B and C1orf115. This molecular mechanism of circNEFM effectively inhibits tumor proliferation while sensitizing glioma cells to chemotherapy. However, conventional delivery systems have inherent limitations, including short systemic circulation time and inadequate local drug concentration. To overcome these challenges, in this study, we engineered a multifunctional GelMA hydrogel scaffold system that integrates three key advantages: the innate ability of exosomes to traverse the BBB while protecting their cargo from enzymatic degradation, aptamer-mediated precise tumor targeting, and the sustained release profile of GelMA hydrogels. This composite scaffold exhibited excellent biomechanical properties and enabled the controlled release of engineered exosomes loaded with circNEFM (exo-circNEFM). Notably, aptamer-functionalized exosomes exhibited enhanced specificity to glioma cells, leading to significant inhibition of cell proliferation through circNEFM-mediated pathways and effective reversal of chemoresistance. This innovative therapeutic platform represents a novel technological solution with considerable translational potential for glioma treatment. - Source: PubMed
Publication date: 2025/10/30
Fu SongningTian ZhisenLiu LuZhou ZongyiLiu TianyuYang QiweiWang Yuanyi - The B-cell CLL/lymphoma 6B (BCL6B) gene, a homolog of , belongs to the ZBTB (zinc finger and BTB domain-containing) protein family and functions as a transcriptional repressor involved in gene regulation and cellular proliferation. In recent years, BCL6B has garnered increasing attention due to its critical involvement in various biological processes, including tumor suppression, immune modulation, stem cell maintenance, and angiogenesis. Moreover, its dysregulation, often through epigenetic modifications such as promoter hypermethylation, has been implicated in the pathogenesis of several malignancies and immune-related disorders. This review provides a comprehensive overview of BCL6B's molecular functions, its roles in human disease, and emerging research advances, highlighting its potential as both a diagnostic biomarker and a therapeutic target. - Source: PubMed
Publication date: 2025/08/16
Pan YuqingLi Ya - We have previously demonstrated that the inhibitory effect of metformin on skeletal muscle mitochondrial respiration was associated with attenuated improvements in whole body insulin sensitivity and cardiorespiratory fitness after aerobic exercise training (AET) in older adults. To identify processes associated with the inhibitory effect of metformin on mitochondrial adaptations to AET, we evaluated the skeletal muscle transcriptome, mitochondrial respiration, and hydrogen peroxide (HO) emissions in 7-mo-old male C57BL6/J mice after 8 wk of nonexercise sedentary control (SED) or progressive AET with and without metformin treatment. Similar to our findings in humans, metformin diminished the improvement in whole body cardiometabolic adaptations and the increase in mitochondrial respiration in both isolated mitochondria and permeabilized muscle fibers after AET in mice. However, AET with or without metformin did not impact resting mitochondrial HO emissions. Metformin decreased the number of differentially expressed genes after AET by ∼50% and suppressed several transcription factors and signal transduction pathways involved in skeletal muscle proteostasis, myogenesis, oxidative capacity, and angiogenesis. A parallel analysis of human resistance exercise data revealed overlapping metformin-sensitive transcription factors and B Cell CLL/Lymphoma 6B (BCL6B)-associated signaling networks implicated in angiogenesis, suggesting a conserved regulatory axis across species and exercise modalities. Collectively, these data demonstrate that attenuation of mitochondrial respiration by metformin coincides with transcriptional repression and identify specific pathways and regulators, such as BCL6B, that may contribute to the suppression of exercise adaptations by metformin. Metformin inhibited skeletal muscle mitochondrial respiration and transcriptional adaptations to aerobic exercise training. The findings from this study suggest BCL6B as a conserved exercise-responsive transcription factor in mice and humans that is sensitive to metformin, enriched in endothelial cells, and implicated in angiogenesis. - Source: PubMed
Publication date: 2025/07/22
Bruss Matthew DElliehausen Christian JClark Josef PMinton Dennis MKonopka Adam R