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anti-Mouse (Murine) BCL6 Antibodies:
anti-Human BCL6 Antibodies:
anti-Rat (Rattus) BCL6 Antibodies:
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Human Polyclonal BCL6 Primary Antibody for IF (p), IHC (p) - ABIN749843
Szabó, Gáspár, Dajnoki, Papp, Fábos, Szegedi, Zeher: Expansion of circulating follicular T helper cells associates with disease severity in childhood atopic dermatitis. in Immunology letters 2017
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Human Monoclonal BCL6 Primary Antibody for IHC, WB - ABIN2668887
García, García, Maestre, Lucas, Sánchez-Verde, Romero-Chala, Piris, Roncador: Genetic immunization: a new monoclonal antibody for the detection of BCL-6 protein in paraffin sections. in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 2005
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Human Polyclonal BCL6 Primary Antibody for ELISA, ICC - ABIN6260236
Huang, Zhang, Hou, Wang, Liu, Zhang, Chen, Zhu: LncRNA AK023391 promotes tumorigenesis and invasion of gastric cancer through activation of the PI3K/Akt signaling pathway. in Journal of experimental & clinical cancer research : CR 2018
Human Polyclonal BCL6 Primary Antibody for WB - ABIN4283623
Margalit, Amram, Amariglio, Simon, Shaklai, Granot, Minsky, Shimoni, Harmelin, Givol, Shohat, Oren, Rechavi: BCL6 is regulated by p53 through a response element frequently disrupted in B-cell non-Hodgkin lymphoma. in Blood 2006
BCL6 forms a complex with BCL6 corepressor (BCoR) on the promoters of selected Notch target genes such as enhancer of split related 1.
These data reveal that by replacing an activating complex of Batf and Irf-4 at the Bcl-6 promoter, Bach2 regulates the transcriptional network of Tfh cells in a different way, as in GC B cells.
Thpok also promoted the expression of Bcl6-independent genes, including the transcription factor Maf.
These studies identify BCL6 as a negative regulator of subcutaneous adipose tissue expansion and metabolic health.
acute loss of BCL6 in germinal center B cells led to remarkable upregulation of mRNA and protein abundance of PD-L1 and PD-L2
PRMT5 contributes to germinal center formation and affinity maturation at least in part through its direct interaction with and methylation of BCL6 at arginine 305 (R305), a modification necessary for the full transcriptional repressive effects of BCL6.
The current study provides evidence for a novel role of Bcl6 in the functional regulation of memory t cells, implying interplay between Bcl6 and transcriptional activators to promote the production of relevant TH2 cytokines, particularly IL-4.
Results provide evidence that LAZ3 is required for negative regulation of cardiac remodeling in the diabetic cardiomyopathy (DCM) heart. Notably, when the heart and cardiomyocytes were subjected to silencing LAZ3, it developed severe inflammation, oxidative stress and apoptosis spontaneously.
Study identified RANKL and BCL6 mRNA as targets of AUF1 p42. Detailed analysis of 3'UTRs revealed for both that full instability required two elements, which are conserved in evolution. In RANKL mRNA both elements are AU-rich and separated by 30 bases, while in BCL6 mRNA one is AU-rich and 60 bases from a non-AU-rich element that potentially forms a stem-loop structure.
results suggest that p53 may block oncogenic transformation by decreasing BCL6 stability via caspase-1 up-regulation, whereas aberrant BCL6 expression inactivates transactivation of p53 target genes, either by inhibiting p53 acetylation by p300 or repressing TP53 gene transcription. These findings have implications for B cell development and lymphomagenesis.
Ezh2 is recruited by Tcf1 to directly activate Bcl6 transcription, with this function requiring Ezh2 phosphorylation at Ser21.
GATA3 and BCL6 inhibit T-regulatory cells from becoming novel Antigen-Presenting Cell-T-regulatory cells .
Bcl-6, expressed in abundance in Tfr cells, inhibits CD25 expression and IL-21-mediated inhibition of CD25 is Bcl-6 dependent.
Together these results identify BCL6 as a potential driver of ETV6-RUNX1-mediated leukemogenesis, which could involve loss of BTG1-dependent suppression of ETV6-RUNX1 function.
this study shows that IL4 and IL21 cooperate to induce the high Bcl6 protein level required for germinal center formation
Although BCL6 controls follicular helper T cells activity in humans and mice, the role of miR-31 is restricted to human follicular helper T cell differentiation, reflecting a species specificity of the miR-31 action.
These findings indicate a role of the interaction between TH2-promoting factors and Bcl6 in promoting appropriate IL-4 production in mTH2 cells and suggest that chronic allergic diseases involve the TH2-promoting factor-mediated functional breakdown of Bcl6, resulting in allergy exacerbation.
Bioinformatics analysis and the dual-luciferase reporter assay demonstrated that miR-10b could target the 3'-untranslated regions of B cell lymphoma 6 (Bcl6) which is an important regulator of osteoblast differentiation.
Def6 limits proliferation of T follicular helper cells in mice via alteration of mTORC1 signaling and inhibition of Bcl6 expression.
The balance between CD4(+) cytotoxic T cell and follicular helper T(Tfh) differentiation heavily depends on the class of infecting virus and is jointly regulated by the Tfh-related transcription factors Bcl6 and Tcf7 (encoding TCF-1) and by the expression of the inhibitory receptors PD-1 and LAG3.
Study provides evidence for an essential role of Bcl6 in the complex regulation of gene transcription during early adipogenesis. The action of Bcl6 is at least partially mediated by the direct transcriptional activation of STAT1.
BCL6 is overexpressed in the bone marrow of methotrexate-resistant children with acute B lymphoblastic leukemia.
findings uncover MLL-dependent transcriptional activation of BCL6 as a previously unrecognized requirement of malignant transformation by oncogenic MLL fusions and identified BCL6 as a novel target for the treatment of MLL-rearranged B-ALL.
Studied expression of myocyte enhancer factor 2B (MEF2B) as part of the diffuse large (DLBCL) B-cell lymphoma 6 (BCL6) transcription complex in diffuse large B-cell lymphoma tissue samples and cell lines. Findings indicate MEF2B to be an essential component of the BCL6 gene transcriptional complex for the regulation of DLBCL growth thru promotion of BCL6 expression.
Low BCL6 expression is associated with MYC-positive diffuse large B-cell lymphoma.
Inhibition of PRMT5 in B-cell lymphoma lines led to significant upregulation of BCL6 target genes, and the concomitant inhibition of both BCL6 and PRMT5 exhibited synergistic killing of BCL6-expressing lymphoma cells.
In univariate time-to-event regression, diffuse large B cell lymphoma patients with either MYC or BCL2 expression and patients with concurrent overexpression of MYC and BCL2 had a 2.1-fold higher (P = 0.009) and 2.4-fold higher (P = 0.009) risk of progression or death within the first 5 years of follow-up than patients without DEL, respectively
Mutual regulation between BCL6 and a specific set of miRNAs controls TFH phenotype in peripheral T-cell lymphoma.
WTAP is a client protein of Hsp90 and can appear in a complex with BCL6 and Hsp90 in DLBCL
ML364 decreases the BCL6 protein stability in K562/G01 by inhibiting the USP2-mediated deubiquitination, and down-regulate the BCL6 protein experssion
BCL6 attenuates proliferation and oxidative stress of vascular smooth muscle cells in hypertension.
Studied role of B cell CLL/lymphoma 6 (BCL6) in malignancy and found BCL6 is expressed at a high level in glioma when compared with non-tumor brain tissues. The downregulation of BCL6 was shown to inhibit proliferation, migration, and invasion, promote apoptosis, and induce cell cycle arrest via the AKT and MAPK pathway.
KRAS, SIRT1 and BCL6 are coordinately over-expressed in eutopic endometrium of women with endometriosis
BCL6 translocation was detected in 15 (12%) cases. Translocation involving MYC and BCL2 was identified in 3 cases (3.8%) and 1 case (1.3%) respectively. One double hit lymphoma was discovered with both MYC/BCL2 translocation (1.3%).
Fluorescence in situ hybridization studies (histologic sections) confirmed translocations of MYC (8q24), BCL2 (18q21) and BCL6 (3q27) in all patients.
our exploratory study suggests that EOMES, BCL6 and GZMB gene expression are aberrant within the PB T cell transcriptome of HT patients. The association of this transcription signature with the heterogeneity of HT and disease control is suggested.
Cryptic t(3;8)(q27;q24) and/or MYC-BCL6 linkage associated with MYC expression by immunohistochemistry is frequent in multiple-hit B-cell lymphomas
BCL6 overexpression in SHR reduced blood pressure, NLRP3 expression and inflammation in the renal cortex of SHR
Aberrant CD10 and BCL6 expression defines a subset of MCLs with higher mean Ki-67 index and higher prevalence of MUM1 expression
The protein encoded by this gene is a zinc finger transcription factor and contains an N-terminal POZ domain. This protein acts as a sequence-specific repressor of transcription, and has been shown to modulate the transcription of START-dependent IL-4 responses of B cells. This protein can interact with a variety of POZ-containing proteins that function as transcription corepressors. This gene is found to be frequently translocated and hypermutated in diffuse large-cell lymphoma (DLCL), and may be involved in the pathogenesis of DLCL. Alternatively spliced transcript variants encoding different protein isoforms have been found for this gene.
B-cell CLL/lymphoma 6
, B-cell CLL/lymphoma 6 (zinc finger protein 51)
, B-cell lymphoma 6 protein
, zinc finger protein 51
, B-cell leukemia/lymphoma 5
, B-cell leukemia/lymphoma 6
, B-cell lymphoma 6 protein homolog
, B-cell lymphoma 5 protein
, B-cell lymphoma 6 protein transcript
, cys-his2 zinc finger transcription factor
, lymphoma-associated zinc finger gene on chromosome 3
, protein LAZ-3
, zinc finger and BTB domain-containing protein 27
, zinc finger transcription factor BCL6S