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anti-Mouse (Murine) BCL6 Anticorps:
anti-Human BCL6 Anticorps:
anti-Rat (Rattus) BCL6 Anticorps:
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Human Monoclonal BCL6 Primary Antibody pour 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. dans The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 2005
Show all 2 Pubmed References
Human Polyclonal BCL6 Primary Antibody pour 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. dans Immunology letters 2017
Human Polyclonal BCL6 Primary Antibody pour 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. dans Blood 2006
Human Polyclonal BCL6 Primary Antibody pour 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. dans Journal of experimental & clinical cancer research : CR 2018
BCL6 forms a complex with BCL6 corepressor (BCoR) on the promoters of selected Notch target genes such as enhancer of split related 1.
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.
These data describe a novel regulatory mechanism through which STAT3 and the Ikaros zinc finger transcription factors Aiolos and Ikaros cooperate to regulate Bcl-6 expression.
Our data reveal a regulatory role of BCL6 in inhibiting antiviral resistance factors in follicular Th cells
data provide a novel mechanism for positive control of gene expression by Bcl6, and illuminate how Bcl6 and Blimp1 control follicular helper T cell differentiation
both mouse and human B cells, IFN-gamma synergized with B cell receptor, toll-like receptor, and/or CD40 activation signals to promote cell-intrinsic expression of the GC master transcription factor, B cell lymphoma 6 protein.
observations reveal that KLF6 repress BCL6 to enhance macrophage inflammatory gene expression and function.
synergistic activity of Card11 mutant and Bcl6 in the development of diffuse large B-cell lymphoma in a mouse model
Bcl6, by interacting with the co-factors NcoR2 and HDAC3, plays a pivotal role in controlling IRF7 induction and antiviral signaling priming.
Bcl6 promoted T follicular helper cell differentiation through antagonizing IL-7R / STAT5a axis.
Bob1 directly binds to and transactivate the Bcl6 promoter during the development of follicular T helper cells .
upon binding to a composite NFAT/BCL6 regulatory element within the Ccl2 promoter, NFATc1/beta proteins release the BCL6-dependent repression of Ccl2 gene in macrophages.
transferred Bcl6-deficient T cells into wildtype hosts. Bcl6-deficient T cells did not develop into GC Tfh, but they still generated CXCR5+ IFN-gamma+ IL-21+ IL-10+ Teff, suggesting that this predominant population is not of the Tfh-lineage
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
Double-hit lymphoma (DHL) is an aggressive form of DLBCL with an unmet treatment need, in which MYC rearrangement is present with either BCL2 or BCL6 rearrangement
BCL6 is a growth promoting factor in glioblastoma and glioma.
IFN gamma induced upregulation of BCL6 was dependent on the classical STAT1 signaling pathway, and affected both major BCL6 variants. Interestingly, although IFN alpha induced stronger STAT1 phosphorylation than IFN gamma, it only slightly upregulated BCL6 in multiple myeloma lines.
Findings demonstrate that BCL6 expression is downregulated by miR-519d which targets its 3 '-UTR. Also, BCL6 mediates the repression of miR-519d on cell proliferation and invasive capability of gastric cancer cells.
In Pakistani population, the frequency of GCB type DLBCL [diffuse large B cell lymphoma ]expressing CD10 and BCL6 is 37.5%, and non- GCB type DLBCL [diffuse large B cell lymphoma ] expressing MUM1 is 62.5%.
BCOR internal tandem duplication and/or nuclear immunoreactivity for BCOR or BCL6 can aid in the diagnosis of primitive myxoid mesenchymal tumor of infancy and help to differentiate it from congenital infantile fibrosarcoma.
our findings provide a novel apoptotic regulatory pathway in which LITAF, as a transcription factor, inhibits the expression of BCL6, which leads to activation of the intrinsic mitochondrial pathway and tumor apoptosis.
Ikaros regulates expression of the BCL6/BACH2 axis in acute lymphoblastic leukemia cells.
our work casts new light on the biology of mantle cell lymphoma (MCL), revealing the role of SOX11 exerting a functional effect through the repression of BCL6 transcription in MCL cells
BCL6 inhibitors have been shown to exert potent effects against these tumor types. Moreover, mechanism-based combinations of BCL6 inhibitors with other agents have yielded synergistic and often quite dramatic activity. Hence, there is a compelling case to accelerate the development of BCL6-targeted therapies for translation to the clinical setting
High BCL6 expression is associated with good response to chemotherapy in acute lymphoblastic leukemia.
this study show that PATZ1 expression correlates positively with BAX and negatively with BCL6 and survival in human diffuse large B cell lymphomas
BCL6 expression is present in isolated cortical neurons, granule cells in the cerebellum, scattered glial cells, and in some cells of the ependyma and choroid plexus.
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