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Validated All-in-One™ qPCR Primer for BCL6(NM_001130845.1) Search again
Product ID:
HQP055166
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BCL5, BCL6A, LAZ3, ZBTB27, ZNF51
Gene Description:
BCL6 transcription repressor
Target Gene Accession:
NM_001130845.1(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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. [provided by RefSeq].
Gene References into function
- BCL6 may regulate apoptosis by means of its repressive effects on PDCD2
- A senescence rescue screen identifies BCL6 as an inhibitor of anti-proliferative p19(ARF)-p53 signaling
- gene reearranged in non-hodkgin's lymphoma
- Class II histone deacetylases are directly recruited by BCL6 transcriptional repressor
- Bcl6 mediates repression of IL-5 gene expression by binding specifically to a DNA sequence on the 3' untranslated region of the IL-5 gene.
- BCL-6 regulates the Blimp-1 promoter through a novel mechanism involving AP-1 elements.
- bcl-2/Jh lymphomas show molecular heterogeneity and that bcl-6 and p53 mutations may be acquired during the evolution of such lymphomas
- REVIEW: those BCL6 translocations with non-immunoglobulin genes placing the rearranged BCL6 gene under the control of the replaced promoter activity; its role in pathogenesis of diffuse large b-cell lymphomas
- Frequent occurrence of BCL6 rearrangements in nodular lymphocyte predominance Hodgkin lymphoma but not in classical Hodgkin lymphoma indicate a significant role of BCL6 in the pathogenesis of NLPHL.
- Role of BCL6 in B cell development and in lymphoma [review]
- the distinct profile of BCL-6 expression in Jijoye/Clone-13 is due to either a missing negative element in a different portion of the gene or that there is an issue of chromatin accessibility operating in BCL-6 gene regulation
- high frequency of BCL-6 mutations discovered in primary mediastinal B-cell lymphoma
- A subset of mutations specifically associated with diffuse large B-cell lymphoma pathogenesis causes deregulated BCL6 transcription by preventing BCL6 from binding its own promoter, thereby disrupting its negative autoregulatory circuit.
- plays a role in immune memory development--review
- role in cell survival and transformation
- Expression of Bcl-6 in primary central nervous system diffuse large B-cell lymphoma may be a prognostic marker for poor overall survival.
- Junctional sequences indicate translocation origins from earlier BCL-6 mutations and switch recombinase events in non-Hodgkin B-cell lymphoma
- tumor specimens expressed BCL6 mRNA predominantly from the rearranged allele that may come under the control of various partner gene promoters
- results show that BCL6 prevents CD40-induced expression of CD80 by binding its promoter region in vivo and suppressing its transcriptional activation by NF-kappaB
- bcl-2 and bcl-6 proteins may play a role in the pathogenesis of transitional cell carcinoma, and bcl-6 expression reflects histopathologic grade.
- BCL6 overexpression was found to inhibit the increase in ROS levels and apoptosis in response to etoposide and other chemotherapeutic reagents.
- BCL-6 oncogene activation plays a role in breast cancers, not just lymphomas.
- This study suggest translocation-mediated BCL6 oncogene activation as a so far unknown pathogenetically relevant mechanism in PCNSL.
- Data describe a 17 residue fragment from SMRT that binds to the BCL6 BTB domain, and report the crystal structure of the complex to 2.2 angstroms.
- BCL6 translocation has a pathogenic in B-cell non-Hodgkin's lymphoma (review)
- Rearrangements of the BCL6 locus were detected in five B-cell lymphomas of the leg, and involved IGH (two cases), IGL (one case), and non-IG genes (two cases).
- REVIEW recently identified deacetylation pathways resulting in the accumulation of inactive acetylated Bcl-6 and thus in cell cycle arrest and apoptosis in B-cell lymphoma cell
- Cytogenetic alterations affecting BCL6 are predominantly found in follicular lymphomas grade 3B with a diffuse large B-cell component
- Nodular lymphocyte-predominant Hodgkin's lymphoma (NLPHL) showed recurrent rearrangement of the BCL6 gene.
- Meta-analysis showed that the preferentially altered sequence motifs of BCL6 in PMBL were TA & AT and TAT. GC & RGYW/WRCY motifs were a target in DLCL & FL but not in PMBL. Nucleotides 150-270 were highly targeted only in PMBL.
- conditional activation of FoxO3a leads to accumulation of BCL6 and down-regulation of cyclin D2 at protein and mRNA levels
- an important function of BCL6 is possibly to allow germinal-centre B cells to tolerate the physiological DNA breaks required for immunoglobulin class switch recombination and somatic hypermutation without inducing a p53-dependent apoptotic response
- Point mutations in the 5' noncoding region of BCL-6 gene are found in Chinese patients with primary gastric lymphomas and MALT lymphomas
- single-nucleotide polymorphisms and acquired somatic mutations of the BCL6 first intron is associated with follicular lymphoma
- Many of the novel binsubf proteins identified in this study suggest additional functional roles for BCL6 beyond transcriptional repression.
- We present here a case of Follicular Lymphoma with leukemic presentation and a complex translocation involving the IgH, BCL2 and BCL6 loci
- BCL6 gene is a new p53 target, regulated through a p53 response element in B-cell lymphoma.
- Our results support the hypothesis that a genetic variant that could alter mRNA transcripts of BCL6 may contribute to the etiology of NHL (non-Hodgkin lymphoma).
- By regulating the induction of several genes implicated in the immune response, including inflammatory cytokines, chemokines and survival genes, BCL6 may represent a pivotal modulator of the afferent branch of the immune response.
- BCL-6 expression was asfavorable prognostic factor in patients with diffuse large B-cell lymphoma of central nervous system origin and peripheral nodal origin.
- BCL6 associates and colocalizes with BCL11A-XL in nuclear paraspeckles.
- Ig/BCL6 translocations occur in germinal center-stage B cells in healthy humans, and Ig/BCL6 translocations per se are not likely sufficient to cause malignant transformation in B cells.
- The bcl6 gene is involved based on the presence of a breakpoint in the alternative breakpoint region and nuclear staining for the BCL6 protein.
- The proto-oncogene BCL6, a potential target of miR-127, was translationally downregulated after treatment with the chromatin-modifying drugs.
- BCL6 has a role in preventing progression of gastric lymphoma
- Stage B immunoproliferative small intestinal disease (IPSID) showed higher expression for bcl6 and p53 than stage A IPSID. bcl6 and p53 expressions correlated with a more advanced disease stage and aggressive tumour behavior.
- Review. BCL6 encodes a nuclear transcriptional repressor, with pivotal roles in germinal center formation & lymphocyte function, differentiation, & survival. It suppresses p53& protects B-cells from apoptosis induced by DNA damage.
- Downregulation of BCL6 is associated with lymphomas
- DNA sequence analysis of the junctional sequences provided evidence that aberrant class switch recombination or somatic hypermutation may be involved in the generation of BCL6 translocations.
- BCOR complex components and mono-ubiquitylated H2A localize to BCL6 targets, indicating that the BCOR complex employs Polycomb Group proteins to expand the repertoire of enzymatic activities that can be recruited by BCL6.
- In EBV-negative diffuse large B-cell lymphoma and Burkitt lymphoma-derived cell lines infected in vitro with a recombinant EBV, high expression of EBNA2 inversely correlated with expression of germinal center-associated genes, BCL6 and TCL1.
- The present study suggests that bcl-6 protein DLBCL requires alternative treatment strategies.
- MUM1 expression dichotomises follicular lymphoma (FL) into low-grade FL of CD10+/Bcl-6+/MUM1-/Ki-67low phenotype, and high-grade FL of CD10+/- /Bcl-6+/weak/MUM1+/ Ki-67high phenotype
- A discrete subset of diffuse large B cell lymphomas are reliant on BCL6 signaling and uniquely sensitive to BCL6 inhibitors.
- HB-EGF carboxyl-terminal fragment is a potent regulator of gene expression via its interaction with the transcriptional repressor Bcl6.
- expression of BCL-6 in human B cell cultures resulted in formation of fewer memory B cells
- repression of programmed cell death 2 by BCL6 is likely important in the pathogenesis of certain human lymphomas
- BCL-6 mutation is associated with splenic and nodal marginal zone B-cell lymphomas
- BCL6 protein over-expression as well as BCL6 gene mutation of the E1.12 fragment may play an important role in the morphological differentiation of transitional call carcinoma
- Bcl-6 mediates the B cell phenotype by directly targeting the ataxia telangiectasia- and Rad3-related (ATR) gene in centroblasts and lymphoma cells.
- lower mutational frequencies & decreased BCL-6 mRNA expression in vivo suggest no major role of aberrant somatic hypermutation in HCV-associated mixed cryoglobulinaemia & B-cell non-Hodgkin lymphoma
- Results suggest that increased squamous metaplasia and lower BCL-6 expression in adenoids may be associated with increased susceptibility to otitis media with effusion.
- analysis of BCL6 molecular alterations and their functional consequences in different subgroups of diffuse large B-cell lymphoma
- Immunohistochemical germinal center-status determined on tissue microarray is not reliable enough to be used for individual treatment decisions in diffuse large B-cell lymphoma, mostly due to difficulties in interpreting BCL6 status
- Sodium arsenite dose dependently alters STAT3 and JAK2 activities via Bcl-6 and this may have a role in arsenic-associated carcinogenesis.
- Chromosomal transloacations or mutations that disrupt the IRF4-responsive region in the BCL6 promoter block its downregulation by CD40 signaling and is associated with B cell lymphoma.
- Study shows that the expression of Bcl-6 is regulated by DNA damage through a signaling pathway that promotes Bcl-6 degradation.
- a novel translocation involving BCL6 may have a role in diffuse large B-cell lymphoma [case report]
- T(3;7)(q27;q32) fusion with BCL6 to a non-coding region at FRA7H near miR-29 results in Diffuse Large B-Cell Lymphomas
- synergistic effect of MYC and BCL6 mutations could explain survival and clonal selection of a t(3;8) carrying cell in lymphoma progression
- analysis of BCL6 chromosomal translocations in MALT lymphoma
- Clinical and histological differences between BCL2-/BCL6+ and BCL2+/BCL6+ tumours could reflect an interplay between both translocations.
- BCL6 can interact with CtBP in vitro & in vivo. CtBP is recruited by BCL6 to its 5' regulatory region. CtBP corepression of BCL6 autoregulation may control the GC stage of B cell development.
- reporter assays demonstrated that Bach2 and Bcl6 cooperate to repress Prdm1 through its intron enhancer region
- findings show that BCL6 can directly bind to a DNA consensus element in the CHEK1 promoter and repress its expression in normal and malignant B-cells
- concomitant down-regulation of BCL6 is absolutely required for completion of the plasma cell differentiation program
- CD40 signaling rapidly disrupts the ability of BCL6 to recruit the SMRT corepressor complex by excluding it from the nucleus, leading to histone acetylation, RNA polymerase II processivity, and activation of BCL6 target genes
- BCL6 gene aberration, especially amplification/3q27 gain, indicates the presence of certain morphological and phenotypical findings in follicular lymphoma cases.
- Bcl-6 expression alone proved to be a prognostic marker in primary nodal DLBCL
- BCL6S is a compact repressor that may have a functional role in normal and neoplastic germinal center B cells.
- In a cohort of 25 children with PTLD, 9 of the patients' tumor specimens were positive for BCL6 protein expression
- BCL-6 expression by diffuse large B-cell lymphoma cells appears to be associated with poorer prognosis.
- A method for the purification and crystallization of the wild-type BCL6 POZ domain is described and the crystal structure to 2.1 A resolution is reported.