Atlas of Genetics and Cytogenetics in Oncology and Haematology


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BCL6 (B-Cell Lymphoma 6)

Identity

Other namesBCL5
LAZ3
ZBTB27
ZNF51
BCL6A
HGNC (Hugo) BCL6
LocusID (NCBI) 604
Location 3q27.3
Location_base_pair Starts at 187439165 and ends at 187454285 bp from pter ( according to hg19-Feb_2009)  [Mapping]
Local_order Gene orientation: telomere - 5' BCL6 3' - centromere.
 
  BCL6 (3q27) - Courtesy Mariano Rocchi, Resources for Molecular Cytogenetics.

DNA/RNA

 
Description The gene is encoded by 11 exons that are located on chromosome 3q27 and is 24,3 kb. The 5' portion encodes for the BTB/POZ domain (broad-complex/tramtrack/bric-a-brac/pox virus/zinc finger), while the 3' end encodes for 6 DNA binding zinc fingers. The first ATG occurs in exon 3.
Transcription 3,8 kb mRNA.

Protein

 
Description The protein product is 706 amino acids with an estimated molecular weight of 78,8 kDa.
Expression Normally expressed in germinal center B and T cells, other lymphoid tissues, in skeletal muscle cells and in keratinocytes. Normally expressed in germinal center B and T cells, other lymphoid tissues, in skeletal muscle cells and in keratinocytes.
Localisation Nuclear paraspeckles/dots.
 
Function Protein domains and functions
The protein can bind to sequence specific DNA and repress its transcription in addition to recruiting other protein repressors. The DNA binding is mediated through the consensus sequence TTCCT(A/C)GAA (see below), while the protein-protein interactions are mediated through the BTB/POZ domain and it has been shown to interact with other zinc finger proteins and corepressors (including Histone Deacetylase 1 (HDAC1) and NCOR2 (Silencing Mediator of Retinoid and Thryoid Receptor 1 (SMRT1))). The carboxy terminus, on the other hand, is responsible for sequence specific DNA binding through its 6 zinc fingers.

Consensus DNA motifs recognized by BCL6
The Zn fingers of BCL6 binds to DNA and recognizes specific DNA motifs: the M00424 motif, a consensus sequence for the NKX-homeobox family of transcription factors, the M2 motif, which mimics an M00424 half site; and the M0 motif (see details in Basso et al., 2010).

BCL6 cellular function
- BCL6 cellular function in germinal centers of lymph nodes follicles
Mature naïve B cells migrate from the bone marrow to lymphoid nodes, meet the antigen, they are stimulated to proliferate and further differentiate into centroblasts in germinal centers (GC) of lymphoid follicles. There, cells are subjects to somatic hypermutation and class switch recombination, to further differenciate into memory B cells or plasma cells. This process also requires the presence of follicular helper T cells. BCL6 has a major role in this process. In particular, BCL6 prevents ATM and TP53 (Phan et al., 2004) to induce apoptosis in response to DNA rearrangements such as those necessary for somatic hypermutation and class switch recombination processes. BCL6 is therefore essential for normal B cell development (reviews in Albagli-Curiel, 2003; Jardin et al., 2007; Parekh et al., 2008; Basso and Dalla-Favera, 2010; Pellicano and Holyoake, 2011; Wagner et al., 2011; Basso and Dalla-Favera, 2012; Okada et al., 2012).
- T follicular helper cells
BCL6 is essential for the development of follicular helper T (Tfh) cells. Tfh cells are defined by the expression of the surface markers CXCR5 and PD-1 and synthesis of IL4 and IL21. BCL6 upregulation of B cells in the outer follicle sustains their interactions with helper T cells and allows them to enter the germinal centers (GC) region (Poholek et al., 2010; Kitano et al., 2011; Baumjohann et al., 2011). ICOS induces BCL6, and BCL6 then induces CXCR5. Tfh cells were lost in the absence of B cells, demonstrating a B cell requirement for maintenance of BCL6 and Tfh cell commitment (Choi et al., 2011). BCL6 and MAF cooperate to induce Tfh cell differentiation (Kroenke et al., 2012).
- Other tissues
BCL6 promotes survival of olfactory sensory neurons (Otaki etal., 2010).
BCL6 associate to NACC1 in brain regions (Korutla et al., 2009).
BCL6 forms a complex with BCOR on the promoters of Notch target genes in Xenopus embryos (Sakano et al., 2010).
BCL6-overexpression inhibits osteoclastogenesis, and the PRDM1 (Blimp-1)/BCL6 balance is essential in regulating the bone homeostasis by controlling osteoclastogenesis (Miyauchi et al., 2010).
BCL6 controls the expression of the CC-type chemokine genes and attenuates allergic airway inflammation in pulmonary epithelium (Seto et al. 2011).

BCL6 repression activity
BCL6 binds to DNA as a homodimer and recruits co-repressor molecules, which, in turn, recruit class I and II histone deacetylases. BCL6 and histone deacetylases (HDACs) form stable complexes. BCL6 binds HDACs both directly through its C-terminal Zn fingers and through its N-terminal BTB/POZ domain and indirectly by recruiting several co-repressors such as BCOR, NCOR1, NCOR2 (which bind in a mutually exclusive way to the BTB/POZ domain), CTBP1 (which binds the BTB/POZ and the PEST domains), and MTA3 (which binds the PEST domain). Deacetylation of histones leads to transcriptional repression of BCL6 targets.
BCL6 interacts with ZBTB17 to repress CDKN1A and BCL2 (Phan et al., 2005). BCL6 has also been found to interact with other POK family members ((POZ and Krüppel)/ZBTB (zing finger and BTB) protein family) such as ZBTB7A (LRF) and ZBTB16 (PLZF).

BCL6 targets
An integrated biochemical and computational approach has recently identified thousands of BCL6 direct target genes, including B cell receptor (BCR; note: nothing to do with BCR, the partner of ABL1) and CD40 signaling genes (involved in signal transduction, MAPK activation, NF-AT activation, and NF-kB activation); T cell-mediated B-cell activation; apoptosis (BCL2, proteins involved in positive and negative regulation of the DISC complex and caspase activation, suggesting a role for BCL6 in balancing pro- and antiapoptotic programs in GC B cells); response to DNA damage (ATM, TP53, CDKN1A, ATR, CHEK1, TP53BP1...); interferon and cytokine signaling (interferon-type and interleukin receptors that lead to activation of JAK/STAT. STAT1, STAT3, and STAT5A were also found to be directly repressed by BCL6); Toll-like receptor signaling; TGFb receptor signaling; and WNT signaling (Basso et al., 2010).

BCL6 regulation
- B cell receptor
B cell receptor (BCR) induces BCL6 phosphorylation by MAPK1 on Ser333 and Ser343, which targets BCL-6 for rapid degradation by the ubiquitin/proteasome pathway (Niu et al., 1998). FBXO11 promotes BCL6 ubiquitylation and degradation (Duan et al., 2012).
- DNA damage
After DNA damage, the kinase ATM promotes BCL6 phosphorylation; follows an interaction with PIN1 required for BCL6 degradation (Phan et al., 2007).
- EP300
EP300 binds and acetylates BCL6, which inactivates BCL6 (acetylation disrupts the ability of BCL6 to recruit histone deacetylases). The same two pathways (HDAC pathway and SIRT2 pathway) that regulate acetylation-mediated activation of TP53 also control acetylation-mediated inactivation of BCL6 (Bereshchenko et al., 2002). BCL6 represses the expression of EP300 and its cofactor BAT3 (Cerchietti et al., 2010). EP300 acetylates and activates PAX5 (He et al., 2011), which enhances BCL6.
- Autoregulation
BCL6 protein binds BCL6 gene promoter, and repress BCL6, mechanism of negative autoregulation (Pasqualucci et al., 2003). PATZ1 interacts with BCL6 and is required for its negative autoregulation (Pero et al., 2012).
- CD40 signaling
CD40 signaling activates various pathways, including NF-kB, NF-AT, and AP-1 (Francis et al., 1995). ILF2 (NF45) and ILF3 (NF90) form the nuclear factor of activated T-cells (NF-AT), a crucial transcription factor essential for productive T cell activation (Kao et al., 1994). CD40 signalling reduces BCL6 expression, through induction of IRF4 by the NF-kB pathway (Saito et al., 2007).
- PRDM1 (review in Crotty et al., 2010)
JUND/AP-1 and activated STATs drive high BCL6 expression in GC B cells (Arguni et al., 2006). STAT5 up-regulates BCL6 expression (Scheeren et al., 2005); in contrast, STAT3 up-regulates PRDM1 (Diehl et al., 2008) (the protein coded from PRDM1 is named Blimp-1). BCL6 directly promotes the expression of BACH2, which repress PRDM1 (Blimp-1). BCL6 also suppresses PRDM1 (Blimp-1) through repression of IRF4. IRF4 binds to and induces PRDM1. PRDM1 (Blimp-1) abrogates BCL6. PAX5 (protein name: BSAP) contributes to BCL6 expression (Nera et al., 2006; Tarlinton, 2011). PAX5 abrogates PRDM1 (Blimp-1), which abrogates PAX5. BCL6 and PAX5 promote the expression of AICDA and UNG (which have a major role in somatic hypermutation and class-switch recombination) (Alinikula et al., 2011). BCL6 positively regulates AICDA, IRF8, and MYB via repression of MIR155 (Basso et al., 2012). BCL6 mediates transcriptional repression by recruiting HDACs. MIR155 directly targets HDAC4 and indirectly attenuates BCL6 expression (Sandhu et al., 2012). PRDM1 (Blimp-1) represses BCL6, and also PAX5, MYC, and AICDA (review in Martins and Calame, 2008). IRF8 is expressed at the high levels in germinal center (GC) B cells. IRF8 binds BCL6 promoter and activates BCL6 (Lee et al., 2006).
It is also to be noted that IRF4 is involved in the t(6;14)(p25;q32) IRF4/IGH. PRDM1 (Blimp-1) is inactivated in about 50% of the activated B cell-like (ABC) subtype of diffuse large B cell lymphoma (ABC- DLBCL) (Mandelbaum et al., 2010).

 
Homology BTB/POZ - Zinc Finger proteins (PLZF, HIC1, KUP, BAZF, ttk (drosophila), BrC (drosophila)...).

Mutations

Note Chromosomal translocations involving BCL6 are found in 40% of diffuse large B-cell lymphomas (DLBCL), 5-10% of follicular lymphomas (FL), and 50% of nodular lymphocyte predominant Hodgkin lymphomas.
Mutations in the autoregulatory region of BCL6 leads to a constitutive BCL6 expression (Pasqualucci et al., 2003).
IRF4 response elements in the BCL6 gene mediate repression of BCL6. Mutations in the IRF4 repression region of BCL6 gene also leads to constitutive expression of BCL6 (Saito et al., 2007).
MYC, BCL2, and BCL6 rearrangements were detected in 6%, 15%, and 29% respectively of diffuse large B-cell lymphoma (DLBCL) patients. Double or triple rearrangements were detected in 3% of these patients. MYC rearrangement was associated with a significantly worse overall survival. BCL6 rearrangement also predicted a significantly shorter overall survival, especially for the non-GC phenotype (Akyurek et al., 2012).
 

Implicated in

Entity 3q27 rearrangements /NHL (non Hodgkin lymphomas)
Disease B cell non-Hodgkin Lymphoma (B-NHL)
Prognosis Generally considered to be a better prognosis if there is increased expression of BCL6. The mechanism by which its expression is increased does not seem to matter (ie different translocation partners increasing its expression results in the same prognosis).
Cytogenetics 3q27 rearrangements/aberrations are diverse and include: translocations, micro-deletions, point mutations and hypermutation. Approximately 50% of 3q27 translocations involves Ig genes at 14q32 (IgH), 2p12 (IgK) and 22q12 (IgL) (e.g. t(3;14)(q27;q32)). Less than half (~40%) include a variety of other chromosomal regions (1q21, 2q21, 4p11, 5q31, 6p21, 7p12, 8q24, 9p13, 11q13, 11q23, 12q11, 13q14-21, 14q11, 15q21; 16p11...). In addition, there are frequent bi-allelic alterations (translocation and deletion or mutation on the non-translocated allele).
Hybrid/Mutated Gene hybrid gene and transcripts are formed following promoter substitution between BCL6 and its different partners. Chimeric transcripts are generally detected containing the 5' part of the gene partner fused to the normal BCL6 exon 2 splice acceptor site. In some cases reciprocal chimeric transcripts driven by the 5' regulatory region of BCL6 fused to the partner gene coding region, have been characterised.
- t(1;3)(q25;q27) the gene in 1q25 is GAS5
- t(2;3)(p12;q27) the gene in 2p12 is IGK
- t(3;3)(q25;q27) the gene in 3q25 is MBNL1
- t(3;3)(q27;q27) the gene in 3q27 is ST6GAL1
- t(3;3)(q27;q27) the gene in 3q27 is EIF4A2
- t(3;3)(q27;q29) the gene in 3q29 is TFRC
- t(3;4)(q27;p13) the gene in 4p13 is RHOH
- t(3;6)(q27;p22) the gene in 6p22 is HIST1H4I
- t(3;6)(q27;p21) the gene in 6p21 is PIM1
- t(3;6)(q27;p21) the gene in 6p21 is SFRS3
- t(3;6)(q27;q15) the gene in 6q15 is SNHG5
- t(3;7)(q27;p12) the gene in 7p12 is IKZF1
- t(3;7)(q27;q32) the gene in 7q32 is FRA7H
- t(3;8)(q27;q24.1) the gene in 8q24.1 is MYC
- t(3;9)(q27;p24) the gene in 9p24 is DMRT1
- t(3;9)(q27;p11) the gene in 9p11 is GRHPR
- t(3;11)(q27;q23) the gene in 11q23 is POU2AF1
- t(3;12)(q27;p13) the gene in 12p13 is GAPDH
- t(3;12)(q27;q12) the gene in 12q12 is LRMP
- t(3;13)(q27;q14) the gene in 13q14 is LCP1
- t(3;14)(q27;q32) the gene in 14q32 is IGH
- t(3;14)(q27;q32) the gene in 14q32 is HSP90AA1
- t(3;16)(q27;p13) the gene in 16p13 is CIITA
- t(3;16)(q27;p11) the gene in 16p11 is IL21R
- t(3;19)(q27;q13) the gene in 19q13 is NAPA
- t(3;22)(q27;q11) the gene in 22q11 is IGL
Abnormal Protein No fusion protein.
  
Entity t(9;22)(q34;q11) leukemias
Disease BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR-ABL1 kinase inhibition (Duy et al. 2011).
In chronic myelogenous leukemia (CML), BCL6 acts as a critical effector downstream of FoxO in self-renewal signaling of CML-initiating cells. Therefore, pharmacological inhibition of BCL6 may represent a novel strategy to eradicate leukemia-initiating cells in CML (Hurtz et al., 2011).
  
Entity Breast cancer
Disease BCL6 protein is elevated in human breast cancers, especially in high-grade, poorly differentiated and metastatic breast cancer cases (Bos et al., 2003; Logarajah et al., 2003; Brill et al., 2010). PRL (prolactin) rapidly suppressed BCL6. Loss of PRL-STAT5a signaling and concomitant upregulation of BCL6 may represent a regulatory switch facilitating undifferentiated histology and poor prognosis (Brill et al., 2010).
  
Entity Bladder transitional cell carcinoma
Disease BCL6 protein overexpression is observed in half of the cases of transitional cell carcinoma. However, BCL6 over-expression has a negative correlation with the histological grade (Cho et al., 2007).
  
Entity Soft tissue tumors
Disease BCL6 expression is more frequent in malignant compared with benign/uncertain solitary fibrous tumors, as well as in leiomyosarcomas compared with leiomyomas (Walters et al., 2011).
  
Entity Neuroblastoma
Disease In the neuroblastic phenotype of neuroblastoma, BCL6 expression is associated with increased time to relapse and increased overall survival (Chamdin et al., 2009).
  
Entity Gastric cancer
Disease In a study of 100 gastric cancer cases, BCL6 was highly expressed in differentiated cancers and reduced or absent in undifferentiated cancers. However, survival was identical in BCL6-positive and BCL6-negative cases (Hirata et al., 2009).
  
Entity Multiple myeloma
Disease IL6 induces transcriptional up-regulation of BCL6 via JAK/STAT3 pathway. TNF (TNF alpha) up-regulates BCL6. BCL6 expression is mediated independantly via both JAK/STAT3 and NF-KB pathways in multiple myeloma cells (Hideshima et al., 2010).
  

Breakpoints

 
Note Clustered in a 3,3 kb EcoRI fragment (MTC) includind exon 1A and intron 1.

External links

Nomenclature
HGNC (Hugo)BCL6   1001
Cards
AtlasBCL6ID20
Entrez_Gene (NCBI)BCL6  604  B-cell CLL/lymphoma 6
GeneCards (Weizmann)BCL6
Ensembl (Hinxton)ENSG00000113916 [Gene_View]  chr3:187439165-187454285 [Contig_View]  BCL6 [Vega]
AceView (NCBI)BCL6
Genatlas (Paris)BCL6
WikiGenes604
SOURCE (Princeton)NM_001130845 NM_001134738 NM_001706 NM_138931
Genomic and cartography
GoldenPath (UCSC)BCL6  -  3q27.3   chr3:187439165-187454285 -  3q27   [Description]    (hg19-Feb_2009)
EnsemblBCL6 - 3q27 [CytoView]
Mapping of homologs : NCBIBCL6 [Mapview]
OMIM109565   
Gene and transcription
Genbank (Entrez)AI624861 AK304325 AK308162 AW337942 AW470156
RefSeq transcript (Entrez)NM_001130845 NM_001134738 NM_001706 NM_138931
RefSeq genomic (Entrez)AC_000135 NC_000003 NC_018914 NG_007149 NT_005612 NW_001838884 NW_004929311
Consensus coding sequences : CCDS (NCBI)BCL6
Cluster EST : UnigeneHs.478588 [ NCBI ]
CGAP (NCI)Hs.478588
Alternative Splicing : Fast-db (Paris)GSHG0022311
Alternative Splicing GalleryENSG00000113916
Gene ExpressionBCL6 [ NCBI-GEO ]     BCL6 [ SEEK ]   BCL6 [ MEM ]
Protein : pattern, domain, 3D structure
UniProt/SwissProtP41182 (Uniprot)
NextProtP41182  [Medical]
With graphics : InterProP41182
Splice isoforms : SwissVarP41182 (Swissvar)
Domaine pattern : Prosite (Expaxy)BTB (PS50097)    ZINC_FINGER_C2H2_1 (PS00028)    ZINC_FINGER_C2H2_2 (PS50157)   
Domains : Interpro (EBI)BTB/POZ-like    BTB/POZ_fold    BTB_POZ    Znf_C2H2    Znf_C2H2-like    Znf_C2H2/integrase_DNA-bd   
Related proteins : CluSTrP41182
Domain families : Pfam (Sanger)BTB (PF00651)   
Domain families : Pfam (NCBI)pfam00651   
Domain families : Smart (EMBL)BTB (SM00225)  ZnF_C2H2 (SM00355)  
DMDM Disease mutations604
Blocks (Seattle)P41182
PDB (SRS)1R28    1R29    1R2B    2EN2    2EOS    2LCE    2YRM    3BIM    3E4U    3LBZ   
PDB (PDBSum)1R28    1R29    1R2B    2EN2    2EOS    2LCE    2YRM    3BIM    3E4U    3LBZ   
PDB (IMB)1R28    1R29    1R2B    2EN2    2EOS    2LCE    2YRM    3BIM    3E4U    3LBZ   
PDB (RSDB)1R28    1R29    1R2B    2EN2    2EOS    2LCE    2YRM    3BIM    3E4U    3LBZ   
Human Protein AtlasENSG00000113916
Peptide AtlasP41182
HPRD00180
IPIIPI00012820   IPI00910067   IPI00816159   IPI00927024   IPI00926569   IPI00926382   IPI00910693   
Protein Interaction databases
DIP (DOE-UCLA)P41182
IntAct (EBI)P41182
FunCoupENSG00000113916
BioGRIDBCL6
InParanoidP41182
Interologous Interaction database P41182
IntegromeDBBCL6
STRING (EMBL)BCL6
Ontologies - Pathways
Ontology : AmiGOprotein import into nucleus, translocation  negative regulation of transcription from RNA polymerase II promoter  cell morphogenesis  negative regulation of cell-matrix adhesion  germinal center formation  regulation of germinal center formation  negative regulation of type 2 immune response  negative regulation of B cell apoptotic process  chromatin binding  sequence-specific DNA binding transcription factor activity  protein binding  nucleus  replication fork  nucleolus  transcription, DNA-templated  inflammatory response  cellular response to DNA damage stimulus  Rho protein signal transduction  spermatogenesis  negative regulation of cell proliferation  actin cytoskeleton organization  B cell differentiation  negative regulation of cell growth  positive regulation of B cell proliferation  chromatin DNA binding  regulation of Rho GTPase activity  negative regulation of mast cell cytokine production  negative regulation of Rho protein signal transduction  type 2 immune response  positive regulation of apoptotic process  regulation of memory T cell differentiation  sequence-specific DNA binding  negative regulation of T-helper 2 cell differentiation  negative regulation of transcription, DNA-dependent  negative regulation of transcription, DNA-dependent  metal ion binding  negative regulation of isotype switching to IgE isotypes  erythrocyte development  regulation of inflammatory response  regulation of immune response  positive regulation of cellular component movement  
Ontology : EGO-EBIprotein import into nucleus, translocation  negative regulation of transcription from RNA polymerase II promoter  cell morphogenesis  negative regulation of cell-matrix adhesion  germinal center formation  regulation of germinal center formation  negative regulation of type 2 immune response  negative regulation of B cell apoptotic process  chromatin binding  sequence-specific DNA binding transcription factor activity  protein binding  nucleus  replication fork  nucleolus  transcription, DNA-templated  inflammatory response  cellular response to DNA damage stimulus  Rho protein signal transduction  spermatogenesis  negative regulation of cell proliferation  actin cytoskeleton organization  B cell differentiation  negative regulation of cell growth  positive regulation of B cell proliferation  chromatin DNA binding  regulation of Rho GTPase activity  negative regulation of mast cell cytokine production  negative regulation of Rho protein signal transduction  type 2 immune response  positive regulation of apoptotic process  regulation of memory T cell differentiation  sequence-specific DNA binding  negative regulation of T-helper 2 cell differentiation  negative regulation of transcription, DNA-dependent  negative regulation of transcription, DNA-dependent  metal ion binding  negative regulation of isotype switching to IgE isotypes  erythrocyte development  regulation of inflammatory response  regulation of immune response  positive regulation of cellular component movement  
Pathways : KEGGFoxO signaling pathway    Transcriptional misregulation in cancer   
REACTOMEBCL6
Protein Interaction DatabaseBCL6
Wikipedia pathwaysBCL6
Gene fusion - rearrangments
Rearrangement : TICdbBCL6 [3q27.3]  -  GAPDH [12p13.31]
Rearrangement : TICdbBCL6 [3q27.3]  -  HIST1H4I [6p22.1]
Rearrangement : TICdbBCL6 [3q27.3]  -  HSP90AA1 [14q32.31]
Rearrangement : TICdbBCL6 [3q27.3]  -  HSP90AB1 [6p21.1]
Rearrangement : TICdbBCL6 [3q27.3]  -  IKZF1 [7p12.2]
Rearrangement : TICdbBCL6 [3q27.3]  -  IL21R [16p12.1]
Rearrangement : TICdbBCL6 [3q27.3]  -  Ig []
Rearrangement : TICdbBCL6 [3q27.3]  -  LCP1 [13q14.13]
Rearrangement : TICdbBCL6 [3q27.3]  -  PIM1 [6p21.2]
Rearrangement : TICdbBCL6 [3q27.3]  -  POU2AF1 [11q23.1]
Rearrangement : TICdbBCL6 [3q27.3]  -  SRSF3 [6p21.31]
Rearrangement : TICdbBCL6 [3q27.3]  -  TFRC [3q29]
Rearrangement : TICdbGAPDH [12p13.31]  -  BCL6 [3q27.3]
Rearrangement : TICdbHIST1H4I [6p22.1]  -  BCL6 [3q27.3]
Rearrangement : TICdbHSP90AA1 [14q32.31]  -  BCL6 [3q27.3]
Rearrangement : TICdbHSP90AB1 [6p21.1]  -  BCL6 [3q27.3]
Rearrangement : TICdbIKZF1 [7p12.2]  -  BCL6 [3q27.3]
Rearrangement : TICdbIL21R [16p12.1]  -  BCL6 [3q27.3]
Rearrangement : TICdbIg [BCL6]  -  3q27.3 []
Rearrangement : TICdbLCP1 [13q14.13]  -  BCL6 [3q27.3]
Rearrangement : TICdbPIM1 [6p21.2]  -  BCL6 [3q27.3]
Rearrangement : TICdbPOU2AF1 [11q23.1]  -  BCL6 [3q27.3]
Rearrangement : TICdbSRSF3 [6p21.31]  -  BCL6 [3q27.3]
Rearrangement : TICdbTFRC [3q29]  -  BCL6 [3q27.3]
Polymorphisms : SNP, mutations, diseases
SNP Single Nucleotide Polymorphism (NCBI)BCL6
SNP (GeneSNP Utah)BCL6
SNP : HGBaseBCL6
Genetic variants : HAPMAPBCL6
1000_GenomesBCL6 
ICGC programENSG00000113916 
Cancer Gene: CensusBCL6 
Somatic Mutations in Cancer : COSMICBCL6 
CONAN: Copy Number AnalysisBCL6 
Mutations and Diseases : HGMDBCL6
OMIM109565   
GENETestsBCL6
Disease Genetic AssociationBCL6
Huge Navigator BCL6 [HugePedia]  BCL6 [HugeCancerGEM]
Genomic VariantsBCL6  BCL6 [DGVbeta]
Exome VariantBCL6
dbVarBCL6
ClinVarBCL6
snp3D : Map Gene to Disease604
General knowledge
Homologs : HomoloGeneBCL6
Homology/Alignments : Family Browser (UCSC)BCL6
Phylogenetic Trees/Animal Genes : TreeFamBCL6
Chemical/Protein Interactions : CTD604
Chemical/Pharm GKB GenePA25312
Clinical trialBCL6
Cancer Resource (Charite)ENSG00000113916
Other databases
Probes
Litterature
PubMed233 Pubmed reference(s) in Entrez
CoreMineBCL6
iHOPBCL6

Bibliography

LAZ3, a novel zinc-finger encoding gene, is disrupted by recurring chromosome 3q27 translocations in human lymphomas.
Kerckaert JP, Deweindt C, Tilly H, Quief S, Lecocq G, Bastard C.
Nat Genet. 1993 Sep;5(1):66-70.
PMID 8220427
 
Alterations of a zinc finger-encoding gene, BCL-6, in diffuse large-cell lymphoma.
Ye BH, Lista F, Lo Coco F, Knowles DM, Offit K, Chaganti RS, Dalla-Favera R.
Science. 1993 Oct 29;262(5134):747-50.
PMID 8235596
 
Cloning and expression of cyclosporin A- and FK506-sensitive nuclear factor of activated T-cells: NF45 and NF90.
Kao PN, Chen L, Brock G, Ng J, Kenny J, Smith AJ, Corthesy B.
J Biol Chem. 1994 Aug 12;269(32):20691-9.
PMID 7519613
 
Gene involved in the 3q27 translocation associated with B-cell lymphoma, BCL5, encodes a Kruppel-like zinc-finger protein.
Miki T, Kawamata N, Hirosawa S, Aoki N.
Blood. 1994 Jan 1;83(1):26-32.
PMID 8274740
 
Induction of the transcription factors NF-kappa B, AP-1 and NF-AT during B cell stimulation through the CD40 receptor.
Francis DA, Karras JG, Ke XY, Sen R, Rothstein TL.
Int Immunol. 1995 Feb;7(2):151-61.
PMID 7537532
 
Antigen receptor signaling induces MAP kinase-mediated phosphorylation and degradation of the BCL-6 transcription factor.
Niu H, Ye BH, Dalla-Favera R.
Genes Dev. 1998 Jul 1;12(13):1953-61.
PMID 9649500
 
Acetylation inactivates the transcriptional repressor BCL6.
Bereshchenko OR, Gu W, Dalla-Favera R.
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Contributor(s)

Written09-1998Jean-Pierre Kerckaert
Unite 124 INSERM, Institut de Recherches sur le Cancer, Place de Verdun, 59045 Lille cedex, France
Updated02-2007Stevan Knezevich
BC Cancer Research Centre (BCCRC), Vancouver, British Columbia, Canada
Updated12-2012Jean-Loup Huret
Genetics, Dept Medical Information, University of Poitiers, CHU Poitiers Hospital, F-86021 Poitiers, France

Citation

This paper should be referenced as such :
Kerckaert JP . BCL6 (B-Cell Lymphoma 6). Atlas Genet Cytogenet Oncol Haematol. September 1998 .
Knezevich S . BCL6 (B-Cell Lymphoma 6). Atlas Genet Cytogenet Oncol Haematol. February 2007 .
Huret JL . BCL6 (B-Cell Lymphoma 6). Atlas Genet Cytogenet Oncol Haematol. December 2012 .
URL : http://AtlasGeneticsOncology.org/Genes/BCL6ID20.html

The various updated versions of this paper are referenced and archived by INIST as such :
http://documents.irevues.inist.fr/bitstream/handle/2042/50185/12-2012-BCL6ID20.pdf?sequence=3   [ Bibliographic record ]
http://documents.irevues.inist.fr/bitstream/handle/2042/50185/12-2012-BCL6ID20.pdf?sequence=3   [ Bibliographic record ]

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