BCL6

Last updated
BCL6
Protein BCL6 PDB 1r28.png
Available structures
PDB Ortholog search: PDBe RCSB
Identifiers
Aliases BCL6 , BCL5, BCL6A, LAZ3, ZBTB27, ZNF51, B-cell CLL/lymphoma 6, B cell CLL/lymphoma 6, transcription repressor, BCL6 transcription repressor
External IDs OMIM: 109565 MGI: 107187 HomoloGene: 7640 GeneCards: BCL6
Orthologs
SpeciesHumanMouse
Entrez

604

12053

Ensembl

ENSG00000113916

ENSMUSG00000022508

UniProt

P41182

P41183

RefSeq (mRNA)

NM_001130845
NM_001134738
NM_001706
NM_138931

NM_009744
NM_001348026

RefSeq (protein)

NP_001124317
NP_001128210
NP_001697

NP_001334955
NP_033874

Location (UCSC) Chr 3: 187.72 – 187.75 Mb Chr 16: 23.78 – 23.81 Mb
PubMed search [3] [4]
Wikidata
View/Edit Human View/Edit Mouse

Bcl-6 (B-cell lymphoma 6) is a protein that in humans is encoded by the BCL6 gene. BCL6 is a master transcription factor for regulation of T follicular helper cells (TFH cells) proliferation. [5] BCL6 has three evolutionary conserved structural domains. [6] The interaction of these domains with corepressors allows for germinal center development and leads to B cell proliferation.

The deletion of BCL6 is known to lead to failure of germinal center formation in the follicles of the lymph nodes, preventing B cells from undergoing somatic hypermutation. [6] Mutations in BCL6 can lead to B cell lymphomas because it promotes unchecked B cell growth. [6] Clinically, BCL6 can be used to diagnose B cell lymphomas and is shown to be upregulated in a number of cancers. [6]

Other BCL genes, including BCL2, BCL3, BCL5, BCL7A, BCL9, and BCL10, also have clinical significance in lymphoma.

Normal physiological function

Structure

The protein encoded by the BCL6 gene is a zinc finger transcription factor that has three evolutionarily conserved domains. BCL6 contains a (1) N-terminal BTB/POZ domain (Broad-complex, Tramtrack and Brick-a-brac/Pox virus and Zin finger family domain), (2) a central RN2 region, and (3) another zinc finger at the C-terminal end. [6] This structure is vital to BCL6’s function – an exon 7 skipping splice variant encodes a shorter form of the protein which lacks the first two zinc fingers of the DNA binding domain, [7] for example.

Function

Bcl-6 is a master transcription factor for the regulation of T follicular helper cells (TFH cells). Bcl-6 is expressed when the cytokines Il-6 and/or Il-21 are recognized; these cytokines can be produced by antigen presenting cells (APCs: B cells, dendritic cells, or macrophages) when activated. This occurs when a naïve T helper cell recognizes antigen and needs to migrate to the follicle as a T follicular helper cell (TFH cell). [8] TFH cells are vital to the generation of germinal centers in the follicles of secondary lymphoid organs, where B cells divide and help fight infections. [5]

As a master transcription factor, BCL6 interacts with a variety of co-repressors and other proteins to influence the T cell lineage. BCL6 has been shown to modulate the STAT-dependent Interleukin 4 (IL-4) responses of B cells [ citation needed ] and suppress the production of BCL2. [6]

Importantly, Bcl-6 should only be expressed when there is an antigen present and further stimulation of the immune system is necessary, since BCL6 prevents cell death (apoptosis). Unchecked growth can lead to lymphomas. Normally, the action of BCL6 is negatively regulated by the gene PRDM1 encoding the transcription factor Blimp-1. [9] The antagonistic effect with Blimp-1 is a powerful role of BCL6, because it shuts off the normal pathway of differentiation toward other cell types.

Differentiation of TFH Cells

BCL6 is currently considered a lineage-defining transcription factor in TFH cell differentiation. [10] Without the expression of BCL6, naïve CD4+ T helper cells will not turn into TFH cells. When a naïve CD4+ T cell binds to MHC class II and an antigen peptide on a dendritic cell, a signaling cascade ensues in which some proliferating T cells become TFH cells. Signaling through the IL-6 receptor leads to TFH cell differentiation, and in turn the expression of BCL6 in TFH lineage-defined cells. BCL6 allows, through transcriptional regulation, unique cell markers to be expressed, resulting in an effective TFH cell. [10]

Transcriptional regulation of BCL6 is vast and complex, but many of the outcomes of BCL6’s transcriptional regulation on TFH cells have been elucidated. TFH cells upregulate CXCR5, IL-6R, and ICOS during their migration to the germinal center. After interacting with a B cell presenting the cognate antigen in the follicle, they also upregulate SAPhi, CD200hi and BTLAhi on their cell surface in the newly formed germinal center. Additionally, BCL6 directly binds and suppresses genes that are downregulated in non-TFH cells, including Ccr7, Selplg, and Gpr183, and other chemokine receptor targets. [10]

Clinical Value

Role in B Cell Lymphomas

BCL6 is found to be frequently translocated and hypermutated in diffuse large B cell lymphoma (DLBCL) [11] [12] [13] and contributes to the pathogenesis of DLBCL. BCL6 is exclusively present in the B-cells of both healthy and neoplastic (cancerous) germinal centers. This allows lymphoma’s to be diagnosed based on immunohistochemical staining, revealing the presence of Burkitt's lymphoma, follicular lymphoma and the nodular lymphocyte predominant subtype of Hodgkin's disease. It is often used together with antibodies to Bcl-2 antigen to distinguish neoplastic follicles from those found in benign hyperplasia, for which Bcl-2 is negative. [14] [ verification needed ]

Many different changes to BCL6 can lead to inhibited activity and are known to be linked with B-cell lymphomas, including direct effects (mutation and post-translational effects) as well as indirect effects (imbalanced interactions with other mutated proteins). Mutations to the transcription factors for BCL6, MEF2B and IRF8, are common in direct transcriptional changes that cause DLBCL. Additionally, post-translational phosphorylation can be affected by mutations in FBXO11. Finally, BCL6’s interaction with other mutated proteins, including CREBBP, EP300, EZH2, and KM2TD, can also lead to B-cell lymphomas. [6] Given its role as a master transcription regulator, many genetic and epigenetic changes can be responsible for B-cell lymphomas; these interacting proteins are likely a few of many that affect BCL6’s function.

Diagnostic Ability

Tracking BLC6 in B cells using immunohistochemical staining or enzyme-linked immunosorbent assay (ELISA) can be used to diagnose cancers and may indicate other illnesses as well. As mentioned previously, tracking BCL6 in tandem with BCL2 can lead to the diagnosis of B-cell lymphomas. More recently, it has been hypothesized that the presence of BCL6 in serum could be used to diagnose endometriosis due to an overactivation of BCL6 in endometriotic females, [15] [16] although this diagnostic method has not been found to work. [17] Nonetheless, the understanding of BCL6 will likely continue to be used to diagnose diseases.

Targeted Therapies

Given BCL6’s role in B-cell lymphomas, it has been suggested as a therapeutic target for cancer treatment. Targeting BCL6 in cancer patients should lead to the deletion of BCL6 in tumor cells. Peptidomimetics, small molecules, and natural compounds have been developed and tested in preclinical models, showing promise of anti-lymphoma activity. [18]

Interactions

BCL6 has been shown to interact with

* BCOR, [19]

See also

Related Research Articles

<span class="mw-page-title-main">B cell</span> Type of white blood cell

B cells, also known as B lymphocytes, are a type of white blood cell of the lymphocyte subtype. They function in the humoral immunity component of the adaptive immune system. B cells produce antibody molecules which may be either secreted or inserted into the plasma membrane where they serve as a part of B-cell receptors. When a naïve or memory B cell is activated by an antigen, it proliferates and differentiates into an antibody-secreting effector cell, known as a plasmablast or plasma cell. In addition, B cells present antigens and secrete cytokines. In mammals, B cells mature in the bone marrow, which is at the core of most bones. In birds, B cells mature in the bursa of Fabricius, a lymphoid organ where they were first discovered by Chang and Glick, which is why the B stands for bursa and not bone marrow, as commonly believed.

<span class="mw-page-title-main">Burkitt lymphoma</span> Cancer of the lymphatic system

Burkitt lymphoma is a cancer of the lymphatic system, particularly B lymphocytes found in the germinal center. It is named after Denis Parsons Burkitt, the Irish surgeon who first described the disease in 1958 while working in equatorial Africa. The overall cure rate for Burkitt lymphoma in developed countries is about 90%, and it is worse in low-income countries. Burkitt lymphoma is uncommon in adults, in whom it has a worse prognosis.

<span class="mw-page-title-main">Memory B cell</span> Cell of the adaptive immune system

In immunology, a memory B cell (MBC) is a type of B lymphocyte that forms part of the adaptive immune system. These cells develop within germinal centers of the secondary lymphoid organs. Memory B cells circulate in the blood stream in a quiescent state, sometimes for decades. Their function is to memorize the characteristics of the antigen that activated their parent B cell during initial infection such that if the memory B cell later encounters the same antigen, it triggers an accelerated and robust secondary immune response. Memory B cells have B cell receptors (BCRs) on their cell membrane, identical to the one on their parent cell, that allow them to recognize antigen and mount a specific antibody response.

<span class="mw-page-title-main">Follicular lymphoma</span> Medical condition

Follicular lymphoma (FL) is a cancer that involves certain types of white blood cells known as lymphocytes. The cancer originates from the uncontrolled division of specific types of B-cells known as centrocytes and centroblasts. These cells normally occupy the follicles in the germinal centers of lymphoid tissues such as lymph nodes. The cancerous cells in FL typically form follicular or follicle-like structures in the tissues they invade. These structures are usually the dominant histological feature of this cancer.

<span class="mw-page-title-main">Germinal center</span> Lymphatic tissue structure

Germinal centers or germinal centres (GCs) are transiently formed structures within B cell zone (follicles) in secondary lymphoid organs – lymph nodes, ileal Peyer's patches, and the spleen – where mature B cells are activated, proliferate, differentiate, and mutate their antibody genes during a normal immune response; most of the germinal center B cells (BGC) are removed by tingible body macrophages. There are several key differences between naive B cells and GC B cells, including level of proliferative activity, size, metabolic activity and energy production. The B cells develop dynamically after the activation of follicular B cells by T-dependent antigen. The initiation of germinal center formation involves the interaction between B and T cells in the interfollicular area of the lymph node, CD40-CD40L ligation, NF-kB signaling and expression of IRF4 and BCL6.

<span class="mw-page-title-main">GLI1</span> Protein-coding gene in humans

Zinc finger protein GLI1 also known as glioma-associated oncogene is a protein that in humans is encoded by the GLI1 gene. It was originally isolated from human glioblastoma cells.

<span class="mw-page-title-main">GLI2</span> Protein-coding gene in the species Homo sapiens

Zinc finger protein GLI2 also known as GLI family zinc finger 2 is a protein that in humans is encoded by the GLI2 gene. The protein encoded by this gene is a transcription factor.

<span class="mw-page-title-main">SIN3A</span> Protein-coding gene in the species Homo sapiens

Paired amphipathic helix protein Sin3a is a protein that in humans is encoded by the SIN3A gene.

<span class="mw-page-title-main">Zinc finger and BTB domain-containing protein 16</span> Protein found in humans

Zinc finger and BTB domain-containing protein 16 is a protein that in humans is encoded by the ZBTB16 gene.

<span class="mw-page-title-main">GPR183</span> Protein-coding gene in the species Homo sapiens

G-protein coupled receptor 183 also known as Epstein-Barr virus-induced G-protein coupled receptor 2 (EBI2) is a protein (GPCR) expressed on the surface of some immune cells, namely B cells and T cells; in humans it is encoded by the GPR183 gene. Expression of EBI2 is one critical mediator of immune cell localization within lymph nodes, responsible in part for the coordination of B cell, T cell, and dendritic cell movement and interaction following antigen exposure. EBI2 is a receptor for oxysterols. The most potent activator is 7α,25-dihydroxycholesterol (7α,25-OHC), with other oxysterols exhibiting varying affinities for the receptor. Oxysterol gradients drive chemotaxis, attracting the EBI2-expressing cells to locations of high ligand concentration. The GPR183 gene was identified due to its upregulation during Epstein-Barr virus infection of the Burkitt's lymphoma cell line BL41, hence its name: EBI2.

<span class="mw-page-title-main">IRF4</span> Protein-coding gene in the species Homo sapiens

Interferon regulatory factor 4 (IRF4) also known as MUM1 is a protein that in humans is encoded by the IRF4 gene,. IRF4 functions as a key regulatory transcription factor in the development of human immune cells. The expression of IRF4 is essential for the differentiation of T lymphocytes and B lymphocytes as well as certain myeloid cells. Dysregulation of the IRF4 gene can result in IRF4 functioning either as an oncogene or a tumor-suppressor, depending on the context of the modification.

<span class="mw-page-title-main">PRDM1</span> Protein-coding gene in the species Homo sapiens

PR domain zinc finger protein 1, or B lymphocyte-induced maturation protein-1 (BLIMP-1), is a protein in humans encoded by the gene PRDM1 located on chromosome 6q21. BLIMP-1 is considered a 'master regulator' of hematopoietic stem cells, and plays a critical role in the development of plasma B cells, T cells, dendritic cells (DCs), macrophages, and osteoclasts. Pattern Recognition Receptors (PRRs) can activate BLIMP-1, both as a direct target and through downstream activation. BLIMP-1 is a transcription factor that triggers expression of many downstream signaling cascades. As a fine-tuned and contextual rheostat of the immune system, BLIMP-1 up- or down-regulates immune responses depending on the precise scenarios. BLIMP-1 is highly expressed in exhausted T-cells – clones of dysfunctional T-cells with diminished functions due to chronic immune response against cancer, viral infections, or organ transplant.

<span class="mw-page-title-main">BCL-6 corepressor</span> Protein-coding gene in humans

BCL-6 corepressor is a protein that in humans is encoded by the BCOR gene.

<span class="mw-page-title-main">ZBTB7A</span> Protein-coding gene in the species Homo sapiens

Zinc finger and BTB domain-containing protein 7A is a protein that in humans is encoded by the ZBTB7A gene.

<span class="mw-page-title-main">BCL11A</span> Protein-coding gene in the species Homo sapiens

B-cell lymphoma/leukemia 11A is a protein that in humans is encoded by the BCL11A gene.

<span class="mw-page-title-main">ZBTB32</span> Protein-coding gene in the species Homo sapiens

Zinc finger and BTB domain-containing protein 32 is a protein that in humans is encoded by the 1960 bp ZBTB32 gene. The 52 kDa protein is a transcriptional repressor and the gene is expressed in T and B cells upon activation, but also significantly in testis cells. It is a member of the Poxviruses and Zinc-finger (POZ) and Krüppel (POK) family of proteins, and was identified in multiple screens involving either immune cell tumorigenesis or immune cell development.

<span class="mw-page-title-main">BCL6B</span> Protein-coding gene in the species Homo sapiens

B-cell CLL/lymphoma 6 member B protein is a protein that in humans is encoded by the BCL6B gene.

<span class="mw-page-title-main">Follicular B helper T cells</span>

Follicular helper T cells (also known as T follicular helper cells and abbreviated as TFH), are antigen-experienced CD4+ T cells found in the periphery within B cell follicles of secondary lymphoid organs such as lymph nodes, spleen and Peyer's patches, and are identified by their constitutive expression of the B cell follicle homing receptor CXCR5. Upon cellular interaction and cross-signaling with their cognate follicular (Fo B) B cells, TFH cells trigger the formation and maintenance of germinal centers through the expression of CD40 ligand (CD40L) and the secretion of IL-21 and IL-4. TFH cells also migrate from T cell zones into these seeded germinal centers, predominantly composed of rapidly dividing B cells mutating their Ig genes. Within germinal centers, TFH cells play a critical role in mediating the selection and survival of B cells that go on to differentiate either into long-lived plasma cells capable of producing high affinity antibodies against foreign antigen, or germinal center-dependent memory B cells capable of quick immune re-activation in the future if ever the same antigen is re-encountered. TFH cells are also thought to facilitate negative selection of potentially autoimmune-causing mutated B cells in the germinal center. However, the biomechanisms by which TFH cells mediate germinal center tolerance are yet to be fully understood.

Gene expression profiling has revealed that diffuse large B-cell lymphoma (DLBCL) is composed of at least 3 different sub-groups, each having distinct oncogenic mechanisms that respond to therapies in different ways. Germinal Center B-Cell like (GCB) DLBCLs appear to arise from normal germinal center B cells, while Activated B-cell like (ABC) DLBCLs are thought to arise from postgerminal center B cells that are arrested during plasmacytic differentiation. The differences in gene expression between GCB DLBCL and ABC DLBCL are as vast as the differences between distinct types of leukemia, but these conditions have historically been grouped together and treated as the same disease.

In situ lymphoid neoplasia is a precancerous condition newly classified by the World Health Organization in 2016. The Organization recognized two subtypes of ISLN: in situ follicular neoplasia (ISFN) and in situ mantle cell neoplasia (ISMCL). ISFN and ISMCL are pathological accumulations of lymphocytes in the germinal centers and mantle zones, respectively, of the follicles that populate lymphoid organs such as lymph nodes. These lymphocytes are monoclonal B-cells that may develop into follicular (FL) and mantle cell (MCL) lymphomas, respectively.

References

  1. 1 2 3 GRCh38: Ensembl release 89: ENSG00000113916 - Ensembl, May 2017
  2. 1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000022508 - Ensembl, May 2017
  3. ↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ↑ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. 1 2 A OJ (2013). Kuby immunology. W.H. Freeman. ISBN   978-1-4292-1919-8. OCLC   820117219.{{cite book}}: CS1 maint: multiple names: authors list (link)
  6. 1 2 3 4 5 6 7 8 9 10 11 12 13 Yang H, Green MR (2019-11-07). "Epigenetic Programing of B-Cell Lymphoma by BCL6 and Its Genetic Deregulation". Frontiers in Cell and Developmental Biology. 7: 272. doi: 10.3389/fcell.2019.00272 . ISSN   2296-634X. PMC   6853842 . PMID   31788471.
  7. ↑ Huang X, Shen Y, Liu M, Bi C, Jiang C, Iqbal J, McKeithan TW, Chan WC, Ding S, Fu K (July 2012). "Quantitative Proteomics Reveals that miR-155 Regulates the PI3K-AKT Pathway in Diffuse Large B-Cell Lymphoma". The American Journal of Pathology. 181 (1): 26–33. doi:10.1016/j.ajpath.2012.03.013. ISSN   0002-9440. PMC   3388146 . PMID   22609116.
  8. ↑ Nurieva RI, Chung Y, Martinez GJ, Yang XO, Tanaka S, Matskevitch TD, Wang Y, Dong C (2009-08-21). "Bcl6 Mediates the Development of T Follicular Helper Cells". Science. 325 (5943): 1001–1005. Bibcode:2009Sci...325.1001N. doi:10.1126/science.1176676. PMC   2857334 . PMID   19628815.
  9. ↑ Johnston RJ, Poholek AC, DiToro D, Yusuf I, Eto D, Barnett B, Dent AL, Craft J, Crotty S (2009-08-21). "Bcl6 and Blimp-1 Are Reciprocal and Antagonistic Regulators of T Follicular Helper Cell Differentiation". Science. 325 (5943): 1006–1010. Bibcode:2009Sci...325.1006J. doi:10.1126/science.1175870. PMC   2766560 . PMID   19608860.
  10. 1 2 3 4 5 6 7 8 9 10 11 12 Choi J, Crotty S (April 2021). "Bcl6-Mediated Transcriptional Regulation of Follicular Helper T cells (TFH)". Trends in Immunology. 42 (4): 336–349. doi:10.1016/j.it.2021.02.002. ISSN   1471-4906. PMC   8021443 . PMID   33663954.
  11. ↑ Ye BH, Lista F, Coco FL, Knowles DM, Offit K, Chaganti RS, Dalla-Favera R (1993-10-29). "Alterations of a Zinc Finger-Encoding Gene, BCL-6, in Diffuse Large-Cell Lymphoma". Science. 262 (5134): 747–750. Bibcode:1993Sci...262..747Y. doi:10.1126/science.8235596. PMID   8235596.
  12. ↑ Kerckaert J, Deweindt C, Tilly H, Quief S, Lecocq G, Bastard C (September 1993). "LAZ3, a novel zinc–finger encoding gene, is disrupted by recurring chromosome 3q27 translocations in human lymphomas". Nature Genetics. 5 (1): 66–70. doi:10.1038/ng0993-66. ISSN   1546-1718. PMID   8220427. S2CID   12575122.
  13. ↑ Migliazza A, Martinotti S, Chen W, Fusco C, Ye BH, Knowles DM, Offit K, Chaganti RS, Dalla-Favera R (1995-12-19). "Frequent somatic hypermutation of the 5' noncoding region of the BCL6 gene in B-cell lymphoma". Proceedings of the National Academy of Sciences. 92 (26): 12520–12524. Bibcode:1995PNAS...9212520M. doi: 10.1073/pnas.92.26.12520 . ISSN   0027-8424. PMC   40389 . PMID   8618933.
  14. ↑ McCluggage WG, Maxwell P (July 1999). <338::aid-path383>3.0.co;2-2 "Manual of diagnostic antibodies for immunohistology. Anthony S.-Y. Leong, Kum Cooper and F. Joel W.-M. Leong. Greenwich Medical Media Ltd., London, 1999. Distributed worldwide by Oxford University Press. No. of pages: 385. ISBN: 1 900151 316". The Journal of Pathology. 188 (3): 338–339. doi:10.1002/(sici)1096-9896(199907)188:3<338::aid-path383>3.0.co;2-2. ISSN   0022-3417.
  15. ↑ Yoo J, Kim TH, Fazleabas AT, Palomino WA, Ahn SH, Tayade C, Schammel DP, Young SL, Jeong J, Lessey BA (2017-07-28). "KRAS Activation and over-expression of SIRT1/BCL6 Contributes to the Pathogenesis of Endometriosis and Progesterone Resistance". Scientific Reports. 7 (1): 6765. Bibcode:2017NatSR...7.6765Y. doi:10.1038/s41598-017-04577-w. ISSN   2045-2322. PMC   5533722 . PMID   28754906.
  16. ↑ Evans-Hoeker E, Lessey BA, Jeong JW, Savaris RF, Palomino WA, Yuan L, Schammel DP, Young SL (2016-05-24). "Endometrial BCL6 Overexpression in Eutopic Endometrium of Women With Endometriosis". Reproductive Sciences. 23 (9): 1234–1241. doi:10.1177/1933719116649711. ISSN   1933-7191. PMC   5933165 . PMID   27222232.
  17. ↑ Sansone AM, Hisrich BV, Young RB, Abel WF, Bowens Z, Blair BB, Funkhouser AT, Schammel DP, Green LJ, Lessey BA, Blenda AV (2021-09-28). "Evaluation of BCL6 and SIRT1 as Non-Invasive Diagnostic Markers of Endometriosis". Current Issues in Molecular Biology. 43 (3): 1350–1360. doi: 10.3390/cimb43030096 . ISSN   1467-3045. PMC   8929102 . PMID   34698105.
  18. ↑ Leeman-Neill RJ, Bhagat G (2018-01-04). "BCL6 as a therapeutic target for lymphoma". Expert Opinion on Therapeutic Targets. 22 (2): 143–152. doi:10.1080/14728222.2018.1420782. ISSN   1472-8222. PMID   29262721. S2CID   22638255.
  19. 1 2 Huynh KD, Fischle W, Verdin E, Bardwell VJ (July 2000). "BCoR, a novel corepressor involved in BCL-6 repression". Genes & Development. 14 (14): 1810–23. doi:10.1101/gad.14.14.1810. PMC   316791 . PMID   10898795.
  20. ↑ Vasanwala FH, Kusam S, Toney LM, Dent AL (August 2002). "Repression of AP-1 function: a mechanism for the regulation of Blimp-1 expression and B lymphocyte differentiation by the B cell lymphoma-6 protooncogene". Journal of Immunology. 169 (4): 1922–9. doi: 10.4049/jimmunol.169.4.1922 . PMID   12165517.
  21. 1 2 David G, Alland L, Hong SH, Wong CW, DePinho RA, Dejean A (May 1998). "Histone deacetylase associated with mSin3A mediates repression by the acute promyelocytic leukemia-associated PLZF protein". Oncogene. 16 (19): 2549–56. doi: 10.1038/sj.onc.1202043 . PMID   9627120.
  22. 1 2 Deltour S, Guerardel C, Leprince D (December 1999). "Recruitment of SMRT/N-CoR-mSin3A-HDAC-repressing complexes is not a general mechanism for BTB/POZ transcriptional repressors: the case of HIC-1 and gammaFBP-B". Proceedings of the National Academy of Sciences of the United States of America. 96 (26): 14831–6. Bibcode:1999PNAS...9614831D. doi: 10.1073/pnas.96.26.14831 . PMC   24733 . PMID   10611298.
  23. 1 2 3 Lemercier C, Brocard MP, Puvion-Dutilleul F, Kao HY, Albagli O, Khochbin S (June 2002). "Class II histone deacetylases are directly recruited by BCL6 transcriptional repressor". The Journal of Biological Chemistry. 277 (24): 22045–52. doi: 10.1074/jbc.M201736200 . PMID   11929873.
  24. ↑ Gupta S, Jiang M, Anthony A, Pernis AB (December 1999). "Lineage-specific modulation of interleukin 4 signaling by interferon regulatory factor 4". The Journal of Experimental Medicine. 190 (12): 1837–48. doi:10.1084/jem.190.12.1837. PMC   2195723 . PMID   10601358.
  25. 1 2 Wong CW, Privalsky ML (October 1998). "Components of the SMRT corepressor complex exhibit distinctive interactions with the POZ domain oncoproteins PLZF, PLZF-RARalpha, and BCL-6". The Journal of Biological Chemistry. 273 (42): 27695–702. doi: 10.1074/jbc.273.42.27695 . PMID   9765306.
  26. ↑ Davies JM, Hawe N, Kabarowski J, Huang QH, Zhu J, Brand NJ, Leprince D, Dhordain P, Cook M, Morriss-Kay G, Zelent A (January 1999). "Novel BTB/POZ domain zinc-finger protein, LRF, is a potential target of the LAZ-3/BCL-6 oncogene". Oncogene. 18 (2): 365–75. doi: 10.1038/sj.onc.1202332 . PMID   9927193.
  27. ↑ Oestreich KJ, Huang AC, Weinmann AS (May 2011). "The lineage-defining factors T-bet and Bcl-6 collaborate to regulate Th1 gene expression patterns". The Journal of Experimental Medicine. 208 (5): 1001–13. doi:10.1084/jem.20102144. PMC   3092354 . PMID   21518797.
  28. ↑ Dhordain P, Albagli O, Honore N, Guidez F, Lantoine D, Schmid M, The HD, Zelent A, Koken MH (December 2000). "Colocalization and heteromerization between the two human oncogene POZ/zinc finger proteins, LAZ3 (BCL6) and PLZF". Oncogene. 19 (54): 6240–50. doi: 10.1038/sj.onc.1203976 . PMID   11175338.

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.

This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.