Affinage

BCL6B

B-cell CLL/lymphoma 6 member B protein · UniProt Q8N143

Length
479 aa
Mass
51.5 kDa
Annotated
2026-06-09
32 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BCL6B (BAZF/ZBTB28/ZNF62) is a sequence-specific transcriptional repressor that recognizes BCL6-consensus DNA elements through its Krüppel-like zinc fingers and silences target genes via its BTB/POZ domain (PMID:9632807, PMID:11374866). Because BCL6B does not bind co-repressors directly, it heterodimerizes with BCL6 through the BTB/POZ domain and recruits the mSin3A/HDAC1 complex indirectly through that association, rendering its repressor activity HDAC-dependent (PMID:9632807, PMID:12659862). In tumor contexts BCL6B acts as a tumor suppressor by directly binding promoters: it transactivates TP53 in competition with BCL6 while repressing BCL6 itself, represses GGT5 to remodel MAPK signaling (lowering ERK and raising p38/JNK activity), and represses CD24 (PMID:31754389, PMID:42083053, PMID:42154583). Independently of its repressor role, VEGF-induced BCL6B assembles with Cullin-3 into an E3 ubiquitin ligase that polyubiquitinates and degrades the Notch effector CBF1, coupling VEGF-driven angiogenesis to Notch suppression in endothelial cells; it also restrains endothelial differentiation by repressing the master factor ETV2 (PMID:22279058, PMID:37078291, PMID:39075623). BCL6B nuclear activity is gated post-translationally, as ABHD17C-mediated depalmitoylation at Cys442 blocks importin-α/β-dependent nuclear import and routes BCL6B to cytoplasmic proteasomal degradation, derepressing CD24 and enabling immune evasion (PMID:42154583). In the immune compartment BCL6B is required for naive CD4+ T cell activation and for the enhanced magnitude of memory CD8+ T cell secondary responses, and it regulates hematopoietic progenitor homeostasis indirectly through CD8+ T cells (PMID:15314041, PMID:15833813, PMID:17526724, PMID:22491947).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1998 High

    Established BCL6B as a nuclear, BCL6-related transcriptional repressor, defining its core domain architecture and DNA-binding behavior.

    Evidence Co-IP, nuclear localization, reporter repression, and domain-deletion analysis of BAZF

    PMID:9632807

    Open questions at the time
    • Physiological target genes not identified
    • Functional consequence of BCL6 association not yet mechanistic
  2. 2001 High

    Defined the precise DNA recognition sequence, showing BCL6B binds a BCL6-identical consensus and can weakly engage STAT6 elements.

    Evidence EMSA with systematic site-directed mutagenesis of binding elements

    PMID:11374866

    Open questions at the time
    • In vitro binding only; genomic occupancy not mapped
    • Biological targets of STAT6-element binding unclear
  3. 2003 High

    Resolved how BCL6B represses transcription — it lacks direct co-repressor binding and instead recruits mSin3A/HDAC1 through BCL6 heterodimerization.

    Evidence Reporter complementation in BCL6-null cells, domain mapping, trichostatin A inhibition, Co-IP

    PMID:12659862

    Open questions at the time
    • Whether BCL6B has any BCL6-independent repressive function not addressed
    • Endogenous target loci not defined
  4. 2004 Medium

    Linked BCL6B to adaptive immunity, showing it is required for naive CD4+ T cell proliferation, proposed to act by modulating BCL6 via heterodimers.

    Evidence BAZF-knockout and lck-BAZF transgenic mice, anti-CD3 proliferation assays

    PMID:15314041

    Open questions at the time
    • Heterodimer mechanism inferred but not demonstrated in vivo
    • Target genes in T cells unknown
  5. 2005 High

    Demonstrated a cell-autonomous role for BCL6B in memory CD8+ T cells, required for the amplified secondary response while sparing primary responses.

    Evidence Gene-interrupted mouse with adoptive transfer/rechallenge across two antigen systems plus in vitro IL-2 assay

    PMID:15833813

    Open questions at the time
    • Transcriptional targets controlling memory expansion not identified
    • Connection to IL-2 signaling mechanistically undefined
  6. 2007 High

    Showed BCL6B regulates hematopoietic progenitor homeostasis indirectly, via a CD8+ T cell-dependent pathway rather than progenitor-intrinsic action.

    Evidence BAZF-knockout mouse, progenitor colony/chemokine assays, CD8+ T cell depletion rescue

    PMID:17526724

    Open questions at the time
    • Mediator signals from CD8+ T cells to progenitors unknown
    • Transcriptional program involved not defined
  7. 2012 High

    Revealed an enzymatic, non-transcriptional role: VEGF-induced BCL6B forms a CUL3 E3 ligase that degrades the Notch effector CBF1 to drive angiogenesis.

    Evidence Reciprocal Co-IP, polyubiquitination assay, knockout mouse with retinal and wound-healing angiogenesis phenotypes

    PMID:22279058

    Open questions at the time
    • How a BTB-zinc finger repressor switches to an E3 ligase adaptor not structurally resolved
    • Other CUL3 substrates unexplored
  8. 2012 High

    Placed BCL6B downstream of FGF2/MAP2K1 signaling in germline stem cells, where excess BCL6B drives self-renewal and is tumorigenic.

    Evidence MAP2K1 inhibition, activated Map2k1 and Bcl6b overexpression, stem cell transplantation tumor assay

    PMID:22491947

    Open questions at the time
    • Direct BCL6B target genes mediating self-renewal not identified
    • Contrast with tumor-suppressor role in other tissues unexplained
  9. 2015 Medium

    Identified BCL6B as a tumor suppressor in carcinomas, activating p53 signaling to induce apoptosis and cell-cycle arrest and sensitize to 5-FU.

    Evidence Re-expression after demethylation and ectopic expression in HCC and colorectal lines, p53-pathway readouts, flow cytometry, invasion assays

    PMID:25909168 PMID:25973304

    Open questions at the time
    • p53 activation shown by protein expression, not direct promoter assay in these studies
    • EGR1 intermediary not mechanistically dissected
  10. 2018 Medium

    Extended tumor-suppressor mechanism to PI3K/AKT inhibition, reducing cyclin D1/MMP-9 and restoring E-cadherin in colorectal cells.

    Evidence BCL6B transfection with pAKT readout and LY294002 co-treatment, proliferation and migration assays

    PMID:29393377

    Open questions at the time
    • Direct versus indirect effect on PI3K/AKT not distinguished
    • Single-lab, no in vivo validation
  11. 2019 High

    Provided direct promoter-level proof of the BCL6B/BCL6 antagonism: BCL6B binds and transactivates TP53 while repressing BCL6, and is upregulated by ZBTB16.

    Evidence ChIP and luciferase reporters on p53/BCL6 promoters, ZBTB16-ZBTB28 Co-IP, xenografts

    PMID:31754389

    Open questions at the time
    • Whether p53 transactivation requires HDAC complex or is repressor-independent unclear
    • Genome-wide occupancy not mapped
  12. 2020 Medium

    Reinforced the ZBTB16-BCL6B partnership as a tumor-suppressive axis antagonizing BCL6 to reverse EMT in breast cancer.

    Evidence Reciprocal Co-IP, luciferase, xenografts, migration/invasion/colony assays

    PMID:32517789

    Open questions at the time
    • Direct EMT target genes not defined
    • Single-lab confirmation
  13. 2021 Medium

    Connected BCL6B to autophagy-dependent apoptosis through FIP200 interaction and Bcl-XL degradation, disrupting the Bcl-XL–BECN1 complex.

    Evidence Ectopic ZBTB28 expression, EM autophagosome detection, interaction/Co-IP, xenograft, flow cytometry

    PMID:33931087

    Open questions at the time
    • Mechanism linking transcriptional repressor to Bcl-XL degradation unresolved
    • FIP200 binding interface undefined
  14. 2022 Medium

    Implicated BCL6B in innate immune surveillance by regulating IFNAR transcription and downregulating anti-phagocytic CD24/CD47 to promote macrophage phagocytosis.

    Evidence Ectopic ZBTB28 expression, IFNAR/ISG expression, flow cytometry, phagocytosis assay, xenograft

    PMID:35048182

    Open questions at the time
    • Direct promoter binding to IFNAR not confirmed
    • Relative contributions of CD24 vs CD47 unclear
  15. 2023 High

    Confirmed the angiogenic VEGF–BCL6B–Notch axis in retinal disease, where BCL6B loss activates Notch and BCL6B siRNA suppresses neovascular pathology.

    Evidence Knockout mice and siRNA in choroidal neovascularization and blood-retinal barrier models, CBF1/NICD readouts, monkey CNV model

    PMID:37078291

    Open questions at the time
    • Therapeutic window and off-target effects of BCL6B knockdown unaddressed
    • Interplay of E3 ligase and repressor functions in this setting unresolved
  16. 2024 High

    Showed BCL6B gates endothelial cell fate by directly repressing the master EC factor ETV2, with ETV2 overexpression rescuing the differentiation block.

    Evidence Inducible hiPSC over/knockdown, ETV2 promoter ChIP-PCR and luciferase, RNA-seq, tube formation, vessel organoids, genetic rescue

    PMID:39075623

    Open questions at the time
    • Upstream signals controlling BCL6B in this program not defined
    • Whether ETV2 repression uses BCL6/HDAC machinery untested
  17. 2026 High

    Defined a direct BCL6B–GGT5 repression event reshaping MAPK signaling toward apoptosis and arrest in AML, with direct DNA binding confirmed.

    Evidence Dual-luciferase, EMSA, RNA-seq, ERK/p38/JNK westerns, gain/loss-of-function in AML, zebrafish and mouse xenografts

    PMID:42083053

    Open questions at the time
    • How GGT5 loss biases MAPK branch selection mechanistically unclear
    • Whether GGT5 axis operates outside AML untested
  18. 2026 High

    Established post-translational control of BCL6B localization: ABHD17C depalmitoylation at Cys442 blocks importin-α/β nuclear import and triggers cytoplasmic degradation, derepressing CD24 for immune evasion.

    Evidence ABHD17C over/knockdown, palmitoylation and Cys442 mutagenesis, fractionation, importin Co-IP, ubiquitination assay, CD24 reporter, phagocytosis assay, orthotopic xenograft

    PMID:42154583

    Open questions at the time
    • The palmitoyltransferase opposing ABHD17C not identified
    • Whether this regulation generalizes beyond pancreatic cancer untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how BCL6B's distinct activities — BCL6-dependent transcriptional repression, BCL6-independent promoter transactivation of TP53, and CUL3-dependent E3 ligase function — are partitioned across cell types and whether common structural determinants or post-translational signals select between them.
  • No structural model integrating repressor and E3-adaptor roles
  • Genome-wide occupancy and direct target catalog incomplete
  • Context-switch between tumor-suppressor and self-renewal/tumorigenic roles unexplained

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 5 GO:0140110 transcription regulator activity 5 GO:0016874 ligase activity 1 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005634 nucleus 2 GO:0005829 cytosol 1
Pathway
R-HSA-74160 Gene expression (Transcription) 5 R-HSA-162582 Signal Transduction 4 R-HSA-1266738 Developmental Biology 3 R-HSA-168256 Immune System 3
Partners
ABHD17CBCL6CBF1CUL3FIP200KPNA (IMPORTIN-ALPHA)ZBTB16
Complex memberships
BCL6B-CUL3 E3 ubiquitin ligase complexmSin3A/HDAC1 co-repressor complex (recruited via BCL6)

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 BAZF (BCL6B) contains BTB/POZ and Krüppel-like zinc finger domains; it associates with BCL6 via its BTB/POZ domain and localizes to the nucleus. BAZF binds specifically to BCL6 DNA-binding sequences and functions as a transcriptional repressor. Repressor activity is associated with both the BTB/POZ domain and a conserved 17-amino-acid sequence in the middle portion of BAZF. Co-immunoprecipitation, nuclear localization assay, reporter gene/transcriptional repression assay, domain deletion analysis Molecular and cellular biology High 9632807
2001 BAZF (BCL6B) binds to a consensus DNA sequence (CBS: 5'-ATTCCTAGAAAG-3') essentially identical to that of BCL6; three nucleotides at positions 6, 8, and 9 are critical for binding. BAZF and BCL6 can also bind STAT6-binding sequences (CD23b, IgE germline ε, IL-4 elements) with weak affinity, and a C-to-T mutation in the IL-4 STAT6-binding element strongly enhances their binding. Electrophoretic mobility shift assay (EMSA), site-directed mutagenesis of binding sequences Biochemical and biophysical research communications High 11374866
2003 BAZF (BCL6B) requires BCL6 to exert transcriptional repression: BAZF cannot function as a repressor in BCL6-deficient fibroblasts or BCL6-null cell lines, but repressor activity is restored when the BTB/POZ domain or the middle portion of BCL6 is reintroduced. BAZF does not directly bind mSin3A or HDAC1; instead it recruits the mSin3A/HDAC1 complex indirectly through association with BCL6. Repressor activity is sensitive to the HDAC inhibitor trichostatin A. Reporter gene assay in BCL6-deficient cells, complementation with BCL6 domain constructs, trichostatin A treatment, co-immunoprecipitation (BTB/POZ and middle-portion binding) Biochemical and biophysical research communications High 12659862
2004 BAZF (BCL6B) is required for TCR-triggered proliferation of naive CD4+ T cells but not memory T cells; BAZF-deficient mice show impaired naive CD4+ T cell proliferation to anti-CD3, while lck-BAZF transgenic mice show augmented proliferation. The data suggest BAZF attenuates BCL6's inhibitory effect on naive T cell activation through BCL6/BAZF heterodimer formation. BAZF-knockout mouse generation, lck-BAZF transgenic mice, T cell proliferation assay with anti-CD3 International immunology Medium 15314041
2005 BCL6B is expressed in a subset of antigen-experienced CD8+ T cells. Ectopic BCL6B expression diminishes CD8+ T cell growth in response to IL-2 in vitro. BCL6B-deficient memory CD8+ T cells show a cell-autonomous defect in effector cell numbers generated upon antigen rechallenge (secondary response), while primary responses are normal. BCL6B is therefore required for the enhanced magnitude of the secondary CD8+ T cell response. BCL6B gene-interrupted mouse model, adoptive transfer/rechallenge assays with vaccinia (H-Y epitope) and influenza (NP peptide), in vitro IL-2 proliferation assay with ectopic BCL6B expression Proceedings of the National Academy of Sciences of the United States of America High 15833813
2007 BAZF (BCL6B)-deficient mice have reduced cycling hematopoietic progenitor cells (HPC) in bone marrow and increased cycling HPC in spleen, mirroring BCL6-deficient mice. HPC from BAZF-deficient mice are resistant to chemokine-induced myelosuppression and lack synergistic response to GM-CSF plus SCF. Depletion of CD8+ T cells in BAZF-deficient mice reverses these hematopoietic defects, indicating BCL6B regulates HPC homeostasis through an indirect CD8+ T cell-dependent pathway. BAZF-knockout mouse, hematopoietic progenitor colony assays, chemokine suppression assays, CD8+ T cell depletion rescue experiment Molecular and cellular biology High 17526724
2012 BAZF (BCL6B) is induced in endothelial cells by VEGF-A, binds to the Notch signaling factor CBF1, and promotes polyubiquitination-dependent degradation of CBF1 through a BAZF-CUL3 E3 ligase complex. BAZF disruption in vivo reduces tip cell number, filopodia protrusion, and vascular plexus formation in mouse retina (phenotype overlapping Notch activation), and impairs angiogenesis in skin-wound healing. Co-immunoprecipitation (BAZF-CBF1, BAZF-CUL3), polyubiquitination assay, BAZF-knockout mouse, retinal vascularization analysis, skin wound-healing angiogenesis model Blood High 22279058
2012 FGF2 activates MAP2K1 (MEK1) signaling to upregulate Bcl6b (and Etv5) in mouse germline stem (GS) cells. An activated form of Map2k1 drives Bcl6b expression and confers FGF2-independent GS cell proliferation. Overexpression of Bcl6b alone in GS cells is sufficient to cause germ cell tumor formation upon transplantation, indicating that excessive Bcl6b-driven self-renewal signals are tumorigenic. MAP2K1 inhibitor (PD0325901) treatment, activated Map2k1 transfection, Bcl6b/Etv5 transfection into GS cells, in vitro proliferation assay, spermatogonial stem cell transplantation tumor formation assay Development (Cambridge, England) High 22491947
2015 BCL6B activates p53 signaling in hepatocellular carcinoma cells by increasing EGR1 expression; restoration of BCL6B re-expression suppresses proliferation, induces apoptosis and G1/S arrest, and sensitizes cells to 5-fluorouracil. 5-aza-2'-deoxycytidine re-expression, western blot for EGR1/p53 pathway components, flow cytometry (apoptosis/cell cycle), cell proliferation assay Oncotarget Medium 25909168
2015 BCL6B re-expression in colorectal cancer cells activates p53 signaling, induces apoptosis and G1/S arrest, and inhibits cell invasion and migration. BCL6B sensitizes cells to 5-fluorouracil. Ectopic BCL6B expression, western blot for p53 pathway, flow cytometry, invasion/migration assays American journal of cancer research Medium 25973304
2018 BCL6B overexpression suppresses colorectal carcinoma cell proliferation and migration by inhibiting PI3K/AKT signaling, reducing AKT phosphorylation, downregulating cyclin D1 and MMP-9, and upregulating E-cadherin. These effects are enhanced by the PI3K inhibitor LY294002. BCL6B transfection, western blot (pAKT), MTT/colony assay, Transwell migration, LY294002 co-treatment International journal of molecular medicine Medium 29393377
2019 ZBTB28 (BCL6B) transactivates TP53 expression by binding to the p53 promoter in competition with BCL6. BCL6 itself is a direct transcriptional target repressed by ZBTB28. ZBTB16 forms heterodimers with ZBTB28 (co-immunoprecipitation) and upregulates ZBTB28 expression to exert tumor suppressor effects. Luciferase reporter assay (p53 promoter), chromatin immunoprecipitation (ChIP) of ZBTB28 on p53 and BCL6 promoters, co-immunoprecipitation (ZBTB16-ZBTB28), gain-of-function in vitro and xenograft experiments Theranostics High 31754389
2020 ZBTB16 forms heterodimers with ZBTB28 (BCL6B) via co-immunoprecipitation, upregulates ZBTB28, and antagonizes BCL6 transcriptional activity to suppress breast cancer cell proliferation and metastasis. ZBTB16 and ZBTB28 together reverse EMT and inhibit colony formation, migration and invasion. Co-immunoprecipitation (ZBTB16-ZBTB28), qRT-PCR, luciferase assay, western blot, xenograft, CCK8/Transwell/colony formation assays Clinical epigenetics Medium 32517789
2021 ZBTB28 (BCL6B) induces autophagy in cervical cancer cells by interacting with the autophagy gene FIP200 and by promoting degradation of Bcl-XL, which reduces the Bcl-XL–BECN1 complex. Autophagy induction by ZBTB28 mediates cellular apoptosis through FIP200 regulation. Ectopic ZBTB28 expression, electron microscopy (autophagosomes), western blot (Bcl-XL, BECN1, FIP200), co-immunoprecipitation or interaction assay, xenograft, flow cytometry Journal of experimental & clinical cancer research Medium 33931087
2022 ZBTB28 (BCL6B) directly regulates IFNAR (interferon-alpha/beta receptor) transcription to activate interferon-stimulated genes. Ectopic ZBTB28 in breast cancer cells downregulates CD24 and CD47 to promote macrophage phagocytosis, demonstrating a role in innate immune surveillance. Ectopic ZBTB28 expression, qRT-PCR and western blot for IFNAR/ISGs, flow cytometry (CD24/CD47), macrophage phagocytosis assay, xenograft Cellular and molecular life sciences Medium 35048182
2023 In retinal endothelial cells, BCL6B expression is induced by VEGF. BCL6B-deficient endothelial cells show Notch signal activation (via CBF1/NICD) and attenuated cord formation by blocking VEGF-VEGFR2 signaling. In BCL6B-knockout mice, breakdown of the inner blood-retinal barrier and pro-angiogenic cytokine induction are abrogated through Notch transcriptional activation. BCL6B-targeting siRNA suppresses choroidal neovascularization lesions and retinal edema in animal models. BCL6B-KO mice, siRNA knockdown in vascular models, optical coherence tomography, immunostaining for CBF1/NICD/Müller cells, in vitro cord formation assay, cynomolgus monkey choroidal neovascularization model Arteriosclerosis, thrombosis, and vascular biology High 37078291
2024 BCL6B suppresses endothelial cell (EC) differentiation from human iPSCs by binding to the promoter region of ETV2 and repressing its transcriptional activity, as demonstrated by ChIP-PCR and luciferase reporter assays. Overexpression of ETV2 rescues the BCL6B-mediated block in EC differentiation. BCL6B overexpression also attenuates tubular structure formation and vessel organoid growth. Doxycycline-inducible hiPSC overexpression/knockdown, luciferase reporter assay (ETV2 promoter), ChIP-PCR (BCL6B on ETV2 promoter), RNA-seq, flow cytometry (EC markers), tube formation assay, vessel organoids Stem cell research & therapy High 39075623
2026 BCL6B directly represses GGT5 transcription by binding to the GGT5 promoter (validated by dual-luciferase reporter and EMSA). Repression of GGT5 by BCL6B modulates MAPK signaling in a GGT5-dependent manner, characterized by decreased ERK phosphorylation and enhanced p38/JNK activation, leading to apoptosis and G0/G1 cell cycle arrest in AML cells. Dual-luciferase reporter assay, electrophoretic mobility shift assay (EMSA), transcriptome sequencing, western blot (ERK/p38/JNK phosphorylation), gain- and loss-of-function in AML lines, zebrafish and nude mouse xenograft models Biology direct High 42083053
2026 ABHD17C-mediated depalmitoylation of BCL6B at Cys442 blocks importin-α/β-mediated nuclear translocation of BCL6B and drives its ubiquitination-dependent degradation in the cytoplasm. Loss of nuclear BCL6B relieves transcriptional repression of the anti-phagocytic signal CD24, increasing its expression and enabling pancreatic cancer cells to evade macrophage phagocytosis. ABHD17C overexpression/knockdown, palmitoylation assay, site-directed mutagenesis (Cys442), subcellular fractionation, co-immunoprecipitation (importin-α/β), ubiquitination assay, CD24 luciferase reporter, macrophage phagocytosis assay, orthotopic xenograft (NSG mice) Advanced science High 42154583

Source papers

Stage 0 corpus · 32 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 FGF2 mediates mouse spermatogonial stem cell self-renewal via upregulation of Etv5 and Bcl6b through MAP2K1 activation. Development (Cambridge, England) 171 22491947
1998 BAZF, a novel Bcl6 homolog, functions as a transcriptional repressor. Molecular and cellular biology 73 9632807
2005 BCL6b mediates the enhanced magnitude of the secondary response of memory CD8+ T lymphocytes. Proceedings of the National Academy of Sciences of the United States of America 66 15833813
2012 BAZF, a novel component of cullin3-based E3 ligase complex, mediates VEGFR and Notch cross-signaling in angiogenesis. Blood 51 22279058
2020 BTB/POZ zinc finger protein ZBTB16 inhibits breast cancer proliferation and metastasis through upregulating ZBTB28 and antagonizing BCL6/ZBTB27. Clinical epigenetics 43 32517789
2001 Binding of BAZF and Bc16 to STAT6-binding DNA sequences. Biochemical and biophysical research communications 39 11374866
2019 Tumor suppressive BTB/POZ zinc-finger protein ZBTB28 inhibits oncogenic BCL6/ZBTB27 signaling to maintain p53 transcription in multiple carcinogenesis. Theranostics 33 31754389
2015 Epigenetic silencing of BCL6B inactivates p53 signaling and causes human hepatocellular carcinoma cell resist to 5-FU. Oncotarget 31 25909168
2015 Epigenetic silencing BCL6B induced colorectal cancer proliferation and metastasis by inhibiting P53 signaling. American journal of cancer research 26 25973304
2022 ZBTB28 inhibits breast cancer by activating IFNAR and dual blocking CD24 and CD47 to enhance macrophages phagocytosis. Cellular and molecular life sciences : CMLS 25 35048182
2013 Promoter hypermethylation of BCL6B gene is a potential plasma DNA biomarker for gastric cancer. Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals 22 24191714
2007 Aberrant regulation of hematopoiesis by T cells in BAZF-deficient mice. Molecular and cellular biology 22 17526724
2003 Bcl6-dependent transcriptional repression by BAZF. Biochemical and biophysical research communications 22 12659862
2021 ZBTB28 induces autophagy by regulation of FIP200 and Bcl-XL facilitating cervical cancer cell apoptosis. Journal of experimental & clinical cancer research : CR 21 33931087
2002 Cloning and characterization of the human BAZF gene, a homologue of the BCL6 oncogene. Biochemical and biophysical research communications 21 11855826
2004 BAZF is required for activation of naive CD4 T cells by TCR triggering. International immunology 20 15314041
2018 Silymarin amplifies apoptosis in ectopic endometrial tissue in rats with endometriosis; implication on growth factor GDNF, ERK1/2 and Bcl-6b expression. Acta histochemica 15 30195499
2015 BCL6B expression in hepatocellular carcinoma and its efficacy in the inhibition of liver damage and fibrogenesis. Oncotarget 15 25970780
2018 BCL6B suppresses proliferation and migration of colorectal carcinoma cells through inhibition of the PI3K/AKT signaling pathway. International journal of molecular medicine 13 29393377
2019 Inhibition of Bcl6b promotes gastric cancer by amplifying inflammation in mice. Cell communication and signaling : CCS 11 31288844
2023 BCL6B Contributes to Ocular Vascular Diseases via Notch Signal Silencing. Arteriosclerosis, thrombosis, and vascular biology 10 37078291
2024 BCL6B-dependent suppression of ETV2 hampers endothelial cell differentiation. Stem cell research & therapy 7 39075623
2022 Carob extract induces spermatogenesis in an infertile mouse model via upregulation of Prm1, Plzf, Bcl-6b, Dazl, Ngn3, Stra8, and Smc1b. Journal of ethnopharmacology 7 36209951
2022 CircTFF1 Promotes Proliferation, Migration and Invasion of Lung Cancer Cells by Facilitating Methylation of BCL6B Promoter via miR-29c-3p/DNMT3A Axis. Molecular biotechnology 7 36376550
2025 Metformin suppresses the mitochondrial and transcriptional response to exercise, revealing a conserved BCL6B-associated angiogenic program. Journal of applied physiology (Bethesda, Md. : 1985) 6 40695624
2018 Expression of the alternative splicing variants of bcl6b in medaka Oryzias latipes. Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology 6 30292753
2021 Epigenetic silencing of ZBTB28 promotes renal cell carcinogenesis. Asia-Pacific journal of clinical oncology 2 34161675
2025 Insight into the Role of the BCL6B Gene in Biological Functions and Disease Progression. Journal of Cancer 1 41049002
2025 Distinct roles of Atf3, Zfp711 and Bcl6b in early embryonic hematopoietic and endothelial lineage specification. Development (Cambridge, England) 1 41200855
2026 BCL6B suppresses acute myeloid leukemia progression by transcriptionally repressing GGT5 and modulating MAPK signaling. Biology direct 0 42083053
2026 ABHD17C-Mediated S-Depalmitoylation of BCL6B Enhances CD24 Transcription to Resist Macrophage Phagocytosis in Pancreatic Cancer. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 0 42154583
2025 [The potential of BCL6B as a therapeutic target for chorioretinal vascular lesions]. Nihon yakurigaku zasshi. Folia pharmacologica Japonica 0 39756899

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