Affinage

BACH2

Transcription regulator protein BACH2 · UniProt Q9BYV9

Length
841 aa
Mass
92.5 kDa
Annotated
2026-06-09
100 papers in source corpus 54 papers cited in narrative 53 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BACH2 is a BTB-bZIP transcriptional repressor that enforces quiescence and restrains terminal differentiation across lymphoid lineages by competing with activating transcription factors at shared regulatory elements (PMID:23728300, PMID:27158840, PMID:32515782). It binds Maf recognition elements (MAREs) as a heterodimer with small Maf proteins such as MafK and recruits co-repressor machinery — SMRT, and an HDAC3-containing NCoR1/NCoR2/TBL1X/RIF1 complex that deacetylates histones at target loci — to silence transcription (PMID:9755173, PMID:17046816, PMID:26786103). In B cells BACH2 represses the plasma-cell master regulator Blimp-1 (Prdm1) by binding MAREs in the Prdm1 promoter and intron 5, delaying Blimp-1 induction to create the time window required for class switch recombination and somatic hypermutation; genetic loss of Blimp-1 restores class switching in Bach2-deficient B cells, placing BACH2 upstream of this network (PMID:15152264, PMID:17046816, PMID:20953163, PMID:26786103), and the BLIMP1–BACH2 balance dictates memory B cell versus plasma cell fate (PMID:38969872). In T cells BACH2 represses effector differentiation programs and is required for regulatory T cell formation, maintaining naive and Treg quiescence by occupying enhancers and attenuating AP-1, BATF-IRF4, and IRF4-driven TCR-induced transcription (PMID:23728300, PMID:27581382, PMID:31937752, PMID:32515782); it likewise establishes stem-like CD8+ T cell programs and suppresses terminal exhaustion during chronic infection (PMID:33574619), restrains T follicular helper differentiation by repressing Bcl-6, Cxcr5, and c-Maf (PMID:30833348, PMID:30971440, PMID:31552021), represses CD25/IL-2R signaling in Tregs (PMID:33979619), and acts as an intrinsic brake on NK cell maturation (PMID:36178457, PMID:36190189). BACH2 activity is controlled post-translationally: PI3K-Akt-mTORC1 phosphorylates BACH2 (notably at S535, and at S521 downstream of BCR/ABL) to drive CRM1-dependent nuclear export and cytoplasmic sequestration (PMID:10809773, PMID:17018862, PMID:26620562, PMID:28993481), SENP3-mediated deSUMOylation promotes nuclear retention (PMID:30089837), heme binds an intrinsically disordered Cys-Pro-motif region to inhibit DNA binding and reduce stability (PMID:21444915, PMID:25444856), and oxidative stress abrogates nuclear export, driving PML-body-associated repression and apoptosis (PMID:10809773, PMID:11923289, PMID:15060166). BACH2 haploinsufficiency, through mutations that disrupt homodimerization or cause aggregation, causes a syndrome of immunodeficiency and autoimmunity (BRIDA) (PMID:28530713). Beyond immune cells, BACH2 functions at the erythro-myeloid bifurcation in a mutual-repression network with C/EBPβ to promote erythropoiesis and B-cell development (PMID:25344725, PMID:28273455, PMID:30250186), and acts as a regulator of pancreatic β-cell survival and type 2 diabetes cell states (PMID:34907913, PMID:24608439).

Mechanistic history

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

    Establishing BACH2 as a sequence-specific repressor defined its core molecular activity: heterodimerization with small Mafs to bind MAREs and recruit co-repressors.

    Evidence Co-IP, EMSA, and reporter assays on the immunoglobulin heavy chain 3' enhancer in B-cell extracts

    PMID:9755173

    Open questions at the time
    • Direct target genes in vivo not yet mapped
    • Co-repressor mechanism not detailed beyond SMRT binding
  2. 2002 High

    Identifying CRM1-dependent nuclear export and oxidative-stress-triggered nuclear accumulation revealed that BACH2 localization, not just expression, gates its repressive activity and links it to redox-induced apoptosis at PML bodies.

    Evidence CLS mutagenesis, leptomycin B, subcellular imaging, retroviral single-cell fate tracking

    PMID:10809773 PMID:11923289

    Open questions at the time
    • Upstream signals controlling CLS not defined in these studies
    • Physiological context of PML-body apoptosis unclear
  3. 2004 High

    Genetic knockout demonstrated BACH2 is required for class switch recombination and somatic hypermutation, and that SUMOylation and the BTB domain govern its recruitment to repressive PML-associated foci.

    Evidence Bach2 knockout mice with isotype analysis; FRAP, mutagenesis, and SUMOylation assays

    PMID:15060166 PMID:15152264

    Open questions at the time
    • Direct CSR target loci not yet identified
    • Link between focus formation and physiological repression incomplete
  4. 2006 High

    Demonstrating direct MARE-mediated repression of Prdm1 and PI3K/S6K phosphorylation at S521 connected BACH2's molecular target (Blimp-1) to a post-translational control circuit.

    Evidence EMSA, ChIP, reporter, shRNA for Prdm1; phospho-mapping and S521A mutagenesis in CML cells

    PMID:17018862 PMID:17046816

    Open questions at the time
    • Full kinase identity not yet resolved (later refined to mTORC1)
    • Quantitative contribution of each phosphosite unknown
  5. 2008 Medium

    Showing cooperative repression of Prdm1 by BACH2 and BCL6 established that BACH2 acts within a partner network rather than alone in germinal center B cells.

    Evidence Co-IP, ChIP, EMSA, reporter assays in B cells

    PMID:18256039

    Open questions at the time
    • BTB-independent BACH2-BCL6 interaction interface not mapped
    • Context-dependence of cooperation vs antagonism not yet recognized
  6. 2010 High

    Genetic epistasis placed BACH2 upstream of a Blimp-1-dependent network, mechanistically explaining how BACH2 timing licenses CSR.

    Evidence Bach2/Blimp-1 double-knockout mice with GRN modeling

    PMID:20953163

    Open questions at the time
    • Quantitative kinetics of the timing window in vivo not fully defined
  7. 2011 High

    Biochemistry and crystallography defined two regulatory inputs: heme binding inhibits DNA binding and destabilizes BACH2, and the POZ/BTB dimer carries a redox-sensitive intersubunit disulfide.

    Evidence In vitro DNA-binding/heme assays, B-cell cultures, in vivo heme; 2.1 Å crystal structure with disulfide detection

    PMID:21444915 PMID:22194330

    Open questions at the time
    • Heme-binding site not yet localized (resolved in 2014)
    • Functional consequence of the POZ disulfide in cells untested
  8. 2013 High

    Genome-wide ChIP-seq across CD4+ and CD8+ T cells established BACH2 as a broad repressor of effector/memory programs required for Treg formation and naive-state maintenance, and revealed its competition with BCL6 to control pre-B p53-dependent selection.

    Evidence Bach2 knockout mice, ChIP-seq, expression profiling, Treg suppression and leukemia transplantation assays

    PMID:23728300 PMID:23754397 PMID:23850379 PMID:23852341

    Open questions at the time
    • Mechanism of activating-complex displacement not yet defined
    • Direct vs indirect targets among many ChIP-seq peaks not fully distinguished
  9. 2014 High

    Mapping heme binding to a disordered Cys-Pro-motif region (331–520) and identifying upstream regulators (Menin) extended the model of how BACH2 levels and activity are set.

    Evidence UV-Vis/CD/DLS/SAXS and GAL4-luciferase; Menin ChIP and T-cell-specific knockout

    PMID:24694524 PMID:25444856

    Open questions at the time
    • In vivo relevance of heme-induced conformational change unclear
    • Interplay between heme region and phosphorylation/SUMO sites untested
  10. 2014 High

    Genetic and ChIP studies revealed a developmental role: BACH2 (with BACH1 and EBF1) represses myeloid genes in lymphoid progenitors to promote B-cell fate.

    Evidence Overexpression in EBF1-deficient pre-pro-B cells, single-cell CLP analysis, ChIP

    PMID:25344725

    Open questions at the time
    • Direct vs cooperative contributions of BACH1 vs BACH2 not fully separated
  11. 2016 High

    Defining the mTORC1-S535 phosphorylation axis, BACH2-BATF complex formation, and AP-1/BATF-IRF4 competition unified the regulatory logic: signaling controls BACH2 localization while BACH2 outcompetes activators at AP-1 motifs; human haploinsufficiency (BRIDA) confirmed dosage sensitivity.

    Evidence MS phospho-mapping and in vitro mTORC1 assay; Co-IP and ChIP for BATF; ATAC-seq/ChIP-seq in CD8+ T cells; human genetics and dimerization/stability assays

    PMID:26620562 PMID:27158840 PMID:27581382 PMID:28530713

    Open questions at the time
    • Structural basis of AP-1 site competition not resolved
    • Generality of competition mechanism across loci incompletely mapped
  12. 2016 High

    Identifying the HDAC3/NCoR co-repressor complex provided the epigenetic effector arm of BACH2 repression at Prdm1.

    Evidence MS purification of the BACH2 complex, ChIP, RNAi, histone modification analysis

    PMID:26786103

    Open questions at the time
    • Whether the same complex operates at non-Prdm1 targets not shown
  13. 2017 High

    Multiple studies mapped upstream transcriptional control of BACH2 (IL-2/ERK/ELK1 super-enhancer repression, NF-κB/c-Rel, PAX5, Ikaros, AHR) and a Bach2–C/EBPβ mutual-repression network, embedding BACH2 in lineage-deciding circuits.

    Evidence ChIP-seq/RNA-seq and reporter assays for the BACH2 super-enhancer; c-Rel, PAX5, Ikaros, AHR ChIP; C/EBPβ co-binding and knockouts

    PMID:21296099 PMID:22858985 PMID:26522720 PMID:28030830 PMID:28273455 PMID:29129929

    Open questions at the time
    • Hierarchy among the many upstream regulators not integrated
    • Some links (Ikaros, AHR, PAX5) rest on single-lab Medium evidence
  14. 2018 High

    Discovery of SENP3-mediated deSUMOylation as a nuclear-retention switch and BACH2/BACH1 roles in erythropoiesis and BCR-driven proliferation broadened both its regulation and its functional reach.

    Evidence Senp3 conditional knockout and SUMO Co-IP; Bach1/Bach2 knockouts and human CD34+ knockdown; BrdU/cell-cycle/ChIP and Bcl-xL rescue

    PMID:29540581 PMID:30089837 PMID:30250186

    Open questions at the time
    • Coordination between SUMO and phospho switches not directly tested
    • SUMO E3/site specificity on BACH2 not fully defined
  15. 2019 Medium

    Context-dependent regulation of Tfh differentiation showed BACH2 can repress Bcl-6, Cxcr5, and c-Maf in T cells, opposite to its cooperative role with BCL6 in GC B cells.

    Evidence Conditional knockouts, ChIP, and reporter assays in Tfh cells

    PMID:30833348 PMID:30971440 PMID:31552021

    Open questions at the time
    • Molecular basis for opposite BACH2-BCL6 relationships across cell types unresolved
    • Several findings are single-lab Medium confidence
  16. 2020 High

    Chromatin-accessibility studies established that BACH2 maintains Treg quiescence by competing with AP-1 and IRF4 for enhancer occupancy, defining a unifying competition mechanism.

    Evidence Bach2 conditional knockout, ChIP-seq, ATAC-seq, Bach2/IRF4 epistasis, tumor models

    PMID:31937752 PMID:32515782

    Open questions at the time
    • Direct biochemical competition for individual sites not structurally resolved
  17. 2021 High

    Single-cell multiomics and conditional genetics defined BACH2 as the gatekeeper of stem-like CD8+ T cell fate and Treg CD25/IL-2R quiescence, and revealed non-immune roles in β-cell/T2D states and HIV-1 Treg persistence.

    Evidence scRNA/scATAC-seq with gain/loss-of-function in chronic infection; ChIP at CD25; islet gain/loss-of-function and BACH inhibitor in diabetic mice; HIV integration sequencing and overexpression in Tregs

    PMID:28887441 PMID:33574619 PMID:33979619 PMID:34907913

    Open questions at the time
    • Mechanism of epigenetic silencing of exhaustion program not fully defined
    • β-cell mechanism partly distinct from canonical lymphoid repression
  18. 2024 High

    Recent single-cell work extended BACH2's role to NK cell maturation, Th17 program diversification, and gut tissue-resident memory, and refined the BLIMP1-BACH2 balance controlling memory B cell recall fate.

    Evidence Conditional knockouts, scATAC/scRNA-seq, EAE and tumor metastasis models; DOGMA/TREK-seq in gut Trms; fate-mapping of MBC subsets

    PMID:36178457 PMID:38969872 PMID:39009838 PMID:40845842

    Open questions at the time
    • Cell-type-specific partner usage across these contexts not yet unified
    • How upstream signals tune BACH2 dosage in each niche incompletely defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple regulatory inputs (mTORC1 phosphorylation, SUMO/SENP3, heme, redox/disulfide) are integrated in real time to set BACH2 nuclear dosage and target selection, and the structural basis of its competition with AP-1/IRF4/BATF complexes, remain unresolved.
  • No integrated model linking the post-translational switches
  • No structure of BACH2 bound to DNA in competition with activating complexes
  • Partner/co-repressor usage across non-B-cell contexts not systematically mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 6 GO:0003677 DNA binding 5 GO:0098772 molecular function regulator activity 2
Localization
GO:0005634 nucleus 4 GO:0005829 cytosol 3
Pathway
R-HSA-168256 Immune System 6 R-HSA-1266738 Developmental Biology 3 R-HSA-4839726 Chromatin organization 3 R-HSA-74160 Gene expression (Transcription) 3
Partners
BATFBCL6HDAC3IRF4MAFKNCOR1SENP3SMRT
Complex memberships
BACH2-BATF complexBACH2-small Maf (MafK) heterodimerHDAC3/NCoR1-NCoR2-TBL1X-RIF1 co-repressor complex

Evidence

Reading pass · 53 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 BACH2 forms heterodimers with small Maf proteins (e.g., MafK) and binds Maf recognition elements (MAREs) in the immunoglobulin heavy chain 3' enhancer, acting as a negative regulator of that enhancer. BACH2 also binds the co-repressor SMRT. Co-immunoprecipitation, EMSA/DNA binding assays, B-cell extract analysis, reporter assays The EMBO journal High 9755173
2000 BACH2 undergoes leptomycin B-sensitive (CRM1/exportin-1-dependent) nuclear export via a C-terminal cytoplasmic localization signal (CLS). Oxidative stress abolishes CLS activity, causing nuclear accumulation of BACH2 and silencing of MARE-dependent transcription. Reporter assays, mutagenesis of CLS, leptomycin B treatment, subcellular localization imaging The Journal of biological chemistry High 10809773
2002 Upon oxidative stress, BACH2 accumulates in the nucleus and forms nuclear foci that associate with PML nuclear bodies, promoting apoptosis. This apoptosis-inducing function is specific to BACH2 (not shared by Bach1) and requires nuclear accumulation beyond what leptomycin B alone provides. Retroviral expression (BACH2-EGFP bicistronic), single-cell fate tracking, immunofluorescence The Journal of biological chemistry Medium 11923289
2004 Transcription activity associated with PML nuclear bodies is selectively repressed upon recruitment of BACH2 around PML bodies following oxidative stress. BACH2 shows rapid turnover in nuclear foci (FRAP). The BTB domain is essential for focus formation, and SUMOylation of BACH2 is required for its recruitment around PML bodies. FRAP, fluorescence microscopy, mutagenesis, sumoylation assays Molecular and cellular biology High 15060166
2004 BACH2 is required for class switch recombination (CSR) and somatic hypermutation (SHM) of immunoglobulin genes in activated B cells. In the absence of Bach2, B cells expressed Blimp-1 and XBP-1 and differentiated into IgM plasma cells but failed to undergo CSR. Genetic ablation (Bach2 knockout mice), in vitro B cell stimulation, immunoglobulin isotype analysis Nature High 15152264
2006 BACH2 represses expression of Blimp-1 (encoded by Prdm1) in B cells by binding, as a heterodimer with MafK, to a MARE in the Prdm1 promoter upstream region and within intron 5. Knockdown of BACH2 accelerates Blimp-1 induction upon BCR stimulation. Reporter gene assays, EMSA, ChIP, co-IP of Bach2/MafK complex, shRNA knockdown The Journal of biological chemistry High 17046816
2006 BCR/ABL signaling phosphorylates BACH2 on serine 521 via the PI3K/S6 kinase pathway, promoting cytoplasmic retention. Substitution S521A leads to nuclear accumulation of BACH2 and greater impairment of CML cell growth. BACH2 transcriptionally represses heme oxygenase-1 (HO-1). Phosphorylation mapping, site-directed mutagenesis (S521A), PI3K inhibitor treatment, reporter assays Blood High 17018862
2007 SMRT recruits HDAC4 to BACH2, and HDAC4 facilitates retention of BACH2 in nuclear foci within the nuclear matrix, enhancing local transcription repression of a chromosomally integrated MARE-driven reporter. Co-IP, confocal microscopy, scratch transcription labeling, 3D reconstruction, reporter assay with chromosomally integrated construct Journal of biochemistry Medium 17383980
2008 BACH2 and BCL6 cooperate to repress the Prdm1 (Blimp-1) gene in B cells. BACH2 (via MafK heterodimer) binds the MARE in intron 5 of Prdm1; BACH2 and BCL6 interact with each other in B cells in a BTB-domain-independent manner. Reporter assays, ChIP, EMSA, Co-IP International immunology Medium 18256039
2010 BACH2 delays Blimp-1 induction in B cells, creating a time window for CSR. Genetic loss of Blimp-1 in Bach2-deficient B cells is sufficient to restore CSR, placing BACH2 upstream of a Blimp-1-dependent GRN. Genetic epistasis (Bach2/Blimp-1 double-knockout mice), in vitro B cell culture, mathematical modeling of GRN The EMBO journal High 20953163
2011 Heme binds to BACH2 and inhibits its DNA-binding activity in vitro. Heme reduces BACH2 half-life in B cells and promotes plasma cell differentiation toward the IgM isotype. Heme oxygenase-1 is repressed by both BACH2 and BACH1 in B cells. In vitro DNA-binding assay (heme inhibition), B-cell primary cultures, in vivo heme injection, reporter assays Blood High 21444915
2011 Crystal structure of the human BACH2 POZ domain at 2.1 Å resolution reveals a dimer that resembles other POZ zinc-finger transcription factors. Dimerization does not require the N-terminal extension implicated in BACH1 dimerization. An intersubunit disulfide bond is present in solution and in eukaryotically expressed protein, suggesting redox regulation of the POZ domain. X-ray crystallography, analytical biochemistry (disulfide bond detection in bacterially and eukaryotically expressed protein) Acta crystallographica. Section D, Biological crystallography High 22194330
2013 BACH2 represses effector differentiation programs in CD4+ T cells and is required for efficient formation of Foxp3+ regulatory T (Treg) cells. In the absence of BACH2, Treg polarization results in inappropriate diversion to effector lineages. BACH2 also constrains full effector differentiation in Th1, Th2, and Th17 lineages. Bach2 knockout mice, genome-wide ChIP-seq, gene expression profiling, Treg suppression assays Nature High 23728300
2013 BACH2 activates p53 to mediate negative selection of pre-B cells that fail productive VH-DJH rearrangement. Pre-BCR signaling ends BACH2-mediated negative selection through BCL6-mediated repression of p53. BACH2 competes with BCL6 for promoter binding and reverses BCL6-mediated repression of p53 and cell cycle checkpoint genes. ChIP-seq, gene expression analysis, genetic models (Bach2+/+ pre-B cells), leukemia transplantation assays Nature medicine High 23852341
2013 BACH2 suppresses effector memory-related genes (e.g., CCR4, ST-2, Blimp-1) in naive T cells to maintain their naive state. ChIP-seq identified direct BACH2 target genes including S100a, HO-1, and PHD3. Bach2-deficient mice, ChIP-seq, forced expression rescue experiments, gene expression analysis Proceedings of the National Academy of Sciences of the United States of America High 23754397
2013 BACH2-MAFK complex binds to regulatory regions of plasma cell genes in germinal center B cells, including PRDM1. BCL6 modulates BACH2 protein stability and their levels are positively correlated in GC B cells. Double heterozygous Bcl6+/-Bach2+/- mice show profound GC reduction, demonstrating cooperative repression. ChIP-seq, double heterozygous mouse genetics, B cell differentiation assays Blood High 24277074
2013 Repression of BACH2 by antigen experience (not simply IgG expression) predisposes IgG1 memory B cells to rapidly differentiate into plasma cells upon rechallenge. Knock-in mouse generating naive IgG1 B cells, antigen rechallenge experiments Immunity Medium 23850379
2014 Heme binds to an intrinsically disordered region (residues 331–520) of BACH2 containing three Cys-Pro motifs, inducing conformational changes (detected by CD, DLS, SAXS) and altering protein interactions mediated by this region. Heme binding involves both 5- and 6-coordinated modes. Spectroscopic analysis (UV-Vis, CD, DLS, SAXS), chemical modification, GAL4-luciferase assay Archives of biochemistry and biophysics High 25444856
2014 Menin binds to the Bach2 locus and maintains histone acetylation there, controlling Bach2 expression. T cell-specific Menin deficiency leads to decreased Bach2 expression and premature CD4+ T cell senescence. Menin ChIP at Bach2 locus, T cell-specific knockout mice, histone acetylation analysis Nature communications Medium 24694524
2014 BACH2 represses myeloid genes in common lymphoid progenitors (CLPs) to promote B cell development, functioning with BACH1 and EBF1. BACH2 and BACH1 bind to presumptive regulatory regions of myeloid genes. Overexpression in EBF1-deficient pre-pro-B cells, single-cell CLP analysis, ChIP Nature immunology High 25344725
2015 BACH2 is phosphorylated at multiple sites in B cells via the PI3K-Akt-mTOR pathway (specifically mTORC1 phosphorylates BACH2 in vitro). Serine 535 is the critical site: a single S535 mutation abolishes cytoplasmic accumulation and promotes nuclear localization. S509 plays an auxiliary role. Mass spectrometry phosphorylation mapping, site-directed mutagenesis, kinase inhibitors, in vitro mTORC1 phosphorylation assay The Journal of biological chemistry High 26620562
2016 BACH2 is recruited to enhancers in naive CD8+ T cells where it limits expression of TCR-driven genes by attenuating availability of AP-1 sites to Jun family transcription factors. Upon effector differentiation, reduced BACH2 expression and its phosphorylation enable unrestrained TCR-driven effector programs. ChIP-seq, ATAC-seq, Bach2 knockout mice, viral infection model Nature immunology High 27158840
2016 BACH2 forms a complex with BATF and binds regulatory regions of Th2 cytokine gene loci, antagonizing recruitment of the BATF-IRF4 complex to AP-1 motifs and suppressing Th2 cytokine production. Bach2 also suppresses Batf and Batf3 expression through two distinct pathways: direct binding to their gene loci and inhibition of IL-4 production. Co-IP of BACH2-BATF complex, ChIP, genetic knockout mice, cytokine assays Nature communications High 27581382
2016 BACH2 haploinsufficiency causes a syndrome of immunodeficiency and autoimmunity (BRIDA). Disease-causing mutations disrupt protein stability by interfering with homodimerization or causing protein aggregation. Analogous lymphocyte defects observed in Bach2-heterozygous mice. Human genetics, protein stability assays, homodimerization assays, heterozygous mouse model Nature immunology High 28530713
2016 BACH2 epigenetically represses the Prdm1 locus by interacting with HDAC3-containing co-repressor complexes (including NCoR1, NCoR2, TBL1X, and RIF1). HDAC3 deacetylates histones H3/H4 at the Prdm1 intron 5 MARE. Knockdown of HDAC3 or NCoR1 in B cells increases Prdm1 expression. Purification of BACH2 complex (mass spectrometry), ChIP, RNAi knockdown, histone modification analysis The Journal of biological chemistry High 26786103
2017 mTORC1 inhibits BACH2 nuclear accumulation and reduces its stability in pre-B cells; mTORC2 inhibits FoxO1, reducing Bach2 mRNA expression. The mTOR-Bach2 cascade regulates cell cycle (via Ccnd3/cyclin D3 as a direct BACH2 target) and class switch recombination. mTOR complex-specific inhibitors, ChIP, expression profiling, Bach2-deficient mice Molecular and cellular biology High 28993481
2017 HIV-1 insertions within the BACH2 locus (upstream of the start codon, same transcriptional orientation) generate chimeric viral-BACH2 mRNAs predicted to encode full-length BACH2. Overexpression of BACH2 in primary T regulatory cells increases their proliferation and survival, providing selective advantage. Integration site sequencing, chimeric mRNA detection, overexpression in primary T regulatory cells, proliferation/survival assays Nature communications Medium 28887441
2017 In B cells, IL-2 signals through ERK/ELK1 to repress BACH2 transcription via an active regulatory region within the BACH2 super-enhancer under ELK1 control. Enforced BACH2 repression in activated B cells unlocks the plasma cell transcriptional program. ChIP-seq, RNA-seq, ELK1 ChIP, reporter assays for BACH2 super-enhancer Nature communications High 29129929
2017 BACH2 promotes tumor immunosuppression through Treg-mediated inhibition of intratumoral CD8+ T cells and IFN-γ. Bach2-deficient mice show markedly impaired tumor growth coinciding with intratumoral activation of adaptive immunity. Bach2 knockout mice, tumor transplantation models, lymphocyte depletion experiments, flow cytometry The Journal of clinical investigation High 26731475
2017 Ikaros directly binds both BCL6 and BACH2 promoters, suppressing BCL6 and promoting BACH2 expression in B-ALL cells. CK2 inhibitors increase Ikaros function, thus regulating BCL6/BACH2 balance. ChIP, CK2 inhibitor treatment, promoter binding assays, gene expression analysis in primary B-ALL cells Oncotarget Medium 28030830
2017 BACH2 represses AP-1-driven interleukin-2 gene transcription in CD4+ T cells by binding to MARE-like sites in the IL-2 proximal promoter in a manner competitive with AP-1. Luciferase reporter assay, ChIP, overexpression and knockdown in primary and transformed CD4+ T cells BMB reports Medium 28855027
2017 Bach2 and C/EBPβ form a mutual repression gene regulatory network in multipotent hematopoietic progenitors: Bach2 represses Cebpb and its target Csf1r; C/EBPβ represses Bach2 and activates Csf1r. Bach2 and C/EBPβ bind overlapping regulatory regions at myeloid target genes. ChIP, expression profiling, genetic knockouts, LPS stimulation Cell reports High 28273455
2018 SENP3-mediated deSUMOylation of BACH2 prevents its nuclear export. SUMOylated BACH2 is exported from the nucleus; SENP3 removes SUMO from BACH2, retaining it in the nucleus where it represses effector T cell differentiation genes and stabilizes Treg gene signatures. SENP3 accumulates in response to ROS. Treg-specific Senp3 knockout mice, co-IP for SUMO-BACH2, subcellular fractionation, gene expression analysis Nature communications High 30089837
2018 Bach2 and Bach1 promote erythropoiesis by repressing C/EBPβ and its myeloid target genes in erythroid-committed cells and at the erythro-myeloid bifurcation. They bind regulatory regions also bound by C/EBPβ. Knockdown of BACH1 or BACH2 in human CD34+ HSPCs impairs erythroid differentiation. Bach2/Bach1 double-knockout mice, overexpression of Bach2 in HSPCs, ChIP, human CD34+ knockdown Nature immunology High 30250186
2018 Bach2 is required for BCR-induced B cell proliferation and survival. Bach2-deficient B cells show reduced BrdU incorporation, increased apoptosis, reduced Bcl-xL expression, and elevated cyclin-dependent kinase inhibitor (Cdkn1a, Cdkn2a, Cdkn2b) expression. ChIP showed Bach2 binds directly to CKI family gene loci. Bach2-deficient mice, BrdU incorporation, cell cycle analysis, ChIP, Bcl-xL reconstitution rescue Journal of immunology High 29540581
2019 In T follicular helper cells, BACH2 directly suppresses Bcl-6 transcription by binding to the Bcl-6 promoter, displacing an activating BATF-IRF4 complex. This is mechanistically distinct from GC B cells where BACH2 and BCL6 cooperate. Ectopic BACH2 overexpression in Tfh cells, reporter assays, ChIP at Bcl-6 promoter Journal of immunology Medium 30833348
2019 Bach2 directly suppresses CXCR5 expression via a novel regulatory element in the CXCR5 locus that negatively regulates CXCR5 promoter activity in a Bach2-dependent manner, controlling Tfh cell differentiation. Bach2-deficient mice, luciferase reporter assay with CXCR5 regulatory element, in vivo differentiation analysis Journal of immunology Medium 30971440
2019 Bach2 directly suppresses Cxcr5 and c-Maf transcription in CD4+ T cells, restraining Tfh cell differentiation. Bach2 deficiency in T cells (but not B cells) results in humoral autoimmunity and Tfh expansion. BCL6 directly suppresses Bach2 expression in Tfh cells. T cell-specific and B cell-specific conditional knockouts, luciferase reporter for Bach2 promoter, ChIP Frontiers in immunology Medium 31552021
2020 BACH2 counteracts IRF4 DNA-binding activity and limits chromatin accessibility at IRF4-dependent loci in Treg cells, thereby attenuating TCR-driven IRF4-dependent transcription and controlling inducible Treg differentiation. Deletion of IRF4 promotes inducible Treg differentiation and rescues pTreg deficiency in Bach2-null mice. Conditional BACH2 knockout in Tregs, ATAC-seq, IRF4 knockout epistasis, ChIP Nature communications High 31937752
2020 In resting Treg cells, BACH2 binds to enhancers of genes involved in activated Treg differentiation and represses their TCR-driven induction by competing with AP-1 factors for DNA binding, maintaining Treg quiescence. Bach2 conditional knockout in Tregs, ChIP-seq, ATAC-seq, tumor models The Journal of experimental medicine High 32515782
2021 BACH2 establishes the transcriptional and epigenetic programs of stem-like CD8+ T cells during chronic infection. BACH2 overexpression enforces stem-like cell fate; BACH2 deficiency impairs stem-like CD8+ T cell differentiation. BACH2 suppresses the terminal exhaustion program via transcriptional repression and epigenetic silencing. BACH2 overexpression and genetic knockout, single-cell scRNA-seq, scATAC-seq, chronic viral infection model Nature immunology High 33574619
2021 BACH2 directly represses CD25 (IL-2Rα) in Treg cells, attenuating IL-2R signaling and controlling quiescence, survival, and maintenance of resting Tregs. BACH2 deficiency in Tregs upregulates CD25/IL-2R signaling, partially counteracting poor survival. BACH2 suppression of CD25/IL-2R signaling in T follicular regulatory cells is required for their differentiation. Treg-specific Bach2 conditional knockout, ChIP at CD25 locus, flow cytometry, IL-2 signaling analysis Cell reports High 33979619
2021 BACH2 inhibition or knockout in T2D islets reverses cellular features of disease and restores insulin secretion. A BACH inhibitor lowers glycemia and increases plasma insulin in diabetic mice. BACH2 is identified as a master regulator driving T2D cell states in pancreatic islets. Single-cell gain- and loss-of-function in islet cells, Ca2+ flux analysis, BACH inhibitor treatment in diabetic mice, human islet experiments The Journal of clinical investigation High 34907913
2021 BACH2 interacts directly with autophagy proteins Beclin-1, Atg3, Atg7, and LC3 in fibroblasts (shown by co-IP). BACH2 modulates UVA-induced senescence through regulation of autophagy; BACH2 knockdown decreases autophagy-related gene expression and enhances senescence. Co-immunoprecipitation, BACH2 knockdown and overexpression, autophagy inhibitor (3-MA), Atg5/Atg7 knockout MEFs Free radical biology & medicine Medium 33882335
2022 BACH2 acts as an intrinsic negative regulator of NK cell maturation and function. BACH2 is expressed in developing and mature NK cells, peaks in immature CD27+CD11b+ cells, and restricts their maturation. BACH2 loss causes accumulation of terminally differentiated, cytotoxically active NK cells and augments control of pulmonary cancer metastasis. NK cell-specific Bach2 conditional knockout, chromatin accessibility (ATAC), flow cytometry, tumor metastasis assay The Journal of experimental medicine High 36178457 36190189
2024 BACH2 promotes immunomodulatory non-pathogenic Th17 programs and restrains proinflammatory TH1-like programs in TH17 cells, both in vitro and in vivo. BACH2 regulates diversification of regulatory vs. proinflammatory chromatin states in TH17 cells. scATAC-seq, scRNA-seq, Bach2 overexpression and deficiency in Th17 cells, in vivo EAE model Nature immunology High 39009838
2024 The relative balance between BLIMP1 and BACH2 determines memory B cell fate upon recall: MBC subsets preferentially producing secondary GCs express comparatively higher BACH2 but lower BLIMP1. Skewing the BLIMP1-BACH2 balance switches fate preferences. IRF4 induces graded PC-specifying epigenetic imprints that progressively shift the balance toward BLIMP1. Fate-mapping of MBC subsets, forced expression experiments, ATAC-seq on history-stamped GC B cells, IRF4 modulation Nature immunology High 38969872
2016 The NF-κB subunit c-Rel directly binds the BACH2 gene in transformed human B cells (shown by ChIP-seq), and c-Rel/RelA deletion or NF-κB/IKK pathway inhibition causes loss of BACH2 expression, revealing BACH2 as an NF-κB target gene in B cells. c-Rel knockout mouse lymphoma model, ChIP-seq in human B cells, NF-κB inhibitor treatment, gene expression analysis Oncogene Medium 26522720
2012 Transcriptional suppression of BACH2 by BCR-ABL is mediated by PAX5 acting as an intermediate effector: BCR-ABL kinase activity reduces PAX5 trans-activation of the BACH2 promoter via a PAX5 binding site, as demonstrated by promoter deletion analysis, transfection assays, and ChIP. BACH2 promoter cloning/deletion analysis, transient transfection, ChIP, PAX5 binding site mutagenesis Leukemia Medium 22858985
2011 The aryl hydrocarbon receptor (AHR), activated by TCDD, directly binds within intron 1 of the Bach2 gene and induces Bach2 expression, leading to increased Bach2 binding to the intron 5 MARE of Prdm1, repression of Prdm1, and suppression of B cell differentiation. ChIP followed by qPCR, EMSA with supershift, RNAi knockdown of Bach2, B cell IgM secretion assay Toxicology and applied pharmacology Medium 21296099
2014 BACH2 inhibition in pancreatic β-cells exacerbates cytokine-induced apoptosis via activation of JNK1 through upregulation of MKK7 and downregulation of PTPN2, leading to phosphorylation of pro-apoptotic BIM. BACH2 overexpression has protective effects. BACH2 siRNA knockdown and overexpression in human and rodent β-cells, cytokine treatment, JNK1/BIM pathway analysis Diabetes Medium 24608439
2017 Bach2 promotes AID-mediated immunoglobulin gene conversion and somatic hypermutation in DT40 B cells by increasing AID expression, in a Blimp-1-independent manner. CRISPR/Cas9 BACH2 knockout in DT40 cells, re-expression rescue, AID expression analysis, gene conversion assay European journal of immunology Medium 28301039
2025 BACH2 shapes gut tissue-resident memory CD4+ T cells (Trms) into long-lived memory and restrains interferon-driven effector function. BACH2 ablation shifts long-lived central memory T cells to effector memory. HIV-1 preferentially infects and persists in BACH2-high gut Trms. Single-cell DOGMA-seq and TREK-seq (chromatin accessibility, transcriptome, surface proteins, TCRs, HIV-1 DNA/RNA), BACH2 ablation experiments, in vitro HIV-1 infection Immunity High 40845842

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 BACH2 represses effector programs to stabilize T(reg)-mediated immune homeostasis. Nature 349 23728300
2016 BACH2 regulates CD8(+) T cell differentiation by controlling access of AP-1 factors to enhancers. Nature immunology 265 27158840
2004 The transcriptional programme of antibody class switching involves the repressor Bach2. Nature 245 15152264
2013 Repression of the transcription factor Bach2 contributes to predisposition of IgG1 memory B cells toward plasma cell differentiation. Immunity 183 23850379
2010 Bach2 represses plasma cell gene regulatory network in B cells to promote antibody class switch. The EMBO journal 182 20953163
2021 BACH2 enforces the transcriptional and epigenetic programs of stem-like CD8+ T cells. Nature immunology 168 33574619
1998 Identification of Bach2 as a B-cell-specific partner for small maf proteins that negatively regulate the immunoglobulin heavy chain gene 3' enhancer. The EMBO journal 157 9755173
2013 Bach2 maintains T cells in a naive state by suppressing effector memory-related genes. Proceedings of the National Academy of Sciences of the United States of America 142 23754397
2006 Plasmacytic transcription factor Blimp-1 is repressed by Bach2 in B cells. The Journal of biological chemistry 138 17046816
2017 BACH2 immunodeficiency illustrates an association between super-enhancers and haploinsufficiency. Nature immunology 125 28530713
2018 SENP3 maintains the stability and function of regulatory T cells via BACH2 deSUMOylation. Nature communications 117 30089837
2014 The transcription repressors Bach2 and Bach1 promote B cell development by repressing the myeloid program. Nature immunology 117 25344725
2007 Recurrent HIV-1 integration at the BACH2 locus in resting CD4+ T cell populations during effective highly active antiretroviral therapy. The Journal of infectious diseases 111 17262715
2013 BACH2 mediates negative selection and p53-dependent tumor suppression at the pre-B cell receptor checkpoint. Nature medicine 101 23852341
2013 Transcription repressor Bach2 is required for pulmonary surfactant homeostasis and alveolar macrophage function. The Journal of experimental medicine 101 24127487
2011 Heme regulates B-cell differentiation, antibody class switch, and heme oxygenase-1 expression in B cells as a ligand of Bach2. Blood 100 21444915
2013 Bach2 regulates homeostasis of Foxp3+ regulatory T cells and protects against fatal lung disease in mice. Journal of immunology (Baltimore, Md. : 1950) 99 24367030
2008 Regulation of the plasma cell transcription factor Blimp-1 gene by Bach2 and Bcl6. International immunology 97 18256039
2017 HIV-1-mediated insertional activation of STAT5B and BACH2 trigger viral reservoir in T regulatory cells. Nature communications 96 28887441
2000 Oxidative stress abolishes leptomycin B-sensitive nuclear export of transcription repressor Bach2 that counteracts activation of Maf recognition element. The Journal of biological chemistry 95 10809773
2017 IL-2 imprints human naive B cell fate towards plasma cell through ERK/ELK1-mediated BACH2 repression. Nature communications 93 29129929
2014 BACH2, a candidate risk gene for type 1 diabetes, regulates apoptosis in pancreatic β-cells via JNK1 modulation and crosstalk with the candidate gene PTPN2. Diabetes 93 24608439
2013 Cooperative transcriptional repression by BCL6 and BACH2 in germinal center B-cell differentiation. Blood 86 24277074
2014 The Menin-Bach2 axis is critical for regulating CD4 T-cell senescence and cytokine homeostasis. Nature communications 83 24694524
2016 Bach2-Batf interactions control Th2-type immune response by regulating the IL-4 amplification loop. Nature communications 82 27581382
2002 Activation of Maf/AP-1 repressor Bach2 by oxidative stress promotes apoptosis and its interaction with promyelocytic leukemia nuclear bodies. The Journal of biological chemistry 82 11923289
2020 Attenuation of TCR-induced transcription by Bach2 controls regulatory T cell differentiation and homeostasis. Nature communications 79 31937752
2015 miR-148a promotes plasma cell differentiation and targets the germinal center transcription factors Mitf and Bach2. European journal of immunology 73 25678371
2014 Orchestration of plasma cell differentiation by Bach2 and its gene regulatory network. Immunological reviews 71 25123280
2016 Epigenetic Regulation of the Blimp-1 Gene (Prdm1) in B Cells Involves Bach2 and Histone Deacetylase 3. The Journal of biological chemistry 65 26786103
2019 Bach2 deficiency leads autoreactive B cells to produce IgG autoantibodies and induce lupus through a T cell-dependent extrafollicular pathway. Experimental & molecular medicine 64 31819031
2020 BACH2 drives quiescence and maintenance of resting Treg cells to promote homeostasis and cancer immunosuppression. The Journal of experimental medicine 60 32515782
2000 Cloning and expression of human B cell-specific transcription factor BACH2 mapped to chromosome 6q15. Oncogene 59 10949928
2016 T Cell Fates Zipped Up: How the Bach2 Basic Leucine Zipper Transcriptional Repressor Directs T Cell Differentiation and Function. Journal of immunology (Baltimore, Md. : 1950) 58 27496973
2021 BACH2 inhibition reverses β cell failure in type 2 diabetes models. The Journal of clinical investigation 57 34907913
2004 Integration of Epstein-Barr virus into chromosome 6q15 of Burkitt lymphoma cell line (Raji) induces loss of BACH2 expression. The American journal of pathology 56 14982850
2016 The transcription factor BACH2 promotes tumor immunosuppression. The Journal of clinical investigation 55 26731475
2006 Bcr-Abl signaling through the PI-3/S6 kinase pathway inhibits nuclear translocation of the transcription factor Bach2, which represses the antiapoptotic factor heme oxygenase-1. Blood 54 17018862
2019 Bach2 Controls T Follicular Helper Cells by Direct Repression of Bcl-6. Journal of immunology (Baltimore, Md. : 1950) 49 30833348
2017 A Bach2-Cebp Gene Regulatory Network for the Commitment of Multipotent Hematopoietic Progenitors. Cell reports 49 28273455
2013 Identification of BACH2 and RAD51B as rheumatoid arthritis susceptibility loci in a meta-analysis of genome-wide data. Arthritis and rheumatism 49 24022229
2012 Duodenal follicular lymphoma lacks AID but expresses BACH2 and has memory B-cell characteristics. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 48 22899287
2019 The Critical Role of Bach2 in Shaping the Balance between CD4+ T Cell Subsets in Immune-Mediated Diseases. Mediators of inflammation 46 32082072
2004 Repression of PML nuclear body-associated transcription by oxidative stress-activated Bach2. Molecular and cellular biology 45 15060166
2003 B-cell-specific transcription factor BACH2 modifies the cytotoxic effects of anticancer drugs. Blood 45 12829606
2019 Bach2 Deficiency Leads to Spontaneous Expansion of IL-4-Producing T Follicular Helper Cells and Autoimmunity. Frontiers in immunology 41 31552021
2019 Inhibition of kras-derived exosomes downregulates immunosuppressive BACH2/GATA-3 expression via RIP-3 dependent necroptosis and miR-146/miR-210 modulation. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 39 31918262
2014 Heme binds to an intrinsically disordered region of Bach2 and alters its conformation. Archives of biochemistry and biophysics 38 25444856
2015 The Transcription Factor Bach2 Is Phosphorylated at Multiple Sites in Murine B Cells but a Single Site Prevents Its Nuclear Localization. The Journal of biological chemistry 37 26620562
2016 Extended exome sequencing identifies BACH2 as a novel major risk locus for Addison's disease. Journal of internal medicine 36 27807919
2013 Nuclear translocation of B-cell-specific transcription factor, BACH2, modulates ROS mediated cytotoxic responses in mantle cell lymphoma. PloS one 35 23936317
2001 Transcription factor BACH2 is transcriptionally regulated by the BCR/ABL oncogene. Genes, chromosomes & cancer 35 11746976
2019 Bach2 Negatively Regulates T Follicular Helper Cell Differentiation and Is Critical for CD4+ T Cell Memory. Journal of immunology (Baltimore, Md. : 1950) 34 30971440
2018 Infection perturbs Bach2- and Bach1-dependent erythroid lineage 'choice' to cause anemia. Nature immunology 33 30250186
2017 The mTOR-Bach2 Cascade Controls Cell Cycle and Class Switch Recombination during B Cell Differentiation. Molecular and cellular biology 33 28993481
2015 The NF-κB subunit c-Rel regulates Bach2 tumour suppressor expression in B-cell lymphoma. Oncogene 33 26522720
2017 Ikaros regulation of the BCL6/BACH2 axis and its clinical relevance in acute lymphoblastic leukemia. Oncotarget 32 28030830
2015 Transcriptome Analysis of CD4+ T Cells in Coeliac Disease Reveals Imprint of BACH2 and IFNγ Regulation. PloS one 32 26444573
2011 Identification of IGHCδ-BACH2 fusion transcripts resulting from cryptic chromosomal rearrangements of 14q32 with 6q15 in aggressive B-cell lymphoma/leukemia. Genes, chromosomes & cancer 32 21319257
2013 BACH2-BCL6 balance regulates selection at the pre-B cell receptor checkpoint. Trends in immunology 31 24332591
2024 Epigenetic recording of stimulation history reveals BLIMP1-BACH2 balance in determining memory B cell fate upon recall challenge. Nature immunology 30 38969872
2022 Bach2: A Key Regulator in Th2-Related Immune Cells and Th2 Immune Response. Journal of immunology research 30 35313725
2018 Promoter methylation of the MGAT3 and BACH2 genes correlates with the composition of the immunoglobulin G glycome in inflammatory bowel disease. Clinical epigenetics 30 29991969
2017 MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression. Bioscience reports 30 28487475
2021 Bach2 attenuates IL-2R signaling to control Treg homeostasis and Tfr development. Cell reports 29 33979619
2018 Bach2 Promotes B Cell Receptor-Induced Proliferation of B Lymphocytes and Represses Cyclin-Dependent Kinase Inhibitors. Journal of immunology (Baltimore, Md. : 1950) 29 29540581
2002 Expression of the oxidative stress-regulated transcription factor bach2 in differentiating neuronal cells. Journal of biochemistry 29 12204112
2022 BACH2 restricts NK cell maturation and function, limiting immunity to cancer metastasis. The Journal of experimental medicine 26 36178457
2017 Bach2 repression mediates Th17 cell induced inflammation and associates with clinical features of advanced disease in chronic pancreatitis. United European gastroenterology journal 25 29511557
2012 Transcriptional suppression of BACH2 by the Bcr-Abl oncoprotein is mediated by PAX5. Leukemia 25 22858985
2013 BACH2: a marker of DNA damage and ageing. DNA repair 24 24075570
2011 Regulation of Bach2 by the aryl hydrocarbon receptor as a mechanism for suppression of B-cell differentiation by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Toxicology and applied pharmacology 24 21296099
2009 Identification of novel Bach2 transcripts and protein isoforms through tagging analysis of retroviral integrations in B-cell lymphomas. BMC molecular biology 24 19159451
2024 BACH2 regulates diversification of regulatory and proinflammatory chromatin states in TH17 cells. Nature immunology 22 39009838
2021 Bach2 regulates autophagy to modulate UVA-induced photoaging in skin fibroblasts. Free radical biology & medicine 22 33882335
2017 SNP co-association and network analyses identify E2F3, KDM5A and BACH2 as key regulators of the bovine milk fatty acid profile. Scientific reports 21 29230020
2016 The double knockout of Bach1 and Bach2 in mice reveals shared compensatory mechanisms in regulating alveolar macrophage function and lung surfactant homeostasis. Journal of biochemistry 21 27387751
2011 A BACH2-BCL2L1 fusion gene resulting from a t(6;20)(q15;q11.2) chromosomal translocation in the lymphoma cell line BLUE-1. Genes, chromosomes & cancer 21 21412927
2022 The transcription factor Bach2 negatively regulates murine natural killer cell maturation and function. eLife 19 36190189
2007 The role of Bach2 in nucleic acid-triggered antiviral innate immune responses. Biochemical and biophysical research communications 19 17991429
2025 Transcription factor BACH2 shapes tissue-resident memory T cell programs to promote HIV-1 persistence. Immunity 18 40845842
2017 Bifurcated BACH2 control coordinates mantle cell lymphoma survival and dispersal during hypoxia. Blood 18 28592433
2016 Charge-state-distribution analysis of Bach2 intrinsically disordered heme binding region. Journal of biochemistry 18 27206783
2022 Diverging regulation of Bach2 protein and RNA expression determine cell fate in early B cell response. Cell reports 17 35793628
2021 Polymorphism in BACH2 gene is a marker of polyglandular autoimmunity. Endocrine 17 33966174
2021 Continuous Culture of Mouse Primary B Lymphocytes by Forced Expression of Bach2. Journal of immunology (Baltimore, Md. : 1950) 16 34389622
2016 A Variant in the BACH2 Gene Is Associated With Susceptibility to Autoimmune Addison's Disease in Humans. The Journal of clinical endocrinology and metabolism 16 27680876
2011 The structure of the Bach2 POZ-domain dimer reveals an intersubunit disulfide bond. Acta crystallographica. Section D, Biological crystallography 16 22194330
2020 Interaction of BACH2 with FUS promotes malignant progression of glioma cells via the TSLNC8-miR-10b-5p-WWC3 pathway. Molecular oncology 15 32892482
2020 Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in systemic lupus erythematosus. FEBS open bio 15 33249782
2018 The critical role of Bach2 in regulating type 2 chronic airway inflammation. International immunology 15 29529253
2017 Bach2 represses the AP-1-driven induction of interleukin-2 gene transcription in CD4＋ T cells. BMB reports 15 28855027
2007 Co-repressor SMRT and class II histone deacetylases promote Bach2 nuclear retention and formation of nuclear foci that are responsible for local transcriptional repression. Journal of biochemistry 15 17383980
2022 CRISPR/Cas9-Mediated Insertion of HIV Long Terminal Repeat within BACH2 Promotes Expansion of T Regulatory-like Cells. Journal of immunology (Baltimore, Md. : 1950) 14 35264460
2020 miR-16-5p and miR-145-5p trigger apoptosis in human gingival epithelial cells by down-regulating BACH2. International journal of clinical and experimental pathology 14 32509061
2019 Age-related changes in the BACH2 and PRDM1 genes in lymphocytes from healthy donors and chronic lymphocytic leukemia patients. BMC cancer 14 30654767
2017 Bach2 regulates AID-mediated immunoglobulin gene conversion and somatic hypermutation in DT40 B cells. European journal of immunology 14 28301039
2017 microRNA-142 is upregulated by tumor necrosis factor-alpha and triggers apoptosis in human gingival epithelial cells by repressing BACH2 expression. American journal of translational research 13 28123644
2008 Regulation of IL-2 expression by transcription factor BACH2 in umbilical cord blood CD4+ T cells. Leukemia 13 18769450
2006 Bach2 is involved in neuronal differentiation of N1E-115 neuroblastoma cells. Experimental cell research 13 16631738

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