Affinage

BACH2

Transcription regulator protein BACH2 · UniProt Q9BYV9

Length
841 aa
Mass
92.5 kDa
Annotated
2026-04-28
100 papers in source corpus 45 papers cited in narrative 45 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BACH2 is a BTB-bZIP transcriptional repressor that functions as a master regulator of lymphoid and hematopoietic cell fate by suppressing effector differentiation programs across multiple immune lineages. It heterodimerizes with small Maf proteins (e.g., MafK) and binds MARE sequences at enhancers and promoters to repress key targets including PRDM1/Blimp-1, thereby creating a temporal window for class switch recombination and somatic hypermutation in B cells, maintaining naive and regulatory states in CD4+ and CD8+ T cells, restraining NK cell maturation, and promoting lymphoid over myeloid commitment in hematopoietic progenitors (PMID:9755173, PMID:15152264, PMID:23728300, PMID:22194330, PMID:36178457, PMID:25344725). BACH2 achieves transcriptional repression by recruiting HDAC3-containing NCoR/SMRT co-repressor complexes and by competing with AP-1 (Jun/Batf) and IRF4 at shared enhancer elements, limiting chromatin accessibility for signal-dependent effector gene activation (PMID:26786103, PMID:27581382, PMID:27158840, PMID:31937752). Its nuclear activity is dynamically regulated: PI3K-Akt-mTORC1-mediated phosphorylation at Ser-535 promotes cytoplasmic retention, SENP3-mediated deSUMOylation prevents nuclear export, oxidative stress inhibits CRM1-dependent export to enforce nuclear accumulation, and heme binding to an intrinsically disordered Cys-Pro-rich region inhibits DNA binding and accelerates degradation (PMID:26620562, PMID:30089837, PMID:10809773, PMID:25444856). Heterozygous loss-of-function mutations in BACH2 cause BACH2-related immunodeficiency and autoimmunity (BRIDA) in humans (PMID:28530713).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 1998 High

    Identification of BACH2 as a B-cell transcriptional repressor that heterodimerizes with small Maf proteins and binds MARE elements established the foundational molecular framework for understanding its repressive function.

    Evidence Co-IP, EMSA, and reporter assays in B-cell extracts identifying MafK heterodimerization and SMRT co-repressor binding

    PMID:9755173

    Open questions at the time
    • Full repertoire of co-repressor complexes unknown
    • Genome-wide binding sites not mapped
    • Regulation of BACH2 activity not understood
  2. 2000 High

    Discovery that BACH2 undergoes CRM1-dependent nuclear export regulated by oxidative stress revealed the first mechanism controlling its subcellular localization and thus repressor activity.

    Evidence Leptomycin B treatment, CLS mutagenesis, and fluorescence microscopy showing oxidative stress blocks nuclear export

    PMID:10809773

    Open questions at the time
    • Identity of reactive cysteines mediating redox sensitivity not defined
    • Physiological oxidative stimuli in immune cells not tested
  3. 2002 High

    Demonstration that oxidative stress drives BACH2 to PML nuclear body-associated foci and promotes apoptosis linked its redox-sensitive localization to a functional cellular outcome.

    Evidence Immunofluorescence co-localization with PML bodies and apoptosis assays in retroviral expression system

    PMID:11923289

    Open questions at the time
    • Whether PML body association is required for apoptosis not resolved
    • Relevance to primary B cells not established
  4. 2004 High

    Genetic ablation of Bach2 proved it is essential for class switch recombination and somatic hypermutation, establishing BACH2 as a central regulator of B-cell diversification rather than merely a repressor of individual genes.

    Evidence Bach2 knockout mice with in vitro B-cell stimulation and immunoglobulin analysis

    PMID:15152264

    Open questions at the time
    • Direct target genes mediating CSR/SHM requirement unknown
    • Mechanism linking BACH2 to AID regulation not defined
  5. 2004 High

    Discovery of BACH2 SUMOylation and its requirement for PML body recruitment, together with the BTB domain's role in focus formation and rapid dynamic turnover, defined how post-translational modification and oligomerization organize BACH2 into functional nuclear compartments.

    Evidence FRAP, sumoylation assays, BTB mutagenesis, and reporter assays

    PMID:15060166

    Open questions at the time
    • SUMO site identity not mapped
    • Whether SUMOylation affects DNA-binding activity not tested
  6. 2006 High

    Identification of PRDM1/Blimp-1 as a direct BACH2 target gene provided the key mechanistic link explaining how BACH2 delays plasma cell differentiation and enables CSR.

    Evidence EMSA, ChIP at PRDM1 MARE, reporter assays, and shRNA knockdown in primary Bach2-deficient B cells

    PMID:17046816

    Open questions at the time
    • Whether PRDM1 repression alone accounts for CSR rescue not tested
    • Genome-wide target repertoire not yet mapped
  7. 2006 High

    Discovery that BCR/ABL-driven PI3K/S6K signaling phosphorylates BACH2 at S521 to promote cytoplasmic retention established that oncogenic signaling inactivates BACH2 by controlling its localization.

    Evidence Site-directed mutagenesis, phosphorylation assays, subcellular fractionation in CML cells

    PMID:17018862

    Open questions at the time
    • Whether this mechanism operates in normal B cells not shown
    • Identity of kinase directly phosphorylating S521 not fully resolved
  8. 2010 High

    Genetic epistasis showing that loss of Blimp-1 in Bach2-null B cells restores CSR proved that BACH2 acts upstream of Blimp-1 in the B-cell gene regulatory network, and that the CSR defect is due to premature Blimp-1 derepression.

    Evidence Bach2/Prdm1 double-knockout mice with mathematical modeling of the GRN

    PMID:20953163

    Open questions at the time
    • Additional BACH2 targets contributing to GC B-cell program not fully defined
    • Whether time-delay model applies across all CSR isotypes not tested
  9. 2011 High

    Biochemical and structural characterization showed heme binds BACH2 to inhibit DNA binding and reduce protein stability, and the BTB domain crystal structure revealed a disulfide-linked homodimer, defining two key regulatory inputs and the structural basis for dimerization.

    Evidence In vitro heme-binding assays, pulse-chase stability assays, X-ray crystallography at 2.1 Å

    PMID:21444915 PMID:22194330

    Open questions at the time
    • Physiological heme concentrations in B cells during differentiation not measured
    • How heme binding is coordinated with phosphorylation/SUMO signals unknown
  10. 2013 High

    A transformative set of studies extended BACH2's role beyond B cells: it was shown to broadly repress effector CD4+ T-cell programs (Th1/Th2/Th17), promote Foxp3+ Treg formation, maintain naive T-cell identity, activate p53 for pre-B cell negative selection, and cooperate with BCL6 genome-wide in GC B cells.

    Evidence Bach2 KO mice with ChIP-seq, genome-wide expression profiling, Treg transfer, pre-B cell leukemia models, and BCL6 co-occupancy analysis

    PMID:23728300 PMID:23754397 PMID:23852341 PMID:24277074

    Open questions at the time
    • Whether BACH2 and BCL6 form a physical complex on chromatin not established by ChIP-seq alone
    • Mechanism by which BACH2 promotes Foxp3 transcription versus repressing competitors not resolved
  11. 2014 High

    BACH2 was shown to repress myeloid genes in common lymphoid progenitors to enforce B-cell lineage commitment and to promote erythroid over myeloid fate at the erythro-myeloid bifurcation, establishing BACH2 as a hematopoietic lineage decision factor beyond adaptive immunity.

    Evidence Bach2/Bach1 KO mice, single-cell CLP analysis, human CD34+ HSPC knockdown, ChIP at myeloid gene loci

    PMID:25344725 PMID:30250186

    Open questions at the time
    • Relative contributions of BACH1 versus BACH2 at overlapping targets not delineated
    • Whether BACH2 directly represses myeloid TFs or acts through Cebpb alone not fully resolved
  12. 2015 High

    Identification of mTORC1 as the kinase directly phosphorylating BACH2 at Ser-535, with this single site being critical for cytoplasmic retention, unified the PI3K-Akt-mTOR signaling axis as the major pathway controlling BACH2 nuclear activity.

    Evidence Mass spectrometry phosphosite mapping, in vitro mTORC1 kinase assay, S535A mutagenesis in B cells

    PMID:26620562

    Open questions at the time
    • Whether additional kinases phosphorylate other functionally relevant sites not fully explored
    • Phosphatase responsible for BACH2 dephosphorylation unknown
  13. 2016 High

    Multiple studies defined BACH2's mechanism in CD8+ T cells and Tregs: it occupies enhancers to compete with AP-1 factors at TCR-responsive elements, recruits HDAC3/NCoR co-repressor complexes to write repressive chromatin marks, and its haploinsufficiency causes human immunodeficiency (BRIDA).

    Evidence ChIP-seq/ATAC-seq in CD8+ T cells, mass spectrometry of BACH2 complex identifying HDAC3/NCoR/Rif1, and human genetics with protein stability assays

    PMID:26786103 PMID:27158840 PMID:28530713

    Open questions at the time
    • Structural basis for AP-1 competition not resolved
    • BRIDA genotype-phenotype spectrum not fully characterized
  14. 2016 High

    Demonstration that BACH2-Batf heterodimers antagonize Batf-IRF4 complexes at AP-1 motifs in Th2 loci provided a specific molecular mechanism by which BACH2 competes for enhancer access with signal-dependent activating complexes.

    Evidence Co-IP, ChIP-seq, Bach2 KO mice with cytokine measurement

    PMID:27581382

    Open questions at the time
    • Stoichiometry of BACH2-Batf versus Batf-IRF4 complexes not measured
    • Whether BACH2-Batf heterodimer has distinct DNA-binding specificity from BACH2-MafK not tested
  15. 2017 High

    The mTORC1/mTORC2 dual regulation of BACH2 (protein localization via mTORC1, mRNA expression via mTORC2-FoxO1) and the identification of BACH2-C/EBPβ mutual repression expanded the signaling network controlling BACH2 and its role in myeloid-lymphoid fate balance.

    Evidence mTOR inhibitor treatment with Bach2 KO epistasis; ChIP at Ccnd3 and Cebpb loci; LPS challenge experiments

    PMID:28273455 PMID:28993481

    Open questions at the time
    • Whether mTORC2-FoxO1 regulation of Bach2 is direct or indirect not fully resolved
    • Kinetics of mTOR-BACH2 axis during in vivo immune responses not measured
  16. 2018 High

    Discovery that SENP3-mediated deSUMOylation of BACH2 prevents nuclear export and stabilizes Treg identity revealed a distinct post-translational mechanism (complementary to phosphorylation and heme binding) that controls BACH2 localization in a cell-type-specific manner.

    Evidence Treg-specific Senp3 conditional KO, SUMOylation assays, subcellular fractionation, tumor models

    PMID:30089837

    Open questions at the time
    • Identity of SUMO acceptor lysines on BACH2 not mapped
    • Whether SENP3 regulation of BACH2 operates in B cells or CD8+ T cells not tested
  17. 2020 High

    Conditional KO studies with ChIP-seq/ATAC-seq in Tregs demonstrated that BACH2 maintains Treg quiescence by competing with AP-1 at enhancers and counteracting IRF4 to limit chromatin accessibility, with genetic epistasis proving BACH2 and IRF4 oppose each other at shared enhancers.

    Evidence Bach2 conditional KO and Bach2/IRF4 double conditional KO in Tregs with ATAC-seq and ChIP-seq

    PMID:31937752 PMID:32515782

    Open questions at the time
    • How BACH2-IRF4 competition is resolved quantitatively during Treg activation not modeled
    • Whether BACH2 directly modifies IRF4 binding or acts indirectly via chromatin state not distinguished
  18. 2021 High

    Single-cell multi-omic profiling during chronic infection showed BACH2 establishes the stem-like CD8+ T-cell transcriptional and epigenetic program, suppressing terminal exhaustion and positioning BACH2 as a central determinant of T-cell longevity during persistent antigen exposure.

    Evidence scRNA-seq, scATAC-seq, BACH2 KO and overexpression in chronic viral infection models

    PMID:33574619

    Open questions at the time
    • Downstream effectors of BACH2 in stem-like CD8+ T cells beyond known targets not identified
    • Whether BACH2 overexpression can rescue exhausted T cells not tested
  19. 2022 High

    Extension to innate lymphocytes showed BACH2 restricts NK cell maturation and terminal differentiation, demonstrating that BACH2's role as a brake on effector programs spans both adaptive and innate lymphoid lineages.

    Evidence Bach2 conditional KO in NK cells with ATAC-seq and tumor metastasis models

    PMID:36178457

    Open questions at the time
    • Direct BACH2 target genes in NK cells not fully catalogued
    • Whether BACH2 interacts with the same co-repressor complexes in NK cells as in T/B cells unknown
  20. 2024 High

    Single-cell epigenomic studies of memory B-cell fate and TH17 plasticity showed that the BACH2-BLIMP1 balance is epigenetically imprinted by IRF4 during primary responses and that BACH2 establishes distinct chromatin landscapes favoring non-pathogenic TH17 programs, refining the model of BACH2 as an epigenetic gatekeeper.

    Evidence scATAC-seq and scRNA-seq in GC/MBC subsets and TH17 cells with genetic manipulation of BACH2-BLIMP1 balance

    PMID:38969872 PMID:39009838

    Open questions at the time
    • Epigenetic marks directly written or maintained by BACH2-recruited complexes at specific loci not mapped genome-wide
    • How BACH2 levels are set in individual cells during stochastic fate decisions not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key open questions include the full structural basis of BACH2-AP-1/IRF4 enhancer competition, the integration of multiple post-translational signals (phosphorylation, SUMOylation, heme, redox) in vivo, and whether BACH2's non-immune roles (e.g., pancreatic β-cells) employ the same co-repressor mechanisms.
  • No full-length BACH2 structure available
  • In vivo quantitative dynamics of BACH2 post-translational modifications during immune activation not measured
  • Mechanism of BACH2 function in pancreatic islets not resolved relative to immune cell mechanism

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 8 GO:0003677 DNA binding 5 GO:0098772 molecular function regulator activity 3
Localization
GO:0005634 nucleus 5 GO:0005829 cytosol 3 GO:0005654 nucleoplasm 2
Pathway
R-HSA-168256 Immune System 9 R-HSA-74160 Gene expression (Transcription) 6 R-HSA-1266738 Developmental Biology 4 R-HSA-4839726 Chromatin organization 4 R-HSA-162582 Signal Transduction 3 R-HSA-5357801 Programmed Cell Death 3
Partners
BATFBCL6HDAC3HDAC4MAFKNCOR1NCOR2RIF1
Complex memberships
BACH2-Batf heterodimerBACH2-HDAC3-NCoR/SMRT co-repressor complexBACH2-MafK heterodimer

Evidence

Reading pass · 45 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 BACH2 was identified as a B-cell-specific transcription factor that forms heterodimers with small Maf proteins (e.g., MafK) and binds to Maf recognition elements (MAREs) in the IgH 3' enhancer, acting as a negative regulator. BACH2 also binds the co-repressor SMRT. Co-immunoprecipitation, EMSA, B-cell extract binding assays, reporter assays The EMBO journal High 9755173
2000 BACH2 is regulated by oxidative stress-sensitive conditional nuclear export via a C-terminal cytoplasmic localization signal (CLS) that directs leptomycin B-sensitive (CRM1/exportin-1-dependent) nuclear export. Oxidative stressors abrogate this CLS activity, causing nuclear accumulation of BACH2 and repression of MARE-dependent transcription. Mutagenesis, leptomycin B treatment, fluorescence microscopy, reporter assays The Journal of biological chemistry High 10809773
2002 Upon oxidative stress, BACH2 forms nuclear foci associated with PML nuclear bodies and promotes apoptosis. BACH2 acts as a generic repressor of TRE-, MARE-, and ARE-driven transcription, and its nuclear accumulation upon oxidative stress is required but not sufficient for apoptosis induction. Retroviral bicistronic reporter, fluorescence microscopy, apoptosis assays, immunofluorescence co-localization with PML bodies The Journal of biological chemistry High 11923289
2004 BACH2 is required for class switch recombination (CSR) and somatic hypermutation (SHM) of immunoglobulin genes in activated B cells. Genetic ablation of Bach2 in mice shows it is not required for plasma cell differentiation per se but is essential for the CSR process. Bach2 knockout mice, in vitro B-cell stimulation, immunoglobulin analysis Nature High 15152264
2004 Upon oxidative stress, BACH2 is sumoylated, which is required for its recruitment around PML nuclear bodies. BACH2 selectively represses transcription associated with PML bodies; FRAP experiments revealed rapid turnover of BACH2 in nuclear foci, and the BTB domain is essential for focus formation. Fluorescence recovery after photobleaching (FRAP), mutagenesis, sumoylation assays, reporter gene assays Molecular and cellular biology High 15060166
2006 BACH2 directly represses expression of Blimp-1 (encoded by Prdm1) in B cells by binding as a heterodimer with MafK to the MARE upstream of the Prdm1 promoter and in intron 5. Loss of BACH2 leads to more rapid and robust Blimp-1 induction and plasma cell differentiation. EMSA, ChIP, reporter assays, shRNA knockdown, primary Bach2-deficient B cells The Journal of biological chemistry High 17046816
2006 BCR/ABL signaling phosphorylates BACH2 at S521 via the PI3K/S6 kinase pathway, which promotes cytoplasmic retention of BACH2 and prevents nuclear accumulation. Mutation of S521 to alanine leads to nuclear accumulation and greater growth inhibition of CML cells. Mutagenesis, phosphorylation assays, subcellular fractionation, cell growth assays Blood High 17018862
2007 SMRT co-repressor mediates HDAC4 binding to BACH2; HDAC4 facilitates retention of BACH2 in nuclear foci. Co-expression of SMRT and HDAC4 enhances BACH2 nuclear focus formation and local transcriptional repression at MARE-containing reporter genes. Co-immunoprecipitation, confocal microscopy, scratch transcription labeling, reporter assays Journal of biochemistry Medium 17383980
2008 BACH2 interacts with BCL6 in B cells in a BTB-domain-independent manner. Both BACH2 and BCL6 bind to separate regulatory elements (MARE and BCL6-binding element, respectively) of the Prdm1 gene and cooperate to repress its expression; co-expression results in greater repression. Co-immunoprecipitation, ChIP, reporter assays International immunology Medium 18256039
2010 BACH2 represses Blimp-1 in B cells to create a time delay in plasma cell differentiation, allowing a window for class switch recombination. Genetic loss of Blimp-1 in Bach2-/- B cells restores CSR, establishing that Bach2 acts upstream of Blimp-1 in the B-cell gene regulatory network. Double-knockout mouse genetics, mathematical modeling of GRN, in vitro B-cell stimulation assays The EMBO journal High 20953163
2011 Heme binds to BACH2 and inhibits its DNA-binding activity in vitro; heme also reduces BACH2 half-life in B cells. Heme treatment of B cells enhances Blimp-1 transcription and skews plasma cell differentiation toward IgM. Heme oxygenase-1 is repressed by both BACH2 and BACH1 in B cells. In vitro DNA-binding assay, pulse-chase protein stability assay, B-cell culture with heme treatment, reporter assays Blood High 21444915
2011 Crystal structure of the human BACH2 POZ/BTB domain dimer was solved at 2.1 Å resolution. The structure reveals an intersubunit disulfide bond present both in bacterially expressed protein and in eukaryotic cells. The BTB domain mediates dimerization and recruits co-repressors including class II HDACs. X-ray crystallography, biochemical validation in solution and in transfected eukaryotic cells Acta crystallographica. Section D, Biological crystallography High 22194330
2013 BACH2 broadly represses effector CD4+ T-cell differentiation programs (Th1, Th2, Th17) while being required for efficient Foxp3+ Treg cell formation. In Bach2-deficient mice, Treg polarization results in inappropriate diversion to effector lineages, and lethal inflammation is suppressed in a Treg-dependent manner. Genome-wide BACH2 occupancy showed enrichment at enhancers of effector differentiation genes. Bach2 knockout mice, ChIP-seq, genome-wide expression profiling, Treg transfer experiments 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 via 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, Bach2 knockout pre-B cells, leukemia transplant experiments Nature medicine High 23852341
2013 BACH2 maintains naive T cells by suppressing effector-memory-related genes including CCR4, ST-2, and Blimp-1. ChIP-seq identified direct BACH2 target genes (S100 calcium binding protein a, Heme oxygenase-1, prolyl hydroxylase 3). Forced expression of BACH2 restored expression of these genes. ChIP-seq, Bach2-deficient mouse T-cell analysis, forced expression experiments Proceedings of the National Academy of Sciences of the United States of America High 23754397
2013 Antigen-experienced IgG1 memory B cells have repressed Bach2 expression compared to non-experienced IgG1 B cells, and this Bach2 repression contributes to predisposition toward plasma cell differentiation upon rechallenge. Engineered mice with non-experienced IgG1 B cells, gene expression analysis, in vivo rechallenge experiments Immunity Medium 23850379
2013 Bach2 cooperates with BCL6 in germinal center B cells to repress the plasma cell program. BCL6 and BACH2 bind overlapping sets of target genes (~30% peak overlap), including PRDM1 cis-regulatory sequences. BACH2 binds predominantly with heterodimer partner MAFK. BCL6 also modulates BACH2 protein stability, and their levels are positively correlated in GC B cells. ChIP-seq, double-heterozygous knockout mice, protein stability assays, B-cell gene expression profiling Blood High 24277074
2013 BACH2 promotes Foxp3 expression in a TCR/TGF-β-induced Treg differentiation assay and represses the competing Gata3-driven Th2 effector program. Bach2-deficient Treg cells show reduced Bcl-2 and Mcl-1 levels and elevated Bim/Bcl-2 ratio, contributing to reduced survival. Bach2 KO mouse, in vitro Treg induction assay, flow cytometry, gene expression analysis Journal of immunology (Baltimore, Md. : 1950) Medium 24367030
2014 BACH2 represses myeloid genes in B-cell progenitors (common lymphoid progenitors) to promote B-cell lineage commitment. Bach2 and Bach1 bind presumptive regulatory regions of myeloid genes. Bach2-high CLPs are resistant to myeloid differentiation even under myeloid culture conditions. Bach2/Bach1 KO mice, single-cell analysis of CLPs, ChIP, overexpression in pre-pro-B cells lacking EBF1 Nature immunology High 25344725
2014 Menin binds to the Bach2 locus and controls its expression through maintenance of histone acetylation. T cell-specific Menin deficiency results in decreased Bach2 expression and premature CD4+ T cell senescence; this Menin-Bach2 axis regulates cytokine homeostasis. T cell-specific Menin conditional KO mice, ChIP at Bach2 locus, histone acetylation analysis Nature communications High 24694524
2014 Heme binds to an intrinsically disordered region (residues 331–520) of BACH2 containing Cys-Pro motifs. Heme binding is in 5- and 6-coordinated modes, induces conformational changes (revealed by CD, SAXS, DLS), and alters protein interactions mediated by this region. The CP-motif mutant lacks 5-coordinated heme binding. Spectroscopic analysis (UV-Vis, CD), dynamic light scattering, small-angle X-ray scattering, chemical modification, GAL4-based luciferase assay Archives of biochemistry and biophysics High 25444856
2015 Bach2 is phosphorylated at multiple sites in B cells via the PI3K-Akt-mTOR pathway. The mTOR complex 1 (mTORC1) phosphorylates Bach2 in vitro. A single phosphorylation site, Ser-535 (murine), is critical: the Ser-535 mutation abolishes cytoplasmic accumulation and promotes nuclear localization, enhancing Bach2 repressor activity. Mass spectrometry phosphosite identification, kinase inhibitors, mTORC1 in vitro phosphorylation assay, site-directed mutagenesis 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 effector genes by attenuating AP-1 site availability to Jun family signal-dependent transcription factors. Upon effector differentiation, reduced BACH2 expression and its phosphorylation enable unrestrained TCR-driven effector programs. ChIP-seq, ATAC-seq, BACH2 KO mouse, viral infection models Nature immunology High 27158840
2016 Bach2 associates with Batf and together the Bach2-Batf complex binds to regulatory regions of Th2 cytokine gene loci. This complex antagonizes the Batf-Irf4 complex at AP-1 motifs, suppressing Th2 cytokine production. Bach2 also regulates Batf/Batf3 expression by inhibiting IL-4 production and directly repressing Batf/Batf3 gene loci. Co-immunoprecipitation, ChIP-seq, Bach2 KO mouse, cytokine measurement assays Nature communications High 27581382
2016 BACH2 haploinsufficiency causes a syndrome of immunodeficiency and autoimmunity (BRIDA). BACH2 mutations disrupt protein stability by interfering with homodimerization or causing aggregation. BACH2 is associated with a super-enhancer architecture, and SE-associated gene haploinsufficiency is enriched among Mendelian immunodeficiency diseases. Human genetics, patient cell studies, protein stability assays, homodimerization assays, SE chromatin analysis Nature immunology High 28530713
2016 BACH2 promotes tumor immunosuppression through Treg-mediated inhibition of intratumoral CD8+ T cells and IFN-γ. In Bach2-deficient mice, tumor growth is markedly impaired, with high frequencies of rapidly proliferating effector T cells and reduced intratumoral Foxp3+ Tregs. Bach2 KO mouse tumor implantation models, adoptive transfer experiments, intratumoral lymphocyte analysis The Journal of clinical investigation High 26731475
2016 The epigenetic regulation of Prdm1 in B cells involves BACH2 interacting with HDAC3-containing co-repressor complexes (including NCoR1, NCoR2, Tbl1x, and Rif1) to write histone deacetylation marks at the Prdm1 intron 5 MARE. ChIP confirmed binding of HDAC3 and Rif1 to the Prdm1 locus; knockdown of HDAC3 or NCoR1 increased Prdm1 expression. Purification of Bach2 complex by mass spectrometry, ChIP, RNA interference knockdown The Journal of biological chemistry High 26786103
2017 mTOR complex 1 (mTORC1) inhibits nuclear accumulation and stability of Bach2, while mTOR complex 2 (mTORC2) inhibits FoxO1 to reduce Bach2 mRNA expression. Bach2 directly regulates Ccnd3 (cyclin D3) expression. The mTOR-Bach2 cascade controls proper cell cycle arrest in B cells, and mTOR inhibition enhances CSR in a Bach2-dependent manner. mTOR inhibitor treatment, Bach2 KO mice, ChIP, expression profiling, cell cycle analysis Molecular and cellular biology High 28993481
2017 Bach2 and C/EBPβ form a mutual repression gene regulatory network in multipotent hematopoietic progenitors. Bach2 represses Cebpb and Csf1r; C/EBPβ represses Bach2 and activates Csf1r. Both factors bind overlapping regulatory regions at myeloid target genes. LPS reduces Bach2 expression, enhancing myeloid differentiation. ChIP, gene expression profiling, KO mouse models, LPS stimulation experiments Cell reports High 28273455
2017 IL-2 drives BACH2 repression via ERK/ELK1 signaling to direct plasma cell lineage commitment in human naive B cells. Enforced BACH2 repression unlocks the plasma cell transcriptional program. An active regulatory region within the BACH2 super-enhancer is under ELK1 control. RNA-seq, ChIP-seq, ERK/ELK1 inhibitors, B-cell differentiation assays Nature communications High 29129929
2018 SENP3-mediated deSUMOylation of BACH2 prevents its nuclear export, thereby repressing effector T-cell differentiation genes and stabilizing Treg cell-specific gene signatures. Treg-specific deletion of Senp3 results in T-cell activation and autoimmune symptoms. ROS accumulation promotes SENP3 accumulation in Treg cells involved in tumor immunosuppression. Treg-specific Senp3 conditional KO mice, SUMOylation assays, subcellular fractionation, ChIP, tumor immunosuppression models Nature communications High 30089837
2018 Bach2 and Bach1 promote erythroid commitment by repressing the myeloid transcription factor gene Cebpb and its targets at the erythro-myeloid bifurcation step. Bach TFs bind to regulatory regions co-occupied by C/EBPβ. Knockdown of BACH1 or BACH2 in human CD34+ HSPCs impairs erythroid differentiation in vitro. ChIP, Bach2/Bach1 KO and overexpression in HSPCs, human CD34+ siRNA knockdown, erythroid differentiation assays Nature immunology High 30250186
2019 Bach2 directly suppresses Bcl-6 transcription in Tfh cells by binding to the Bcl-6 promoter and replacing an activating Batf-Irf4 complex, thereby controlling the Tfh cell transcriptional network. This is mechanistically distinct from GC B cells, where Bach2 and Bcl-6 are co-expressed. Ectopic overexpression in murine Tfh cells, reporter assays, ChIP at Bcl-6 promoter Journal of immunology (Baltimore, Md. : 1950) Medium 30833348
2019 Bach2 directly suppresses CXCR5 and c-Maf expression in CD4+ T cells by binding to a regulatory element in the CXCR5 locus. Bach2 deficiency results in preferential Tfh cell differentiation but ultimately collapsed CD4+ T cell memory. Bach2 KO mouse, identification of novel CXCR5 regulatory element by reporter assay, in vivo viral infection models Journal of immunology (Baltimore, Md. : 1950) Medium 30971440
2020 BACH2 in resting Treg cells 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, thereby maintaining Treg quiescence. Bach2 conditional KO in Tregs, ChIP-seq, ATAC-seq, tumor immunosuppression models The Journal of experimental medicine High 32515782
2020 BACH2 counteracts the DNA-binding activity of IRF4 and limits chromatin accessibility, thereby attenuating IRF4-dependent transcription in Treg cells. Loss of Bach2 normalizes eTreg differentiation of IRF4-deficient Tregs, establishing genetic epistasis between BACH2 and IRF4. Bach2/IRF4 double conditional KO epistasis experiments, ATAC-seq, ChIP-seq Nature communications High 31937752
2021 BACH2 establishes the transcriptional and epigenetic programs of stem-like CD8+ T cells during chronic infection; BACH2 overexpression enforces stem-like cell fate while BACH2 deficiency impairs stem-like CD8+ T cell differentiation. BACH2 suppresses the terminal exhaustion program through transcriptional repression and epigenetic silencing. BACH2 KO, overexpression, single-cell transcriptomics, single-cell epigenomics (scATAC-seq), chronic viral infection models Nature immunology High 33574619
2021 BACH2 directly represses CD25 (IL-2Rα) transcription in Treg cells, thereby attenuating IL-2R signaling. Upregulated CD25/IL-2R signaling in Bach2-deficient resting Tregs partially counteracts poor survival. Bach2 also suppresses CD25/IL-2R signaling in T follicular regulatory cells to enable their full differentiation. Bach2 conditional KO in Tregs, ChIP at CD25 locus, flow cytometry, in vivo Tfr analysis Cell reports High 33979619
2021 BACH2 knockdown in T2D pancreatic islets reverses cellular features of the disease, restoring a non-diabetic phenotype. BACH2 is identified as a master regulator of T2D islet cell states via single-cell gain- and loss-of-function analyses and glucose-induced Ca2+ flux assays. Single-cell gain/loss-of-function, Ca2+ flux assays, BACH2 KO in T2D islets, BACH inhibitor treatment in diabetic mice and human islets The Journal of clinical investigation Medium 34907913
2022 BACH2 acts as an intrinsic negative regulator of NK cell maturation and function by restricting maturation in the presence of weak stimulatory signals. BACH2 expression positively correlates with TCF1 and negatively correlates with NK effector molecules; lack of BACH2 causes changes in chromatin accessibility and accumulation of activated, terminally differentiated NK cells with augmented anti-tumor cytotoxicity. Bach2 conditional KO in NK cells, ATAC-seq, flow cytometry, tumor metastasis models The Journal of experimental medicine High 36178457
2014 BACH2 regulates apoptosis in pancreatic β-cells via JNK1 modulation: BACH2 inhibition exacerbates cytokine-induced β-cell apoptosis via the mitochondrial pathway by upregulating MKK7 and downregulating PTPN2, leading to increased JNK1 and BIM phosphorylation. BACH2 siRNA knockdown and overexpression in human and rodent β-cells, kinase activity assays, apoptosis assays Diabetes Medium 24608439
2017 Bach2 directly represses the AP-1-driven induction of the interleukin-2 gene in CD4+ T cells by binding to multiple MARE-like sites on the IL-2 proximal promoter in a manner competitive with AP-1 factors. Luciferase reporter assay, ChIP, BACH2 overexpression and knockdown in primary and transformed CD4+ T cells BMB reports Medium 28855027
2018 Bach2 promotes BCR-induced B-cell proliferation and survival by repressing cyclin-dependent kinase inhibitors (Cdkn1a, Cdkn2a, Cdkn2b) and maintaining expression of anti-apoptotic Bcl-xL. ChIP showed direct binding of Bach2 to CKI family gene loci. Bach2 KO mice, BrdU incorporation, ChIP, transcriptome analysis, Bcl-xL reconstitution Journal of immunology (Baltimore, Md. : 1950) High 29540581
2024 The relative strength of BLIMP1 versus BACH2 progressively increases in favor of BLIMP1 in antigen-responding B cells through primary responses, with epigenetic imprinting driven by IRF4 determining MBC fate upon recall. Skewing the BLIMP1-BACH2 balance in fate-predisposed MBC subsets can switch their fate preferences. Single-cell epigenomics, ATAC-seq, genetic manipulation of BLIMP1-BACH2 balance in MBC subsets, history-stamped GC B cell analysis Nature immunology High 38969872
2024 BACH2 promotes immunomodulatory non-pathogenic TH17 programs and restrains proinflammatory TH1-like programs in TH17 cells. BACH2 establishes distinct chromatin landscapes in npTH17 versus pTH17 cells in vitro and in vivo, sharing accessible chromatin configurations with Treg cells in npTH17 cells. scATAC-seq, scRNA-seq, Bach2 KO in TH17 cells, in vitro and in vivo inflammatory disease models Nature immunology High 39009838

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 344 23728300
2016 BACH2 regulates CD8(+) T cell differentiation by controlling access of AP-1 factors to enhancers. Nature immunology 259 27158840
2004 The transcriptional programme of antibody class switching involves the repressor Bach2. Nature 244 15152264
2010 Bach2 represses plasma cell gene regulatory network in B cells to promote antibody class switch. The EMBO journal 181 20953163
2013 Repression of the transcription factor Bach2 contributes to predisposition of IgG1 memory B cells toward plasma cell differentiation. Immunity 178 23850379
2021 BACH2 enforces the transcriptional and epigenetic programs of stem-like CD8+ T cells. Nature immunology 160 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 139 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 122 28530713
2018 SENP3 maintains the stability and function of regulatory T cells via BACH2 deSUMOylation. Nature communications 113 30089837
2014 The transcription repressors Bach2 and Bach1 promote B cell development by repressing the myeloid program. Nature immunology 113 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 110 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 100 24127487
2011 Heme regulates B-cell differentiation, antibody class switch, and heme oxygenase-1 expression in B cells as a ligand of Bach2. Blood 98 21444915
2008 Regulation of the plasma cell transcription factor Blimp-1 gene by Bach2 and Bcl6. International immunology 97 18256039
2013 Bach2 regulates homeostasis of Foxp3+ regulatory T cells and protects against fatal lung disease in mice. Journal of immunology (Baltimore, Md. : 1950) 96 24367030
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 HIV-1-mediated insertional activation of STAT5B and BACH2 trigger viral reservoir in T regulatory cells. Nature communications 93 28887441
2017 IL-2 imprints human naive B cell fate towards plasma cell through ERK/ELK1-mediated BACH2 repression. Nature communications 92 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 92 24608439
2013 Cooperative transcriptional repression by BCL6 and BACH2 in germinal center B-cell differentiation. Blood 84 24277074
2014 The Menin-Bach2 axis is critical for regulating CD4 T-cell senescence and cytokine homeostasis. Nature communications 83 24694524
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
2016 Bach2-Batf interactions control Th2-type immune response by regulating the IL-4 amplification loop. Nature communications 79 27581382
2020 Attenuation of TCR-induced transcription by Bach2 controls regulatory T cell differentiation and homeostasis. Nature communications 77 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 70 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 63 31819031
2000 Cloning and expression of human B cell-specific transcription factor BACH2 mapped to chromosome 6q15. Oncogene 59 10949928
2020 BACH2 drives quiescence and maintenance of resting Treg cells to promote homeostasis and cancer immunosuppression. The Journal of experimental medicine 58 32515782
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) 57 27496973
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 55 14982850
2021 BACH2 inhibition reverses β cell failure in type 2 diabetes models. The Journal of clinical investigation 54 34907913
2016 The transcription factor BACH2 promotes tumor immunosuppression. The Journal of clinical investigation 54 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
2013 Identification of BACH2 and RAD51B as rheumatoid arthritis susceptibility loci in a meta-analysis of genome-wide data. Arthritis and rheumatism 49 24022229
2019 Bach2 Controls T Follicular Helper Cells by Direct Repression of Bcl-6. Journal of immunology (Baltimore, Md. : 1950) 48 30833348
2017 A Bach2-Cebp Gene Regulatory Network for the Commitment of Multipotent Hematopoietic Progenitors. Cell reports 48 28273455
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
2003 B-cell-specific transcription factor BACH2 modifies the cytotoxic effects of anticancer drugs. Blood 45 12829606
2019 The Critical Role of Bach2 in Shaping the Balance between CD4+ T Cell Subsets in Immune-Mediated Diseases. Mediators of inflammation 44 32082072
2004 Repression of PML nuclear body-associated transcription by oxidative stress-activated Bach2. Molecular and cellular biology 44 15060166
2019 Bach2 Deficiency Leads to Spontaneous Expansion of IL-4-Producing T Follicular Helper Cells and Autoimmunity. Frontiers in immunology 39 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 38 31918262
2016 Extended exome sequencing identifies BACH2 as a novel major risk locus for Addison's disease. Journal of internal medicine 36 27807919
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 36 26620562
2014 Heme binds to an intrinsically disordered region of Bach2 and alters its conformation. Archives of biochemistry and biophysics 36 25444856
2001 Transcription factor BACH2 is transcriptionally regulated by the BCR/ABL oncogene. Genes, chromosomes & cancer 35 11746976
2013 Nuclear translocation of B-cell-specific transcription factor, BACH2, modulates ROS mediated cytotoxic responses in mantle cell lymphoma. PloS one 34 23936317
2018 Infection perturbs Bach2- and Bach1-dependent erythroid lineage 'choice' to cause anemia. Nature immunology 33 30250186
2015 The NF-κB subunit c-Rel regulates Bach2 tumour suppressor expression in B-cell lymphoma. Oncogene 33 26522720
2019 Bach2 Negatively Regulates T Follicular Helper Cell Differentiation and Is Critical for CD4+ T Cell Memory. Journal of immunology (Baltimore, Md. : 1950) 32 30971440
2017 Ikaros regulation of the BCL6/BACH2 axis and its clinical relevance in acute lymphoblastic leukemia. Oncotarget 32 28030830
2017 The mTOR-Bach2 Cascade Controls Cell Cycle and Class Switch Recombination during B Cell Differentiation. Molecular and cellular biology 32 28993481
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
2015 Transcriptome Analysis of CD4+ T Cells in Coeliac Disease Reveals Imprint of BACH2 and IFNγ Regulation. PloS one 31 26444573
2013 BACH2-BCL6 balance regulates selection at the pre-B cell receptor checkpoint. Trends in immunology 31 24332591
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
2022 Bach2: A Key Regulator in Th2-Related Immune Cells and Th2 Immune Response. Journal of immunology research 29 35313725
2018 Bach2 Promotes B Cell Receptor-Induced Proliferation of B Lymphocytes and Represses Cyclin-Dependent Kinase Inhibitors. Journal of immunology (Baltimore, Md. : 1950) 28 29540581
2021 Bach2 attenuates IL-2R signaling to control Treg homeostasis and Tfr development. Cell reports 27 33979619
2002 Expression of the oxidative stress-regulated transcription factor bach2 in differentiating neuronal cells. Journal of biochemistry 27 12204112
2012 Transcriptional suppression of BACH2 by the Bcr-Abl oncoprotein is mediated by PAX5. Leukemia 25 22858985
2022 BACH2 restricts NK cell maturation and function, limiting immunity to cancer metastasis. The Journal of experimental medicine 24 36178457
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
2024 Epigenetic recording of stimulation history reveals BLIMP1-BACH2 balance in determining memory B cell fate upon recall challenge. Nature immunology 23 38969872
2017 Bach2 repression mediates Th17 cell induced inflammation and associates with clinical features of advanced disease in chronic pancreatitis. United European gastroenterology journal 23 29511557
2013 BACH2: a marker of DNA damage and ageing. DNA repair 23 24075570
2009 Identification of novel Bach2 transcripts and protein isoforms through tagging analysis of retroviral integrations in B-cell lymphomas. BMC molecular biology 23 19159451
2021 Bach2 regulates autophagy to modulate UVA-induced photoaging in skin fibroblasts. Free radical biology & medicine 22 33882335
2013 Identification of BACH2 as a susceptibility gene for Graves' disease in the Chinese Han population based on a three-stage genome-wide association study. Human genetics 22 24346624
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
2024 BACH2 regulates diversification of regulatory and proinflammatory chromatin states in TH17 cells. Nature immunology 20 39009838
2007 The role of Bach2 in nucleic acid-triggered antiviral innate immune responses. Biochemical and biophysical research communications 19 17991429
2017 Bifurcated BACH2 control coordinates mantle cell lymphoma survival and dispersal during hypoxia. Blood 18 28592433
2022 Diverging regulation of Bach2 protein and RNA expression determine cell fate in early B cell response. Cell reports 17 35793628
2022 The transcription factor Bach2 negatively regulates murine natural killer cell maturation and function. eLife 17 36190189
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 Charge-state-distribution analysis of Bach2 intrinsically disordered heme binding region. Journal of biochemistry 16 27206783
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
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
2017 Bach2 represses the AP-1-driven induction of interleukin-2 gene transcription in CD4＋ T cells. BMB reports 15 28855027
2011 The structure of the Bach2 POZ-domain dimer reveals an intersubunit disulfide bond. Acta crystallographica. Section D, Biological crystallography 15 22194330
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
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
2018 The critical role of Bach2 in regulating type 2 chronic airway inflammation. International immunology 14 29529253
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) 13 35264460
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
2017 Bach2 regulates AID-mediated immunoglobulin gene conversion and somatic hypermutation in DT40 B cells. European journal of immunology 13 28301039
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