| 1995 |
B-ATF (BATF) is a nuclear bZIP protein that heterodimerizes with JUN family members (JunB, c-Jun, JunD) but not efficiently with c-Fos, and the B-ATF/c-Jun heterodimer binds AP-1 consensus DNA (TRE sites), establishing BATF as a tissue-specific modulator of AP-1 transcription. |
Yeast two-hybrid library screen, GST pulldown with in vitro translated proteins, EMSA |
Oncogene |
High |
8570175
|
| 1996 |
B-ATF physically associates with IFP 35, a leucine zipper protein translocated to the nucleus after interferon treatment, forming B-ATF:IFP 35 heterodimers as an interferon-inducible event. |
Co-immunoprecipitation, in vitro binding assay |
Biochemical and biophysical research communications |
Medium |
8954125
|
| 1996 |
SFA-2 (BATF) does not homodimerize efficiently but forms heterodimers preferentially with c-Jun; the SFA-2/c-Jun heterodimer binds preferentially to AP-1 (TRE) and CRE sites. |
In vitro dimerization assay, EMSA |
Biochemical and biophysical research communications |
Medium |
8630063
|
| 2000 |
B-ATF lacks a conventional transcriptional activation domain; Jun/B-ATF dimers bind TRE sites with a bias over CRE sites; B-ATF inhibits AP-1-mediated transcription in a dose-dependent manner by forming transcriptionally inert Jun/B-ATF heterodimers that compete with Fos for Jun; stable expression of B-ATF blocks focus formation by H-Ras and v-Fos oncoproteins. |
GAL4 chimeric reporter assay, EMSA, transient transfection reporter assay, focus-formation assay in C3H10T1/2 cells |
Oncogene |
High |
10777209
|
| 2001 |
Murine BATF/Jun heterodimers bind AP-1 consensus DNA and are transcriptionally inert; overexpression of BATF in thymic T cells reduces AP-1 transactivation in vivo, demonstrating BATF is a negative regulator of AP-1 activity in the thymus. |
In situ hybridization, AP-1 luciferase reporter transgenic mouse cross, transgenic overexpression |
European journal of immunology |
Medium |
11466704
|
| 2002 |
BATF expression is induced as an early transcriptional response to IL-6/LIF stimulation and Stat3 activation in M1 myeloid leukemia cells; BATF forms complexes with c-Jun in these cells; forced BATF expression reduces cell growth rate. |
Representational difference analysis, immunoblot, co-immunoprecipitation, forced expression growth assay |
Oncogene |
Medium |
12444555
|
| 2003 |
BATF is phosphorylated in vivo on multiple serine and threonine residues and at least one tyrosine residue; phosphorylation of serine-43 within the DNA-binding domain (modeled by S43D mutation) converts BATF from a DNA-binding to a non-DNA-binding inhibitor of AP-1 activity while retaining dimerization with Jun and nuclear localization. |
In vivo phosphorylation labeling, reverse-polarity PAGE, site-directed mutagenesis (S43D), EMSA, nuclear localization assay, AP-1 reporter assay |
The Biochemical journal |
High |
12809553
|
| 2003 |
EBNA2 and activated Notch up-regulate BATF expression in B cells within 24 h of EBV infection; BATF negatively impacts BZLF1 reporter expression and reduces the frequency of EBV lytic replication in latently infected cells. |
Differential gene expression analysis, reporter assay, viral replication frequency assay |
Journal of virology |
Medium |
12719594
|
| 2003 |
Transgenic overexpression of BATF in T cells causes a severe deficiency of NKT cells, demonstrating that precise control of AP-1 activity mediated by BATF is critical for NKT cell development. |
Transgenic mouse model, flow cytometry, in vivo cytokine production assay |
Journal of immunology |
Medium |
12594265
|
| 2009 |
BATF is required for TH17 cell differentiation; Batf−/− T cells fail to induce RORγt and IL-21, are resistant to experimental autoimmune encephalomyelitis, and BATF binds conserved intergenic elements in the Il17a-Il17f locus and the Il17, Il21, and Il22 promoters after TH17 differentiation. |
Batf knockout mouse, ChIP, EMSA, retroviral overexpression, EAE model |
Nature |
High |
19578362
|
| 2010 |
BATF is required for Th17, Th2, and Tfh cell differentiation and for B-cell class-switch recombination; adoptive transfer experiments established that the B-cell CSR defect is driven by T-cell intrinsic BATF loss, while B-cell-intrinsic BATF is also required for in vitro CSR. |
Batf knockout mouse (BatfΔZ/ΔZ), adoptive transfer, in vitro B-cell stimulation, Ig class-switch analysis |
The Journal of experimental medicine |
High |
20421391
|
| 2010 |
PD-1 ligation upregulates BATF in exhausted CD8+ T cells; enforced BATF expression is sufficient to impair T cell proliferation and cytokine secretion; BATF knockdown reduces PD-1-mediated inhibition and rescues HIV-specific T cell function. |
Gene expression profiling of HIV-specific CD8+ T cells, lentiviral BATF overexpression, siRNA knockdown, T cell functional assays |
Nature medicine |
High |
20890291
|
| 2011 |
BATF directly controls expression of Bcl-6 and c-Maf in T cells (required for Tfh development), and AID and germline IH-CH transcripts in B cells (required for CSR); coexpression of Bcl-6 and c-Maf restores Tfh activity in Batf−/− T cells. |
Batf knockout mouse, ChIP, in vivo complementation/rescue experiments, adoptive transfer |
Nature immunology |
High |
21572431
|
| 2011 |
BATF promotes effector CD8+ T-cell differentiation by inhibiting Sirt1 expression (together with c-Jun), resulting in increased histone acetylation of the T-bet locus and elevated cellular NAD+/ATP levels that support effector differentiation and survival. |
BATF-deficient mouse, ChIP for histone acetylation, NAD+/ATP measurement, transcriptional reporter assay |
Proceedings of the National Academy of Sciences |
Medium |
21873234
|
| 2011 |
BATF induction downstream of Stat3 signaling in M1 myeloid leukemia cells is required for growth arrest and terminal macrophage differentiation; Stat3 binds the Batf promoter to drive its transcription; Batf in turn represses c-Myb to enable differentiation. |
RNA interference knockdown, rescue expression, ChIP for Stat3 at Batf promoter, gene expression analysis |
Molecular cancer research |
Medium |
21296860
|
| 2012 |
In CD4+ T cells, BATF-JUN complexes cooperate with IRF4 to bind AP1-IRF composite elements (AICEs; 5'-TGAnTCA/GAAA-3'); BATF binding is diminished in Irf4−/− T cells and IRF4 binding is diminished in Batf−/− T cells, demonstrating functional co-dependence; BATF-JUN-IRF4 complexes cooperatively promote Il10 transcription. |
ChIP-seq, EMSA, reporter assay, Irf4 and Batf KO T cells |
Nature |
High |
22992523
|
| 2012 |
BATF (and BATF2) can compensate for BATF3 in CD8α+ dendritic cell development during infection; compensation is based on the shared capacity of BATF leucine zipper domains to interact with IRF4 and IRF8, mediating cooperative gene activation; reciprocal compensation between BATF and BATF3 also occurs in T cells for IL-10 and CTLA4 expression. |
Batf3 KO mouse, cytokine-driven rescue experiments, leucine zipper domain interaction studies, gene expression analysis |
Nature |
High |
22992524
|
| 2013 |
BATF is required for Th9 cell differentiation and IL-9 expression in both human and mouse T cells; BATF is enriched in Th9 cells and regulates a Th9-specific transcriptional network. |
Microarray, BATF KO mouse, BATF overexpression, allergic inflammation model |
The Journal of clinical investigation |
High |
24216482
|
| 2013 |
BATF is required for normal expression of gut-homing receptors CCR9 and α4β7 on T helper cells in response to retinoic acid; BATF-deficient T cells show defective RARα binding and histone acetylation at the regulatory regions of the CCR9 and Itg-α4 genes. |
BATF KO mouse, ChIP for RARα and histone acetylation, flow cytometry, intestinal T cell functional assays |
The Journal of experimental medicine |
Medium |
23460729
|
| 2013 |
Egr-2 interacts physically with BATF in CD4 T cells and suppresses its interaction with DNA sequences from the IL-17 promoter, thereby inhibiting Th17 differentiation; Egr-2 control of IL-17 is dependent on BATF inhibition without affecting STAT3 or RORγt. |
Co-immunoprecipitation, EMSA/DNA binding competition assay, Egr-2 KO mouse, Th17 differentiation assay |
Journal of immunology |
Medium |
23203924
|
| 2013 |
EBNA3C binds strongest to BATF/IRF4 (AICE) and SPI1/IRF4 (EICE) composite sites genome-wide in LCLs; EBNA3C co-immunoprecipitates with Sin3A and is tethered to DNA through BATF-containing complexes; EBNA3C/Sin3A at promoters correlates with transcription downregulation including repression of p14ARF. |
ChIP-seq, co-immunoprecipitation, conditional EBNA3C inactivation |
Proceedings of the National Academy of Sciences |
Medium |
24344258
|
| 2014 |
BATF is essential for early effector CD8+ T cell differentiation; BATF-deficient CD8+ T cells show proliferative and metabolic catastrophe early after antigen encounter; BATF together with IRF4 and Jun proteins binds regulatory regions and promotes early expression of T-bet and Blimp-1 while paradoxically repressing IFN-γ and granzyme B genes. |
Batf KO mouse, ChIP-seq, genome-wide transcriptional profiling, adoptive transfer |
Nature immunology |
High |
24584090
|
| 2014 |
EBNA3A is tethered to DNA through BATF-containing protein complexes; ChIP-re-ChIP confirmed complexes of EBNA3A on DNA together with BATF; EBNA3A coincidence with BATF-IRF4 or RUNX3 is associated with stronger EBNA3A ChIP-seq signals. |
ChIP-seq, ChIP-re-ChIP |
Proceedings of the National Academy of Sciences |
Medium |
25540416
|
| 2014 |
BATF is required for sustained CD8+ T cell effector function during LCMV infection; absence of BATF results in reduced CD8+ T cell responses and promotes viral persistence; IRF4 and BATF cooperate as necessary partners for antiviral cytotoxic T cell immunity. |
Irf4 KO and Batf KO mouse, LCMV infection model, T cell proliferation and effector function assays |
Cell death and differentiation |
Medium |
24531538
|
| 2014 |
BATF is required to initiate but not maintain CD8+ T-cell effector differentiation; inducible in vivo RNAi showed BATF is essential for the initial commitment of naive CD8+ T cells to effector development but becomes dispensable by 72 h post-activation. |
Inducible in vivo RNAi (bone marrow chimera with inducible shRNA), flow cytometry, adoptive transfer |
Proceedings of the National Academy of Sciences |
High |
25548173
|
| 2015 |
IL-21 induces and sustains BATF expression in CD8+ T cells during chronic viral infection; BATF cooperates with IRF4 to preserve Blimp-1 expression and sustain CD8+ T cell effector function; BATF overexpression rescues 'unhelped' CD8+ T cells during chronic LCMV infection. |
Chronic LCMV infection model, conditional BATF KO, BATF overexpression, flow cytometry, gene expression |
Cell reports |
Medium |
26527008
|
| 2015 |
BATF and IRF4 are necessary for VAT-Treg cell differentiation through direct regulation of ST2 and PPARγ expression. |
BATF and IRF4 conditional KO mice, ChIP, flow cytometry, metabolic phenotyping |
Nature immunology |
Medium |
25599561
|
| 2015 |
BATF, in cooperation with IRF4 along with STAT3 and STAT6, directly binds the CNS2 region of the IL-4 locus in Tfh cells to promote IL-4 expression; Batf-to-c-Maf signaling is an important determinant of IL-4 expression in Tfh cells. |
ChIP, reporter assay, BATF KO mouse, retroviral overexpression, allergic asthma model |
Nature communications |
Medium |
26278622
|
| 2016 |
Bach2 physically associates with BATF and binds regulatory regions of Th2 cytokine gene loci; the Bach2-BATF complex antagonizes recruitment of the BATF-IRF4 complex to AP-1 motifs, suppressing Th2 cytokine production; Bach2 also regulates Batf and Batf3 expression by inhibiting IL-4 production and by directly binding the Batf and Batf3 gene loci. |
Co-immunoprecipitation, ChIP, cytokine production assays, Bach2 KO mouse |
Nature communications |
High |
27581382
|
| 2016 |
BATF/JUN-B and BATF/C-JUN complexes form in chondrocytes; overexpression of BATF induces upregulation of matrix-degrading enzymes and downregulation of cartilage matrix molecules; ChIP confirmed BATF and JUN binding to promoter regions of catabolic gene candidates; BATF knockout suppresses experimental osteoarthritis. |
ChIP, adenoviral BATF overexpression, BATF KO mouse, DMM and intra-articular injection OA models |
Annals of the rheumatic diseases |
Medium |
27147707
|
| 2016 |
In Th2 cells, BATF is enriched at the Rad50 hypersensitivity sites (RHS6 and RHS7) of the Th2 locus control region rather than at proximal cytokine promoters; BATF-deficient CD4+ T cells fail to acquire permissive epigenetic modifications at the Th2 locus linked to RHS6/7 function. |
ChIP-seq, BATF KO mouse, helminth infection model, epigenetic (H3K4me3/H3K27ac) profiling |
Journal of immunology |
Medium |
27798167
|
| 2017 |
IRF1 and BATF are induced early by IL-27 during Tr1 cell differentiation and are required for differentiation and function; both transcription factors influence chromatin accessibility and expression of genes required for Tr1 cell function, with unique pioneering functions. |
ATAC-seq, ChIP-seq, IRF1 and BATF KO T cells, in vitro and in vivo Tr1 differentiation |
Nature immunology |
High |
28166218
|
| 2017 |
The BATF-IRF4 ternary complex shows a spectrum of occupancy at enhancers that correlates with sensitivity of gene expression to TCR signal strength; DNA sequences flanking the AICE motif control the affinity of BATF-IRF4 for direct binding to DNA; ChIP-exo identified a high-affinity AICE2 motif at a human CTLA-4-associated SNP. |
ChIP-seq, ChIP-exo, graded TCR stimulation, direct binding affinity measurements |
Nature immunology |
High |
28346410
|
| 2017 |
A Foxp3 A384T missense mutation (IPEX patient-derived) impairs BATF expression in Treg cells by altering Foxp3-DNA binding specificity, broadening it at Batf target sites; repressed BATF expression contributes to tissue-restricted inflammation and impaired Treg competition in non-lymphoid tissues. |
Knock-in Foxp3 mutant mouse models, ChIP, Treg functional assays |
Immunity |
Medium |
28778586
|
| 2018 |
BATF, IRF4, and IRF8 are recruited to and bind AP1-IRF composite elements (AICEs) in the il12a, ebi3, and il10 loci in activated B cells (Bregs), driving IL-35 and IL-10 production. |
EMSA, ChIP assay on activated B cells |
Journal of leukocyte biology |
Medium |
30117603
|
| 2018 |
BATF quantitative DNA binding preferences (as BATF-JUNB heterodimer and BATF-JUNB-IRF4/8 heterotrimer) were determined in vitro; without IRF, all three BATF family heterodimers show similar TRE/CRE preferences; IRF4/8 binding adjacent to BATF sites increases affinity substantially through protein-protein interactions and alters CRE vs TRE preference. |
Spec-seq (in vitro quantitative binding to large sequence collections), recombinant proteins |
BMC molecular biology |
High |
29587652
|
| 2018 |
BATF controls formation of colon-infiltrating IL-7R+GM-CSF+ donor T effector memory cells that are sufficient to promote intestinal GVHD; this T cell subset's formation is dependent on T cell-intrinsic BATF expression. |
MHC-mismatched and miHA-mismatched GVHD mouse models, BATF KO adoptive transfer, flow cytometry |
The Journal of clinical investigation |
Medium |
29376889
|
| 2019 |
Batf pioneers chromatin accessibility in developing effector T cells and controls developmentally regulated recruitment of the architectural factor Ctcf to promote chromatin looping associated with lineage-specific gene transcription; the Ctcf recruitment by Batf is largely dependent on Ets1 and does not require Batf-Irf complexes at AICE sites. |
ChIP-seq for Batf, Ctcf, and Ets1; ATAC-seq; Hi-C/chromatin interaction assays; Batf KO and Ets1 KO T cells |
Cell reports |
High |
31665634
|
| 2019 |
BATF function in Th subsets is specified by its interacting partners: JunB and c-Jun (but not JunD) cooperate with BATF to promote IL-9 in Th9 cells; low Jun expression in Th17 cells limits BATF-driven IL-9; Bach2 cooperates with BATF to induce IL-9 by directly binding the Il9 gene. |
Primary mouse T cell culture, ectopic expression, ChIP, cytokine production assays |
Journal of immunology |
Medium |
31451674
|
| 2020 |
BATF is required for the molecular tissue program of nonlymphoid tissue Treg cell precursors residing in secondary lymphoid organs; global chromatin profiling showed BATF drives stepwise acquisition of chromatin accessibility toward the tissue Treg phenotype. |
scRNA-seq, ATAC-seq, BATF KO validation in precursor populations, Nfil3 reporter mice |
Immunity |
High |
31924477
|
| 2020 |
STAT5 is the earliest factor binding and remodeling the Il9 locus in Th9 cells, and this is required for BATF binding at the Il9 locus; STAT5 mediates accessibility for BATF at the Il9 locus in multiple Th lineages, allowing acquisition of an IL-9-secreting phenotype; STAT5 and BATF together can convert Th17 cells to IL-9 producers. |
ChIP-seq, ATAC-seq, STAT5 and BATF KO T cells, retroviral overexpression, allergy and tumor models |
Nature communications |
High |
32985505
|
| 2020 |
BATF is selectively required for the development and function of IL-25-responsive migratory iILC2s (IL-17RBhigh, KLRG1high) during helminth infection; BATF directly binds cis-regulatory elements of wound healing genes in ILC2s and maintains their chromatin accessibility; BATF also supports the IL-33-ST2 feed-forward loop sustaining ILC2 identity. |
BATF KO mouse, Nippostrongylus infection, scRNA-seq, ChIP-seq, flow cytometry |
Science immunology |
Medium |
31924686
|
| 2020 |
BATF is induced during ILC development at the α-lymphoid progenitor stage in response to IL-7; BATF binds and activates transcription of the Nfil3 gene to promote ILC hematopoiesis; BATF deficiency causes ILC lymphopenia affecting ILC1, ILC2, ILC3, and NK cells. |
BATF KO mouse, ChIP, IL-7 stimulation assays, bone marrow progenitor analysis, enteric infection model |
Science immunology |
Medium |
33277375
|
| 2021 |
BATF and IRF4 cooperate to counter T cell exhaustion in tumor-infiltrating CAR T cells; BATF overexpression in CAR T cells promotes survival, expansion, effector cytokine production, decreased TOX/inhibitory receptor expression, and generation of long-lived memory T cells; these responses require BATF-IRF4 protein-protein interaction, as a BATF variant unable to interact with IRF4 failed to mediate these effects. |
CAR T cell tumor models (mouse), BATF overexpression, BATF-IRF4 interaction-deficient BATF mutant, flow cytometry, tumor growth assays |
Nature immunology |
High |
34282330
|
| 2021 |
BATF maintains a permissive chromatin structure allowing transition from TCF-1+ progenitor CD8+ T cells to CX3CR1+ cytotoxic effector cells during chronic viral infection; BATF directly binds regulatory regions near Tbx21 and Klf2 to modulate their enhancer accessibility. |
Genetic deletion of Batf in chronic LCMV model, ATAC-seq, ChIP-seq, gene regulatory network analysis |
Nature immunology |
High |
34282329
|
| 2021 |
BATF promotes ILC2 proliferation and function and restricts ILC2-to-ILC3 plasticity during influenza infection; BATF directly binds cis-regulatory elements of wound healing genes and maintains their chromatin accessibility; BATF plays a role in an IL-33-ST2 feed-forward loop supporting ILC2 identity. |
BATF KO mouse, influenza infection model, scRNA-seq, ChIP-seq, ATAC-seq |
Science immunology |
High |
35030033
|
| 2021 |
BATF directly binds and up-regulates a subset of exhaustion-related genes in human CAR T cells; knocking out BATF shifts the CAR T cell population toward a more central memory subset and enhances antitumor activity against solid tumors. |
Candidate gene screen, BATF KO (CRISPR) in human CAR T cells, ChIP, tumor xenograft models, transcriptomic analysis |
Cancer cell |
High |
36240777
|
| 2022 |
BATF mediates chromatin organization at several levels in CD8+ T cells including regulatory region accessibility, enhancer-gene interactions, and TF co-binding; Batf and Irf4 together (not Batf alone) are sufficient to increase accessibility and transcription at key T cell function loci in fibroblasts; addition of Runx3 and T-bet further fine-tunes changes and is essential for establishing T cell-characteristic chromatin loops. |
ATAC-seq, ChIP-seq, Hi-C chromatin interaction mapping, ectopic TF overexpression in fibroblasts, Batf KO CD8+ T cells |
Science immunology |
High |
35179948
|
| 2022 |
BATF is a key regulator of Treg cell differentiation and activation in the tumor microenvironment, controlling activation-associated gene expression epigenetically; BATF deficiency in Treg cells inhibits tumor growth in mouse models. |
scRNA-seq, scATAC-seq, BATF KO in Treg cells (mouse), CUT&Tag, tumor growth assay |
Science immunology |
Medium |
36206353
|
| 2022 |
BATF is required for maintenance of ILC3 lineage identity in the gut; BATF directly binds cis-regulatory elements of type 1 effector genes and restrains their chromatin accessibility; BATF also promotes chromatin accessibility of MHCII antigen presentation genes to facilitate transition to MHCII+ ILC3s. |
ILC3-specific BATF KO mouse, ATAC-seq, ChIP-seq, antibiotic treatment, IFN-γ blockade epistasis experiments |
The Journal of experimental medicine |
High |
36048018
|
| 2022 |
FOSL1, FOSL2, and BATF share occupancy over regulatory regions of Th17 lineage commitment genes and share protein-interacting partners in human T cells; these AP-1 factors functionally interact during early human Th17 differentiation with BATF promoting the Th17 lineage. |
ChIP-seq, co-immunoprecipitation, siRNA knockdown in human T cells, genome-wide binding analysis |
Nucleic acids research |
Medium |
35511484
|
| 2023 |
Batf stabilizes Th17 cell identity by restraining IL-2 expression and IL-2-induced Stat5 activation, which in turn limits Stat5-dependent recruitment of Ets1-Runx1 factors to Th1- and Treg-specific gene loci; Batf thus acts indirectly to inhibit a competing Stat5-Ets1-Runx1 enhanceosome. |
Batf KO T cells, ChIP-seq for Stat5/Ets1/Runx1, IL-2 manipulation, Th17 stability assays |
The EMBO journal |
High |
36917143
|
| 2023 |
BATF is a central component of a gene regulatory network governing TNFR+ intratumoral Treg cells; CRISPR-mediated BATF KO in human activated Tregs limits excessive activation and promotes survival of activated Tregs in vitro. |
scRNA-seq, CRISPR-Cas9 KO in human Tregs, bulk RNA-seq, immunophenotyping, in vitro functional suppression assay |
Science immunology |
Medium |
37713508
|
| 2023 |
BATF represses BIM (Bcl2l11) expression in anergic T cells to sustain peripheral tolerance; BATF-deficient tolerized CD4+ T cells resist anergy induction and undergo clonal deletion due to BIM upregulation; simultaneous Batf and Bcl2l11 double knockdown restores anergic T cell survival. |
In vivo antigen-driven anergy model, BATF KO and Bcl2l11 KO mouse, double-knockdown epistasis, ChIP/ATAC-seq |
The Journal of experimental medicine |
High |
37862030
|
| 2023 |
BATF is required for Treg stability and FOXP3 expression; BATF regulates demethylation and chromatin accessibility of the CNS2 region of the Foxp3 locus; Treg-specific BATF KO causes multiorgan autoimmune pathology. |
Treg-specific BATF KO mouse, ATAC-seq, bisulfite sequencing (CNS2 methylation), ChIP-seq, flow cytometry |
Advanced science |
High |
37587835
|
| 2023 |
Tox-induced IL-10 expression in T cells is dependent on BATF; Tox and BATF co-bind regulatory regions of the IL-10 gene along with IRF4 and JunB; cosilencing of BATF abolishes Tox-mediated IL-10 induction but not PD-1 upregulation. |
ChIP, co-occupancy analysis, BATF siRNA knockdown, Tox overexpression in multiple Th subsets |
Frontiers in immunology |
Medium |
38054003
|
| 2024 |
METTL3 stabilizes BATF mRNA through m6A modification read by IGF2BP2, promoting BATF expression in inflammatory microglia; elevated BATF directly binds promoters of inflammatory cytokine and chemokine genes (including CXCL2) and drives TNF-dependent neurotoxicity; this METTL3-m6A-BATF axis promotes neuroinflammation after TBI. |
MeRIP-seq, CUT&Tag sequencing, METTL3 conditional KO in microglia, BATF ChIP, in vitro and in vivo TBI/stroke models |
Cell death and differentiation |
High |
38902548
|
| 2024 |
BATF is directly regulated by SMAD2/3 downstream of TGF-β/integrin signaling in NK cells; BATF in turn binds key NK cell exhaustion genes (HAVCR2, LAG3, TIGIT, CTLA4); BATF deletion enhances NK cell function against AML in vitro and in vivo. |
TGF-β/SMAD pathway inhibition, BATF KO in NK cells, ChIP-seq for BATF at exhaustion gene loci, in vitro and in vivo AML models |
Science translational medicine |
High |
39259809
|
| 2024 |
BATF directly binds the TGF-β1 promoter in AML cells, transcriptionally enhancing TGF-β1 expression and activating the TGF-β1/Smad2-3/MMP2/9 axis to promote AML cell migration and invasion. |
ChIP assay, luciferase reporter assay, siRNA knockdown and overexpression in AML cells, in vitro migration/invasion assays, in vivo AML model |
Molecular carcinogenesis |
Medium |
38477642
|
| 2021 |
BATF directly binds the TGF-β1 promoter in breast cancer cells (confirmed by ChIP and dual luciferase reporter assay), increasing TGF-β1 mRNA and protein levels and promoting EMT; TGF-β1 knockdown reduces migration of BATF-overexpressing cells. |
Dual luciferase reporter assay, ChIP, siRNA knockdown, BATF overexpression in breast cancer cell lines |
Aging |
Medium |
34096887
|
| 2021 |
BATF directly binds the GBP-5 promoter and transcriptionally activates GBP-5 expression, which promotes NLRP3 inflammasome activation and hepatocyte death in sepsis-associated liver injury. |
ChIP, luciferase reporter assay, BATF overexpression, NLRP3 inflammasome activation assay, LPS-induced SALI mouse model |
FASEB journal |
Medium |
34042221
|
| 2018 |
BATF regulates B cell class-switch recombination by positively regulating Nfil3 and miR155hg, and negatively regulating Wnt10a; inducible BATF deletion demonstrated these are early regulatory targets upstream of germline transcript activation and Aicda induction. |
Inducible BATF deletion mouse model, ChIP, gene expression analysis, in vitro CSR assay |
European journal of immunology |
Medium |
29898247
|