Affinage

IRF2BP2

Interferon regulatory factor 2-binding protein 2 · UniProt Q7Z5L9

Length
587 aa
Mass
61.0 kDa
Annotated
2026-04-28
52 papers in source corpus 23 papers cited in narrative 24 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

IRF2BP2 is a nuclear transcriptional co-repressor that uses its RING domain to recognize a conserved RxSVI motif in diverse partner proteins—including IRF2, VGLL4, ZBTB16, and NFAT1—thereby modulating inflammatory, metabolic, and differentiation programs across multiple tissues (PMID:39616187, PMID:28716987). In macrophages and microglia, IRF2BP2 activates KLF2 expression through MEF2 and suppresses NF-κB, STAT1, and AP-1/ATF7-JDP2 inflammatory signaling; its loss causes exaggerated inflammatory responses, impaired cholesterol efflux, and worsened stroke outcomes (PMID:26195219, PMID:28769762, PMID:38801077). IRF2BP2 directly represses metabolic target genes such as ATF3 in hepatocytes and LIPE in adipocytes, and its hepatocyte- or adipocyte-specific deletion exacerbates hepatic steatosis or adipose inflammation, respectively (PMID:31529495, PMID:39752494). In hematopoiesis, IRF2BP2 is essential for fetal erythropoiesis and megakaryocytic differentiation, cooperates with TRIM28/DNMT1 to silence transposable elements in AML, and is required for T-ALL cell survival through super-enhancer-driven regulation of MYC/E2F pathways (PMID:35865523, PMID:39616187, PMID:39454110).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2008 High

    Establishing IRF2BP2 as a p53-responsive transcriptional modulator answered how cells fine-tune p53-mediated apoptosis and cell-cycle arrest, revealing a feedback loop in which p53 induces its own co-repressor.

    Evidence Luciferase reporters, siRNA knockdown, and overexpression in multiple cell lines treated with actinomycin D/doxorubicin

    PMID:19042971

    Open questions at the time
    • Direct chromatin occupancy at p21/Bax promoters not demonstrated
    • Physiological relevance in vivo not tested
    • Mechanism of repression (corepressor recruitment vs. direct interference) unresolved
  2. 2010 High

    Identifying IRF2BP2 as a component of the TEAD4/VGLL4 complex that activates VEGFA expression established that IRF2BP2 can function as a transcriptional co-activator, not solely a repressor.

    Evidence Yeast two-hybrid from human heart library, reciprocal Co-IP, mammalian two-hybrid, siRNA knockdown in C2C12 cells

    PMID:20702774

    Open questions at the time
    • Mechanism by which IRF2BP2 switches from repressor to activator function unknown
    • In vivo vascular phenotype not assessed
  3. 2015 High

    Conditional knockout in macrophages demonstrated that IRF2BP2 is required for MEF2-dependent KLF2 activation, linking it to cholesterol efflux and anti-inflammatory macrophage polarization—the first in vivo loss-of-function evidence for its immune-regulatory role.

    Evidence Macrophage-specific conditional KO mice, luciferase promoter assays, cholesterol efflux assays, KLF2 genetic rescue

    PMID:26195219

    Open questions at the time
    • Whether IRF2BP2 directly contacts MEF2 at the KLF2 promoter not shown by ChIP
    • Upstream signals regulating IRF2BP2 expression in macrophages unclear
  4. 2017 High

    Two studies established IRF2BP2 as a critical anti-inflammatory and cardioprotective factor: cardiomyocyte-specific KO proved IRF2BP2 restrains NFAT1-driven hypertrophy, while microglia-specific KO showed it mediates IFNβ-dependent neuroprotection after stroke.

    Evidence Cardiomyocyte- and microglia-specific conditional KO and transgenic OE mice, Co-IP of IRF2BP2-NFAT1, epistasis rescue by NFAT1 blockade, photothrombotic stroke model

    PMID:28716987 PMID:28769762

    Open questions at the time
    • Structural basis of IRF2BP2-NFAT1 interaction unresolved at the time
    • Whether cardiac and microglial mechanisms share a common IRF2BP2-dependent chromatin program unknown
  5. 2019 High

    Three discoveries expanded IRF2BP2's mechanistic repertoire: its RING domain sequesters repressive activity via VGLL4 binding in erythropoiesis, it co-regulates glucocorticoid receptor–NF-κB crosstalk genome-wide, and the IRF2BP2/KLF2 axis controls osteoclast-osteoblast balance.

    Evidence CRISPR KO zebrafish with epistasis rescue (VGLL4-IRF2BP2-alas2), ChIP-seq in A549 cells for GR/IRF2BP2 co-binding, overexpression/KD in osteoclast precursor and osteoblast differentiation assays

    PMID:31145973 PMID:31186082 PMID:31539803

    Open questions at the time
    • Human erythropoiesis relevance of VGLL4-IRF2BP2 axis not tested
    • Whether GR directly recruits IRF2BP2 or they co-bind independently unclear
    • Osteoclast data based on overexpression only, no KO
  6. 2020 High

    ChIP-seq identification of ATF3 as a direct IRF2BP2 target gene in hepatocytes, combined with hepatocyte-specific KO exacerbating steatosis, established IRF2BP2 as a metabolic gatekeeper in liver lipid homeostasis.

    Evidence Hepatocyte-specific conditional KO and AAV overexpression in HFD-fed mice, ChIP-seq, luciferase assay, ATF3 siRNA rescue

    PMID:31529495

    Open questions at the time
    • Whether IRF2BP2 represses ATF3 via E3 ligase activity or corepressor recruitment unresolved
    • Human liver disease correlation not established
  7. 2022 Medium

    Identifying IRF2BP2 as an HNF4α co-repressor whose activity depends on E3 ubiquitin ligase function, and demonstrating that germline Irf2bp2 KO is near-lethal due to failed fetal erythropoiesis, defined IRF2BP2 as essential for development and revealed a catalytic mechanism for its repressive function.

    Evidence Novel proteomic detection of labile HNF4α interaction, E3 ligase domain mutant analysis, germline KO mice with transcriptomic profiling of fetal liver

    PMID:35609419 PMID:35865523

    Open questions at the time
    • E3 ubiquitin ligase substrates not identified
    • HNF4α interaction detected by novel method only, not by conventional Co-IP
    • Cause of lethality (erythroid vs. cardiac vs. combined) not fully dissected
  8. 2024 High

    Structural resolution of the RING domain bound to the RxSVI motif of IRF2, VGLL4, and ZBTB16 unified the molecular basis for IRF2BP2's diverse partnerships and linked the ZBTB16 interaction to megakaryocytic differentiation.

    Evidence X-ray crystallography/structural analysis, biochemical binding assays, megakaryocyte differentiation assays

    PMID:39616187

    Open questions at the time
    • Whether all cellular partners use the same RxSVI motif or alternative interfaces exist unknown
    • No full-length IRF2BP2 structure available
  9. 2024 High

    Context-dependent oncogenic roles were established: in T-ALL, super-enhancer-driven IRF2BP2 sustains MYC/E2F programs and is essential for leukemic growth; in neuroblastoma, AP-1 cooperates with IRF2BP2 to activate ALK expression; and in AML, IRF2BP2 counteracts ATF7/JDP2-driven inflammatory gene activation to maintain proliferation.

    Evidence CUT&Tag, ChIP-seq, conditional KO mice for T-ALL, xenograft models for neuroblastoma, Co-IP and ChIP with functional KO in AML cells

    PMID:38801077 PMID:38864832 PMID:39454110

    Open questions at the time
    • Whether IRF2BP2 is a viable therapeutic target in these cancers not tested with specific inhibitors
    • Relative contribution of inflammatory suppression vs. TE silencing in AML proliferation unclear
  10. 2024 Medium

    Domain-level analysis of human IRF2BP2 variants showed that RING domain mutations cause cytoplasmic aggregation and impair nuclear translocation of both IRF2 and NF-κB1, while a patient mutation (c.625_665del) fails to suppress STAT1, linking IRF2BP2 dysfunction to interferon hyperactivation.

    Evidence Confocal microscopy of EGFP-fused mutants in HEK293, Western blot for nuclear IRF2/NF-κB1, luciferase STAT1 reporter, patient PBMC analysis

    PMID:34451894 PMID:39059757

    Open questions at the time
    • No Mendelian disease formally defined from these variants
    • Structural consequences of RING domain mutations not solved
    • Patient cohort small
  11. 2025 High

    Adipocyte-specific Irf2bp2 deletion proved that IRF2BP2 directly represses LIPE to restrain lipolysis, with its loss causing adipose inflammation and glucose intolerance, extending the metabolic gatekeeper role from liver to adipose tissue.

    Evidence ChIP-seq, RNA-seq, adipocyte-specific conditional KO mice, primary human adipocyte knockout and overexpression

    PMID:39752494

    Open questions at the time
    • Upstream metabolic signals that regulate IRF2BP2 in adipocytes unknown
    • Whether hepatic and adipose IRF2BP2 functions are coordinately regulated unclear
  12. 2025 Medium

    MCL1-mediated cytoplasmic sequestration of IRF2BP2 in drug-resistant AML derepresses the fatty acid oxidation gene ACSL1, defining a non-transcriptional mechanism of IRF2BP2 inactivation in cancer; separately, IRF2BP2 cooperates with TRIM28/DNMT1 to epigenetically silence transposable elements in AML.

    Evidence (preprint) Co-IP/mass spectrometry for MCL1 interaction, subcellular fractionation, ACSL1 inhibition assay; (preprint) Perturb-seq screen, CRISPR activation/silencing of HERV-K

    PMID:40475530

    Open questions at the time
    • Both findings are preprints awaiting peer review
    • Whether MCL1 sequestration occurs in non-AML contexts unknown
    • Relative contribution of TE derepression vs. ACSL1 upregulation to AML drug resistance not dissected

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the identity of E3 ubiquitin ligase substrates, whether IRF2BP2's activator vs. repressor switch is determined by partner identity or post-translational modification, and whether pharmacological disruption of the RING-RxSVI interface is therapeutically feasible.
  • No bona fide ubiquitination substrate identified
  • Molecular switch between co-activator and co-repressor modes uncharacterized
  • No small-molecule modulator of IRF2BP2 reported

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 8 GO:0098772 molecular function regulator activity 3 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005634 nucleus 6 GO:0005829 cytosol 2
Pathway
R-HSA-74160 Gene expression (Transcription) 9 R-HSA-168256 Immune System 5 R-HSA-1266738 Developmental Biology 3 R-HSA-1430728 Metabolism 3 R-HSA-162582 Signal Transduction 3 R-HSA-4839726 Chromatin organization 1
Partners
HNF4AIRF2MCL1NFAT1TEAD4TRIM28VGLL4ZBTB16
Complex memberships
ATF7/JDP2/IRF2BP2IRF2BP2/TRIM28/DNMT1TEAD4/VGLL4/IRF2BP2

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2010 IRF2BP2 was identified as a novel component of the TEAD4/VGLL4 transcription factor complex via yeast 2-hybrid screen from a human heart cDNA library, confirmed by coimmunoprecipitation and mammalian 2-hybrid assays. Coexpression of IRF2BP2 with TEAD4/VGLL4 or TEAD1 potently activated VEGFA expression, while knockdown of IRF2BP2 reduced VEGFA expression in C2C12 muscle cells. Yeast 2-hybrid, coimmunoprecipitation, mammalian 2-hybrid, siRNA knockdown FASEB journal High 20702774
2008 IRF2BP2 was identified as a direct transcriptional target of p53. Upregulation of IRF2BP2 after actinomycin D treatment is p53-dependent. Overexpressed IRF2BP2 impedes p53-mediated transactivation of p21 and Bax genes. Knockdown of IRF2BP2 leads to upregulation of p21 and faster induction of apoptosis after doxorubicin or actinomycin D treatment, indicating IRF2BP2 modulates cell survival decisions during p53 stress response. Luciferase reporter assay, siRNA knockdown, overexpression in multiple cell lines, actinomycin D/doxorubicin treatment Nucleic acids research High 19042971
2015 IRF2BP2 is required for MEF2-dependent activation of KLF2 (Krüppel-like factor 2) in macrophages. Promoter studies revealed this dependence. IRF2BP2-deficient macrophages have markedly reduced KLF2 expression, impaired cholesterol efflux due to inability to activate ABCA1, and increased M1 inflammatory activation. Restoring KLF2 in IRF2BP2-deficient macrophages rescued these defects. Macrophage-specific conditional knockout mice, promoter/luciferase assay, cholesterol efflux assay, genetic rescue experiment Circulation research High 26195219
2016 Ectopic expression of IRF2BP2 in murine primary CD4 T cells reduced CD25 expression, STAT5 phosphorylation, CD69 expression, and impaired proliferative capacity. In vivo, IRF2BP2-overexpressing transferred cells displayed impaired expansion, establishing IRF2BP2 as a repressor of naive CD4 T cell activation and clonal expansion downstream of TCR triggering. Retroviral transduction of primary murine CD4 T cells, in vivo adoptive transfer, flow cytometry, phospho-STAT5 analysis Journal of leukocyte biology Medium 27286791
2017 IRF2BP2 directly interacted with the C-terminal transactivation domain of NFAT1, competing with MEF2C and disturbing their transcriptional synergism, thereby inhibiting NFAT1-transactivated hypertrophic transcriptome. Cardiomyocyte-specific Irf2bp2 knockout exacerbated aortic banding- and angiotensin II-induced cardiac hypertrophy, while Irf2bp2 transgenic overexpression was protective. The effect of Irf2bp2 deficiency was rescued by NFAT1 blockade. Cardiomyocyte-specific conditional KO and transgenic overexpression mice, Co-IP, epistasis rescue by NFAT1 blockade, aortic banding/angiotensin II models Hypertension High 28716987
2017 Loss of IRF2BP2 in microglia leads to increased inflammatory cytokine expression in response to LPS and impaired anti-inflammatory marker activation in response to IL-4. IRF2BP2-deficient mice had larger brain infarctions after photothrombotic stroke with fewer anti-inflammatory M2 microglia. IRF2BP2 also mediates the anti-inflammatory and neuroprotective effect of IFNβ, which was lost in IRF2BP2-deficient macrophages. Macrophage/microglia-specific conditional KO mice, photothrombosis stroke model, LPS/IL-4 stimulation, cytokine measurement, IFNβ treatment Frontiers in cellular neuroscience High 28769762
2019 IRF2BP2 overexpression suppresses osteoclast differentiation and enhances osteoblast differentiation; these effects were reversed by KLF2 knockdown, establishing the IRF2BP2/KLF2 axis as a regulator of osteoclast and osteoblast differentiation. Overexpression and siRNA knockdown in osteoclast precursor cells and osteoblasts, differentiation assays, marker gene expression BMB reports Medium 31186082
2019 IRF2BP2 modulates glucocorticoid receptor (GR) and NF-κB transcriptional activity. GC treatment changes chromatin binding of IRF2BP2, with IRF2BP2-binding sites co-occurring with GR binding sites. Depletion of IRF2BP2 modulates transcription of GC-regulated genes and alters responses to both glucocorticoids and TNF in A549 cells, positioning IRF2BP2 as a coregulator of GR-NF-κB crosstalk. ChIP-seq, siRNA knockdown, transcriptomic analysis in HEK293 and A549 cells Journal of steroid biochemistry and molecular biology Medium 31145973
2019 In zebrafish, VGLL4 sequesters IRF2BP2 via the VGLL4 TDU1 and IRF2BP2 RING finger domains, thereby inhibiting IRF2BP2's repression of alas2 (aminolevulinate synthase 2) expression and heme biosynthesis. IRF2BP2 depletion rescued impaired erythroid terminal differentiation in vgll4b-deficient zebrafish, establishing an oxygen-sensing pathway: NOTCH1→HIF1α→VGLL4→IRF2BP2→alas2. CRISPR/Cas9 knockout zebrafish, genetic epistasis rescue (irf2bp2 depletion rescuing vgll4b mutant), domain-mapping experiments Redox biology High 31539803
2020 IRF2BP2 directly binds the promoter region of ATF3 (activating transcription factor 3) as a transcriptional repressor, as demonstrated by ChIP-seq and luciferase assay. Hepatocyte-specific Irf2bp2 knockout exacerbated high-fat diet-induced hepatic steatosis, while Irf2bp2 overexpression was protective. ATF3 knockdown significantly relieved IRF2BP2 knockout-exaggerated hepatosteatosis in vitro. Hepatocyte-specific conditional KO and adeno-associated virus overexpression in mice, ChIP-seq, luciferase assay, digital gene expression, ATF3 siRNA rescue Hepatology High 31529495
2020 miR-155-5p targets IRF2BP2 mRNA (validated by luciferase reporter assay). Immunoprecipitation showed that IRF2BP2 binds NFAT1, and oroxylin A increases this binding, reducing iNOS-driven inflammation. shRNA knockdown of miR-155-5p in bone marrow ameliorated LPS-induced acute lung injury in mice. Luciferase reporter assay, immunoprecipitation, shRNA in vivo, LPS-induced lung injury mouse model American journal of physiology. Cell physiology Medium 33052070
2021 IRF2BP2 is required to attenuate STAT1 transcriptional activity; IRF2BP2 c.625_665del mutation failed to suppress STAT1 transcriptional activity in a luciferase reporter system. Patient cells with this mutation showed overexpression of STAT1 protein and increased constitutive activation of STAT1 and STAT5, as well as elevated interferon-inducible gene expression. Luciferase reporter system, flow cytometry (phospho-STAT), patient PBMC analysis, NanoString gene expression Pharmaceuticals Medium 34451894
2022 IRF2BP2 was identified as a novel HNF4α co-repressor. This interaction could not be detected by conventional immunoprecipitation but was identified through novel proteomic techniques sensitive to biochemically labile interactions. IRF2BP2 repressed HNF4α transcriptional activity dependent on its E3 ubiquitin ligase activity. IRF2BP2 deficiency in HepG2 cells induced gluconeogenic genes comparable to forskolin-treated wild-type cells. Novel proteomic approach for biochemically labile interactions, luciferase reporter assay, IRF2BP2 gene deletion in HepG2 cells, E3 ubiquitin ligase domain mutant Biochemical and biophysical research communications Medium 35609419
2023 Agmatine binds directly to IRF2BP2 (identified by protein microarray). This competitive binding frees IRF2BP2-bound IRF2, allowing free IRF2 to translocate to the nucleus of BV2 microglia. Translocated IRF2 activates KLF4 transcription, increasing CD206-positive (M2) microglia cells. Protein microarray binding screen, cell treatment with agmatine, nuclear translocation assay, flow cytometry Inflammation research Medium 37314519
2024 IRF2BP2 interacts with the AP-1 heterodimer ATF7/JDP2, is recruited by this dimer to chromatin, and counteracts its gene-activating function. Loss of IRF2BP2 leads to overactivation of inflammatory pathways and strongly reduced AML cell proliferation, defining a pro-oncogenic inflammatory equilibrium maintained by the ATF7/JDP2-IRF2BP2 regulatory axis. Co-immunoprecipitation, ChIP, siRNA/KO loss-of-function, transcriptomic analysis in AML cells Nucleic acids research High 38801077
2024 Structural and biochemical studies revealed that the RING domain of IRF2BP2 binds a conserved RxSVI motif present in IRF2, VGLL4, and ZBTB16. The motif-containing peptides form a short loop and β-strand recognized by the RING domain. IRF2BP2 regulates megakaryocytic differentiation through its interaction with ZBTB16 via this RxSVI motif. Motif discovery, X-ray crystallography/structural analysis, biochemical binding assays, cell biological differentiation assays Nature communications High 39616187
2024 In T-ALL cells, IRF2BP2 is driven by a super-enhancer activated by master transcription factors ERG, ELF1, and ETS1. IRF2BP2 cooperates with master TFs to target the enhancer of the RAG1 gene and modulate its expression. Loss of IRF2BP2 affects MYC and E2F pathways. Hematopoietic-specific IRF2BP2 knockout mice showed minimal impact on normal T cell development but IRF2BP2 was crucial for T-ALL cell growth and survival in vitro and in vivo. CUT&Tag, immunoprecipitation, conditional KO mice, in vitro and in vivo T-ALL growth assays, transcriptomic analysis Advanced science High 39454110
2024 In neuroblastoma, super-enhancer-driven IRF2BP2 is activated by master transcription factors MYCN, MEIS2, and HAND2. AP-1 family proteins shape chromatin accessibility to expose IRF2BP2 binding sites, enabling AP-1 and IRF2BP2 to collaboratively stimulate expression of the ALK susceptibility gene, thereby maintaining the highly proliferative NB phenotype. ChIP-seq, chromatin accessibility analysis, transcriptome sequencing, loss-of-function experiments, in vivo xenograft models Neuro-oncology Medium 38864832
2025 IRF2BP2 directly represses lipolysis-related genes including LIPE (encoding hormone sensitive lipase) in adipocytes, as shown by ChIP-seq demonstrating direct promoter binding. Adipocyte-selective Irf2bp2 deletion in mice increased Lipe expression and free fatty acid levels, causing adipose tissue inflammation and glucose intolerance. RNA-seq, ChIP-seq, adipocyte-specific conditional KO mice, primary human adipocyte KO and OE Science advances High 39752494
2025 In ven/aza-resistant AML, MCL1 was identified as an IRF2BP2 binding partner by co-immunoprecipitation and mass spectrometry. This MCL1-IRF2BP2 interaction results in cytoplasmic sequestration of IRF2BP2, causing loss of transcriptional repression and increased expression of IRF2BP2 target gene ACSL1, an enzyme required for fatty acid oxidation. Inhibition of ACSL1 impaired ven/aza-resistant leukemic stem cells. Co-IP + mass spectrometry, subcellular fractionation, ACSL1 inhibition functional assay, metabolite profiling bioRxivpreprint Medium 40475530
2025 IRF2BP2 cooperates with TRIM28 and DNMT1 to epigenetically silence transposable elements (TEs), particularly HERV-K/LTR5_Hs, in AML cells. Loss of IRF2BP2 induced differentiation, apoptosis, and TE transcriptional activation. CRISPR-mediated activation of HERV-K/LTR5_Hs recapitulated IRF2BP2 loss phenotypes, and re-silencing of HERV-K partially rescued these effects. Single-cell Perturb-seq screen, CRISPR activation/silencing, co-immunoprecipitation, AML patient primary cells bioRxivpreprint Medium
2025 The IRF2BP2::JAK2 fusion protein localizes to the cytoplasm and drives constitutive JAK-STAT signaling, conferring cytokine-independent growth in Ba/F3 cells engineered by CRISPR-Cas9 to express the fusion. Both type I (ruxolitinib) and type II (CHZ868) JAK inhibitors potently inhibited this fusion kinase. CRISPR-Cas9 genome engineering of Ba/F3 cells, cytokine-independent growth assay, JAK inhibitor treatment, subcellular localization Genes, chromosomes & cancer High 41711169
2024 Variants in the C-terminal RING finger domain of IRF2BP2 caused irregular aggregate formation and non-nuclear distribution, while N-terminal zinc finger domain variants retained normal nuclear localization. Immunoblotting revealed impaired IRF2 and NFκB1 (p50) nuclear localization in IRF2BP2 mutants compared to wild-type, indicating that IRF2BP2 controls nuclear translocation of both IRF2 and NF-κB. Confocal fluorescence microscopy, Western blotting, overexpression of EGFP-fused mutants in HEK293 cells Clinical immunology Medium 39059757
2022 Irf2bp2 is required for fetal hepatic erythropoiesis through the expansion of erythromyeloid progenitors. Germline ablation of Irf2bp2 caused near-complete lethality with predominantly upregulation of interferon-responsive genes and elevation of hematopoietic stem cell-enriched transcription factors (Etv6, Fli1, Ikzf1, Runx1) in Irf2bp2-null livers. Germline KO mice, transcriptome profiling (liver, heart, skeletal muscle), FISH for chimerism Frontiers in immunology Medium 35865523

Source papers

Stage 0 corpus · 52 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Whole-transcriptome sequencing identifies novel IRF2BP2-CDX1 fusion gene brought about by translocation t(1;5)(q42;q32) in mesenchymal chondrosarcoma. PloS one 74 23185413
2015 IRF2BP2 Reduces Macrophage Inflammation and Susceptibility to Atherosclerosis. Circulation research 69 26195219
2010 IRF2BP2 is a skeletal and cardiac muscle-enriched ischemia-inducible activator of VEGFA expression. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 63 20702774
2016 Mutation in IRF2BP2 is responsible for a familial form of common variable immunodeficiency disorder. The Journal of allergy and clinical immunology 58 27016798
2019 IRF2BP2: A new player in the regulation of cell homeostasis. Journal of leukocyte biology 46 31022319
2008 The novel p53 target gene IRF2BP2 participates in cell survival during the p53 stress response. Nucleic acids research 46 19042971
2017 Loss of IRF2BP2 in Microglia Increases Inflammation and Functional Deficits after Focal Ischemic Brain Injury. Frontiers in cellular neuroscience 43 28769762
2015 Identification of a novel fusion gene, IRF2BP2-RARA, in acute promyelocytic leukemia. Journal of the National Comprehensive Cancer Network : JNCCN 43 25583766
2019 The IRF2BP2-KLF2 axis regulates osteoclast and osteoblast differentiation. BMB reports 28 31186082
2021 The Transcriptional Co-factor IRF2BP2: A New Player in Tumor Development and Microenvironment. Frontiers in cell and developmental biology 25 33996817
2020 Hepatic IRF2BP2 Mitigates Nonalcoholic Fatty Liver Disease by Directly Repressing the Transcription of ATF3. Hepatology (Baltimore, Md.) 25 31529495
2016 New variant of acute promyelocytic leukemia with IRF2BP2-RARA fusion. Cancer science 25 27193600
2019 IRF2BP2 modulates the crosstalk between glucocorticoid and TNF signaling. The Journal of steroid biochemistry and molecular biology 20 31145973
2019 The NOTCH1-dependent HIF1α/VGLL4/IRF2BP2 oxygen sensing pathway triggers erythropoiesis terminal differentiation. Redox biology 19 31539803
2020 Inhibition of miR-155 potentially protects against lipopolysaccharide-induced acute lung injury through the IRF2BP2-NFAT1 pathway. American journal of physiology. Cell physiology 18 33052070
2016 IRF2BP2 transcriptional repressor restrains naive CD4 T cell activation and clonal expansion induced by TCR triggering. Journal of leukocyte biology 18 27286791
2017 Control of Pathological Cardiac Hypertrophy by Transcriptional Corepressor IRF2BP2 (Interferon Regulatory Factor-2 Binding Protein 2). Hypertension (Dallas, Tex. : 1979) 17 28716987
2017 IRF2BP2-deficient microglia block the anxiolytic effect of enhanced postnatal care. Scientific reports 17 28852125
2022 OIP5-AS1 Inhibits Oxidative Stress and Inflammation in Ischemic Stroke Through miR-155-5p/IRF2BP2 Axis. Neurochemical research 13 36460840
2024 Super-enhancer-driven IRF2BP2 enhances ALK activity and promotes neuroblastoma cell proliferation. Neuro-oncology 12 38864832
2023 Novel mutation and expanding phenotype in IRF2BP2 deficiency. Rheumatology (Oxford, England) 12 36193988
2019 A rare case of acute promyelocytic leukemia with IRF2BP2-RARA fusion; and literature review. OncoTargets and therapy 12 31447564
2022 A novel IRF2BP2::CDX2 Gene fusion in digital intravascular myoepithelioma of soft tissue: An enigma! Genes, chromosomes & cancer 11 36448218
2021 IRF2BP2 prevents ox-LDL-induced inflammation and EMT in endothelial cells via regulation of KLF2. Experimental and therapeutic medicine 11 33767776
2024 miR‑155 promotes an inflammatory response in HaCaT cells via the IRF2BP2/KLF2/NF‑κB pathway in psoriasis. International journal of molecular medicine 10 39219281
2023 Agmatine-IRF2BP2 interaction induces M2 phenotype of microglia by increasing IRF2-KLF4 signaling. Inflammation research : official journal of the European Histamine Research Society ... [et al.] 10 37314519
2021 IRF2BP2 Mutation Is Associated with Increased STAT1 and STAT5 Activation in Two Family Members with Inflammatory Conditions and Lymphopenia. Pharmaceuticals (Basel, Switzerland) 10 34451894
2019 Primary mesenchymal chondrosarcoma of the kidney without HEY1-NCOA2 and IRF2BP2-CDX1 fusion: A case report and review. Oncology letters 10 31897203
2018 Suppressing Irf2bp2 expressions accelerates metabolic syndrome-associated brain injury and hepatic dyslipidemia. Biochemical and biophysical research communications 10 30131248
2024 Super-Enhancer-Driven IRF2BP2 is Activated by Master Transcription Factors and Sustains T-ALL Cell Growth and Survival. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 7 39454110
2024 IRF2BP2 counteracts the ATF7/JDP2 AP-1 heterodimer to prevent inflammatory overactivation in acute myeloid leukemia (AML) cells. Nucleic acids research 6 38801077
2023 Case Report: A novel IRF2BP2 mutation in an IEI patient with recurrent infections and autoimmune disorders. Frontiers in immunology 5 37350971
2022 IRF2BP2 is a novel HNF4α co-repressor: Its role in gluconeogenic gene regulation via biochemically labile interaction. Biochemical and biophysical research communications 5 35609419
2025 Transcriptional regulation of adipocyte lipolysis by IRF2BP2. Science advances 4 39752494
2024 Novel hypermorphic variants in IRF2BP2 identified in patients with common variable immunodeficiency and autoimmunity. Clinical immunology (Orlando, Fla.) 4 39059757
2023 IRF2BP2 drives lymphatic metastasis in OSCC cells by elevating mitochondrial fission-dependent fatty acid oxidation. Molecular carcinogenesis 4 37737489
2021 IRF2BP2 3'UTR Polymorphism Increases Coronary Artery Calcification in Men. Frontiers in cardiovascular medicine 4 34760935
2025 IRF2BP2 deficiency: An important form of common variable immunodeficiency with inflammation. The Journal of allergy and clinical immunology 3 40090425
2025 Laminarin-coated Genexol-PM pH sensitive nanomicelles targeting miR-620/IRF2BP2 axis for inhibition of cell proliferation and induction of apoptosis in Invitro thyroid carcinoma. International journal of biological macromolecules 3 40246117
2023 Novel frameshift variants expand the map of the genetic defects in IRF2BP2. Frontiers in immunology 3 37876937
2022 Savior Siblings Might Rescue Fetal Lethality But Not Adult Lymphoma in Irf2bp2-Null Mice. Frontiers in immunology 3 35865523
2022 LncRNA ATP1A1-AS1 inhibits cell proliferation and promotes cell apoptosis in thyroid carcinoma by regulating the miR-620/IRF2BP2 axis. The American journal of the medical sciences 3 36002076
2024 CDYL loss promotes cervical cancer aggression by increasing PD-L1 expression via the suppression of IRF2BP2 transcription. Translational oncology 2 38991463
2023 Fusion of the Genes for Interferon Regulatory Factor 2 Binding Protein 2 (IRF2BP2) and Caudal Type Homeobox 1 (CDX1) in a Chondrogenic Tumor. In vivo (Athens, Greece) 2 37905608
2024 IRF2BP2 binds to a conserved RxSVI motif of protein partners and regulates megakaryocytic differentiation. Nature communications 1 39616187
2024 RETRACTED: IAV Antagonizes Host Innate Immunity by Weakening the LncRNA-LRIR2-Mediated Antiviral Functions. Biology 1 39765665
2026 IRF2BP2::JAK2 Defines a Novel Kinase-Activating Fusion in Pediatric T-Cell Acute Lymphoblastic Leukemia. Genes, chromosomes & cancer 0 41711169
2025 Therapy resistance in AML is mediated by cytoplasmic sequestration of the transcriptional repressor IRF2BP2. bioRxiv : the preprint server for biology 0 40475530
2025 An IRF2BP2 Variant in a Pediatric Patient with Common Variable Immunodeficiency. Pediatric allergy, immunology, and pulmonology 0 40689779
2025 Myoepithelial Tumor of Soft Tissue With the Novel IRF2BP2::CDX1 Gene Fusion. Cureus 0 40978976
2025 Case Report: Novel IRF2BP2 variant in a Japanese patient with impaired B-cell differentiation, Th1 polarization, and systemic immune dysregulation. Frontiers in immunology 0 41246352
2024 Transcriptional regulation of adipocyte lipolysis by IRF2BP2. bioRxiv : the preprint server for biology 0 39211193