Affinage

IRF2BP2

Interferon regulatory factor 2-binding protein 2 · UniProt Q7Z5L9

Length
587 aa
Mass
61.0 kDa
Annotated
2026-06-10
52 papers in source corpus 26 papers cited in narrative 26 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

IRF2BP2 is a nuclear transcriptional co-regulator that controls gene programs governing inflammation, lipid metabolism, hematopoietic differentiation, and cancer cell survival, generally acting as a co-repressor but also as a context-dependent co-activator (PMID:20702774, PMID:38801077, PMID:39752494). It engages transcription factor partners through a C-terminal RING finger domain that recognizes a conserved RxSVI motif present in IRF2, VGLL4, and ZBTB16, with structural and biochemical data showing the motif forms a short loop and β-strand that docks into the RING domain (PMID:39616187). Through these interactions IRF2BP2 directly represses target genes: it binds and represses the ATF3 promoter in hepatocytes to protect against high-fat-diet steatosis and insulin resistance (PMID:31529495), represses LIPE and other lipolysis genes in adipocytes to restrain free fatty acid release and adipose inflammation (PMID:39752494), and acts as an HNF4α co-repressor in a manner dependent on its E3 ubiquitin ligase activity to restrain gluconeogenic genes (PMID:35609419). In macrophages and microglia IRF2BP2 is required for MEF2-dependent activation of KLF2, driving anti-inflammatory and cholesterol-efflux programs whose loss worsens atherosclerosis and stroke outcome (PMID:26195219, PMID:28769762), and the same IRF2BP2/KLF2 axis governs osteoclast versus osteoblast differentiation (PMID:31186082). It restrains hypertrophic and immune transcription by competing with MEF2C for the NFAT1 transactivation domain in cardiomyocytes and by binding NFAT1 to limit inflammatory signaling (PMID:28716987, PMID:33052070). In the nucleus IRF2BP2 is recruited to chromatin by the ATF7/JDP2 AP-1 dimer to counteract gene activation (PMID:38801077), cooperates with TRIM28 and DNMT1 to silence HERV-K transposable elements in AML [PMID:bio_10.1101_2025.11.12.688028], and supports leukemia and tumor proliferation, being driven by super-enhancers and cooperating with master transcription factors to regulate targets such as RAG1 in T-ALL and ALK in neuroblastoma (PMID:39454110, PMID:38864832). Loss-of-function and RING-domain mutations in humans cause an immunodeficiency with impaired B-cell/plasmablast maturation, defective repression of NFAT and STAT1, and aberrant cytoplasmic mislocalization and aggregation of the protein (PMID:27016798, PMID:34451894, PMID:39059757, PMID:40090425).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2008 High

    Established the first functional context for IRF2BP2 by showing it is a p53 target that dampens the apoptotic response, framing it as a transcriptional modulator of stress programs.

    Evidence Reporter assays, siRNA knockdown, overexpression, and apoptosis assays in human cells

    PMID:19042971

    Open questions at the time
    • Did not define direct DNA-binding or repressive mechanism at p53 target promoters
    • No partner protein identified
  2. 2010 High

    Identified IRF2BP2 as a TEAD4/VGLL4 complex component that activates VEGFA, demonstrating it can act as a co-activator within a defined transcription factor complex.

    Evidence Yeast 2-hybrid, reciprocal co-IP, mammalian 2-hybrid, and knockdown with VEGFA readout in C2C12 cells

    PMID:20702774

    Open questions at the time
    • Mechanism of VEGFA activation not resolved at chromatin level
    • Did not establish whether activation versus repression is partner-determined
  3. 2015 High

    Defined an IRF2BP2/MEF2/KLF2 axis controlling macrophage anti-inflammatory and cholesterol-efflux programs, linking IRF2BP2 to atherosclerosis in vivo.

    Evidence Macrophage-specific conditional KO mice, promoter assays, and KLF2 rescue with cholesterol efflux readout

    PMID:26195219

    Open questions at the time
    • Whether IRF2BP2 acts as activator or repressor at the KLF2 promoter not fully resolved
    • Direct chromatin occupancy not shown
  4. 2016 Medium

    Extended IRF2BP2 function to adaptive immunity by showing it restrains CD4 T-cell activation and to humans by linking a heterozygous mutation to CVID with impaired plasmablast formation.

    Evidence Retroviral transduction of primary CD4 T and B cells, flow cytometry, in vivo transfer, and exome sequencing of a CVID family

    PMID:27016798 PMID:27286791

    Open questions at the time
    • Direct target genes in T/B cells not identified
    • Mechanism connecting mutation to plasmablast defect undefined
  5. 2017 High

    Revealed a competitive co-repression mechanism in which IRF2BP2 binds the NFAT1 transactivation domain to displace MEF2C and limit hypertrophic transcription, validated by genetic epistasis.

    Evidence Cardiomyocyte-specific KO and transgenic mice with aortic banding, reciprocal co-IP, NFAT1 blockade rescue

    PMID:28716987

    Open questions at the time
    • Structural basis of NFAT1/MEF2C competition not resolved
    • Did not address whether other partners use the same competitive mechanism
  6. 2017 High

    Showed IRF2BP2 controls macrophage/microglial inflammatory polarization and IFNβ responses, connecting it to stroke injury outcomes.

    Evidence Conditional macrophage/microglia KO mice, photothrombotic stroke model, cytokine and IFNβ epistasis assays

    PMID:28769762

    Open questions at the time
    • Direct transcriptional targets in microglia not mapped
    • Relationship to the KLF2 axis in this context not formalized
  7. 2019 High

    Established IRF2BP2 as a direct hepatic transcriptional repressor of ATF3 and a regulator of metabolic homeostasis, and extended the KLF2 axis to bone cell differentiation.

    Evidence Hepatocyte-specific KO/overexpression mice with ChIP-seq, luciferase and ATF3 rescue; osteoclast/osteoblast differentiation with KLF2 rescue

    PMID:31186082 PMID:31529495

    Open questions at the time
    • Cofactors mediating ATF3 promoter repression not identified
    • Whether RING/E3 activity is required for ATF3 repression not tested
  8. 2019 Medium

    Connected IRF2BP2 to nuclear receptor and stress signaling by mapping glucocorticoid-dependent chromatin binding co-occurring with GR, and to erythropoiesis via VGLL4 sequestration that releases alas2 repression.

    Evidence ChIP-seq/RNA-seq with siRNA depletion in A549/HEK293 cells; CRISPR vgll4b zebrafish with irf2bp2-depletion rescue and TDU1/RING domain mapping

    PMID:31145973 PMID:31539803

    Open questions at the time
    • Whether IRF2BP2 directly contacts GR not established
    • Domain-level data did not yet define the partner-binding motif
  9. 2020 Medium

    Demonstrated IRF2BP2 acts as a ubiquitin-ligase-dependent HNF4α co-repressor and confirmed NFAT1 binding as a node modulated by miRNA and small molecules.

    Evidence Specialized proteomic interaction detection, reporter assays with E3-ligase mutant, CRISPR KO HepG2; co-IP, miR-155 reporter assay, shRNA in mice

    PMID:33052070 PMID:35609419

    Open questions at the time
    • HNF4α interaction undetectable by conventional IP, leaving stoichiometry uncertain
    • Ubiquitination substrate of the E3 activity not identified
  10. 2021 Medium

    Linked human IRF2BP2 deficiency to dysregulated STAT signaling by showing a deletion variant fails to suppress STAT1, with patients showing constitutive STAT1/STAT5 activation.

    Evidence Luciferase reporter, phospho-STAT flow cytometry, NanoString in patient samples

    PMID:34451894

    Open questions at the time
    • Direct mechanism by which IRF2BP2 represses STAT1 transcription not defined
    • Single family/lab
  11. 2024 High

    Provided the structural and biochemical basis for IRF2BP2 partner selection, defining RING-domain recognition of a conserved RxSVI motif shared by IRF2, VGLL4, and ZBTB16, and a role in megakaryocytic differentiation.

    Evidence Motif discovery, biochemical binding assays, structural determination, and differentiation assays

    PMID:39616187

    Open questions at the time
    • Whether all functional partners use the RxSVI motif not exhaustively tested
    • How motif binding dictates repression versus activation unresolved
  12. 2024 High

    Established IRF2BP2 as a chromatin co-repressor of AP-1 (ATF7/JDP2) and an oncogenic dependency in leukemia driven by super-enhancers cooperating with master transcription factors.

    Evidence Co-IP and chromatin recruitment assays with RNA-seq in AML; CUT&Tag, IP, conditional KO mice in T-ALL targeting RAG1; ChIP/ATAC-seq with loss-of-function in neuroblastoma targeting ALK

    PMID:38801077 PMID:38864832 PMID:39454110

    Open questions at the time
    • How IRF2BP2 switches between repressing AP-1 and co-activating master TF targets not reconciled
    • Direct versus indirect effects on MYC/E2F pathways not separated
  13. 2024 Medium

    Connected human RING-domain mutations to a cell-biological defect: aberrant cytoplasmic aggregation and impaired nuclear translocation of IRF2 and NF-κB1.

    Evidence Confocal microscopy and immunoblotting of EGFP-fused mutants with NF-κB1 reporter in HEK293

    PMID:39059757

    Open questions at the time
    • Whether aggregation is a direct cause of partner mislocalization or a downstream consequence unclear
    • Overexpression system may not reflect endogenous behavior
  14. 2025 High

    Defined IRF2BP2 as a direct transcriptional repressor of adipocyte lipolysis genes including LIPE, establishing its role in systemic metabolic and inflammatory homeostasis.

    Evidence ChIP-seq, RNA-seq, adipocyte-specific KO mice, primary human adipocyte deletion/overexpression with FFA measurement

    PMID:39752494

    Open questions at the time
    • Cofactors required for LIPE promoter repression not identified
    • Relationship to hepatic ATF3 repression mechanism not compared
  15. 2025 Medium

    Revealed regulation of IRF2BP2 by spatial sequestration and an epigenetic silencing partnership: MCL1 traps it in the cytoplasm to de-repress fatty-acid-oxidation genes in drug-resistant AML, and it cooperates with TRIM28/DNMT1 to silence transposable elements.

    Evidence Co-IP/MS, subcellular fractionation, ACSL1 functional assays (preprint); Perturb-seq, CRISPR activation/re-silencing of HERV-K, TRIM28/DNMT1 co-occupancy (preprint)

    PMID:40475530 PMID:bio_10.1101_2025.11.12.688028

    Open questions at the time
    • Preprint findings not yet peer-reviewed
    • Whether cytoplasmic sequestration is reversible/regulated physiologically unknown
  16. 2026 Medium

    Showed an IRF2BP2::JAK2 fusion is an oncogenic, cytoplasmically localized driver of constitutive JAK-STAT signaling that is targetable by JAK inhibitors.

    Evidence CRISPR-engineered Ba/F3 cytokine-independence, localization, and JAK-inhibitor sensitivity assays

    PMID:41711169

    Open questions at the time
    • Contribution of the IRF2BP2 portion to fusion activity not dissected
    • Single experimental system

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how IRF2BP2 chooses between transcriptional repression and activation at different partners and loci, and what substrate its E3 ubiquitin ligase activity acts upon.
  • No identified ubiquitination substrate despite an E3-activity-dependent repression function
  • No unified model linking RxSVI-motif binding to activator versus repressor outcome
  • Regulation of nuclear/cytoplasmic partitioning under physiological conditions undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 6 GO:0060090 molecular adaptor activity 3 GO:0003677 DNA binding 2 GO:0016874 ligase activity 1
Localization
GO:0005634 nucleus 4 GO:0005829 cytosol 3
Pathway
R-HSA-1643685 Disease 4 R-HSA-168256 Immune System 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1430728 Metabolism 3 R-HSA-4839726 Chromatin organization 2
Complex memberships
ATF7/JDP2 AP-1 chromatin complexTEAD4/VGLL4 transcription factor complexTRIM28/DNMT1 silencing complex

Evidence

Reading pass · 26 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2010 IRF2BP2 was identified as a component of the TEAD4/VGLL4 transcription factor complex via yeast 2-hybrid screen from a human heart cDNA library, confirmed in vivo by co-immunoprecipitation and mammalian 2-hybrid assays. Co-expression of IRF2BP2 with TEAD4/VGLL4 or TEAD1 potently activated VEGFA expression, while knockdown reduced VEGFA expression in C2C12 muscle cells. Yeast 2-hybrid, co-immunoprecipitation, mammalian 2-hybrid, knockdown with gene expression readout FASEB journal High 20702774
2008 IRF2BP2 is a direct transcriptional target of p53; its upregulation after actinomycin D treatment is p53-dependent. Overexpressed IRF2BP2 impedes p53-mediated transactivation of p21 and Bax genes, diminishes apoptosis after doxorubicin treatment, and its knockdown leads to upregulation of p21 and faster apoptosis induction. Reporter assays, loss-of-function (siRNA knockdown), gain-of-function (overexpression), cell viability/apoptosis assays Nucleic acids research High 19042971
2015 IRF2BP2 is required for MEF2-dependent activation of KLF2 (Krüppel-like factor 2) in macrophages, as shown by promoter studies. IRF2BP2-deficient macrophages have markedly reduced KLF2 expression, impaired ABCA1 activation in response to cholesterol loading, and worsened atherosclerosis; restoring KLF2 in IRF2BP2-deficient macrophages rescued anti-inflammatory gene activation and cholesterol efflux. Macrophage-specific conditional knockout mice, promoter assays, rescue experiments with KLF2 restoration, cholesterol efflux assays Circulation research High 26195219
2017 IRF2BP2 directly interacts with the C-terminal transactivation domain of NFAT1 by competing with MEF2C, disturbing their transcriptional synergism and impeding NFAT1-transactivated hypertrophic transcriptome in cardiomyocytes. Cardiomyocyte-specific Irf2bp2 knockout exacerbated cardiac hypertrophy, while Irf2bp2 transgenic overexpression was protective; the effect of Irf2bp2 deficiency was rescued by NFAT1 blockage. Cardiomyocyte-specific KO and transgenic mouse models, co-immunoprecipitation of IRF2BP2-NFAT1 interaction, aortic banding and angiotensin II infusion models Hypertension High 28716987
2016 Ectopic expression of IRF2BP2 in murine primary CD4 T cells reduced CD25 expression, STAT5 phosphorylation, and proliferative capacity following TCR stimulation; IRF2BP2-overexpressing cells showed impaired in vivo expansion capacity. IRF2BP2 expression was decreased in CD4 T cells upon activation. Retroviral transduction of primary CD4 T cells, flow cytometry, in vivo adoptive transfer Journal of leukocyte biology Medium 27286791
2016 A heterozygous IRF2BP2 mutation (c.1652G>A:p.[S551N]) was identified in a family with CVID. Transduction of mutant IRF2BP2 into control human B cells decreased production of plasmablasts in vitro, demonstrating a role for IRF2BP2 in B-cell differentiation. Whole-exome sequencing, retroviral transduction into human B cells, in vitro plasmablast differentiation assay, protein immunoblots The Journal of allergy and clinical immunology Medium 27016798
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 macrophages/microglia lost the anti-inflammatory effect of IFNβ, and mice lacking IRF2BP2 in macrophages/microglia showed larger infarctions and worse functional outcomes after photothrombotic stroke. Conditional macrophage/microglia-specific KO mice, photothrombotic stroke model, cytokine measurements, IFNβ treatment Frontiers in cellular neuroscience High 28769762
2019 IRF2BP2 overexpression suppressed osteoclast differentiation and enhanced osteoblast differentiation; these effects were reversed by KLF2 knockdown, establishing an IRF2BP2/KLF2 axis in bone cell differentiation. KLF2 overexpression inhibited osteoclast differentiation by downregulating c-Fos, NFATc1, and TRAP. Overexpression, siRNA knockdown, osteoclast/osteoblast differentiation assays BMB reports Medium 31186082
2019 IRF2BP2 modulates glucocorticoid (GC) receptor (GR) and NF-κB signaling: GC changes chromatin binding of IRF2BP2, GC-induced IRF2BP2-binding sites co-occur with GR binding sites and associate with GC-induced genes. Depletion of IRF2BP2 modulates GC-regulated gene transcription and alters responses to both GC and TNFα. ChIP-seq (chromatin immunoprecipitation sequencing), siRNA depletion, RNA-seq in A549 and HEK293 cells The Journal of steroid biochemistry and molecular biology Medium 31145973
2019 In zebrafish, VGLL4 sequesters IRF2BP2 via their respective TDU1 and RING finger domains, thereby preventing IRF2BP2 from repressing alas2 expression and heme biosynthesis during erythroid terminal differentiation. irf2bp2 depletion rescued the impaired erythroid phenotype of vgll4b mutant zebrafish. CRISPR/Cas9 vgll4b mutant zebrafish, genetic rescue by irf2bp2 depletion, domain mapping (TDU1/RING finger) Redox biology Medium 31539803
2020 IRF2BP2 directly represses ATF3 gene expression in hepatocytes by binding to the ATF3 promoter region, as demonstrated by ChIP-seq and luciferase assay. Hepatocyte-specific Irf2bp2 knockout exacerbated high-fat diet-induced hepatic steatosis, insulin resistance and inflammation, while hepatic overexpression was protective; ATF3 knockdown relieved the effects of IRF2BP2 knockout. Hepatocyte-specific KO and overexpression mouse models, ChIP-seq, luciferase assay, digital gene expression analysis, ATF3 siRNA rescue Hepatology High 31529495
2020 IRF2BP2 binds to NFAT1, and this interaction is increased by the natural compound Oroxylin A. IRF2BP2 binding to NFAT1 was demonstrated by immunoprecipitation assay and is linked to regulation of inducible nitric oxide synthase and inflammatory signaling. miR-155-5p targets IRF2BP2 mRNA (validated by reporter assay), reducing IRF2BP2 levels. Immunoprecipitation assay, miRNA array, luciferase reporter assay, shRNA injection in mice American journal of physiology. Cell physiology Medium 33052070
2021 IRF2BP2 is required to attenuate STAT1 transcriptional activity; an IRF2BP2 deletion variant (c.625_665del) failed to suppress STAT1 transcription in a luciferase reporter system. Patients with this mutation showed overexpression and constitutive activation of STAT1, upregulated IFN-JAK-STAT signaling, and elevated STAT5 phosphorylation in CD4+ T cells. Luciferase reporter assay, flow cytometry for phospho-STAT quantification, NanoString gene expression, clinical patient samples Pharmaceuticals Medium 34451894
2022 IRF2BP2 represses transcriptional activity of HNF4α and functions as a novel HNF4α co-repressor. The IRF2BP2-HNF4α interaction was detectable only by novel proteomic techniques (not conventional immunoprecipitation). IRF2BP2 repressed HNF4α transcriptional activity in a manner dependent on its E3 ubiquitin ligase activity, and IRF2BP2 gene deficiency in HepG2 cells induced gluconeogenic genes. Novel proteomic interaction techniques, reporter assay, CRISPR KO of IRF2BP2 in HepG2 cells, gluconeogenic gene expression measurement Biochemical and biophysical research communications Medium 35609419
2024 The RING domain of IRF2BP2 binds to a conserved RxSVI motif present in interacting partners IRF2, VGLL4, and ZBTB16. Biochemical and structural data show that motif-containing peptides form a short loop with a short β-strand facilitating RING domain recognition. IRF2BP2 plays a regulatory role in megakaryocytic differentiation through its interaction with ZBTB16. Motif discovery, biochemical binding assays, structural determination (crystal/NMR), cell biological assays of megakaryocytic differentiation Nature communications High 39616187
2024 IRF2BP2 interacts with the AP-1 heterodimer ATF7/JDP2 and is recruited to chromatin by this dimer, where it counteracts ATF7/JDP2 gene-activating function. Loss of IRF2BP2 causes overactivation of inflammatory pathways in AML cells, resulting in strongly reduced proliferation. Co-immunoprecipitation, chromatin recruitment assays, IRF2BP2 loss-of-function in AML cells with RNA-seq Nucleic acids research High 38801077
2024 IRF2BP2 is driven by a super-enhancer in T-ALL regulated by master TFs (ERG, ELF1, ETS1). CUT&Tag and immunoprecipitation show IRF2BP2 cooperates with T-ALL master TFs to target the enhancer of RAG1 and modulate its expression. IRF2BP2 is crucial for T-ALL cell growth and survival in vitro and in vivo, and loss affects MYC and E2F pathways. CUT&Tag, immunoprecipitation, conditional KO mice (hematopoietic-specific), in vitro and in vivo T-ALL models Advanced science High 39454110
2024 In neuroblastoma, a super-enhancer driven by master TFs MYCN, MEIS2, and HAND2 activates IRF2BP2 expression. AP-1 family members shape chromatin accessibility to expose IRF2BP2 binding sites, and AP-1 and IRF2BP2 collaboratively stimulate expression of the NB susceptibility gene ALK to maintain the highly proliferative NB phenotype. ChIP-seq, ATAC-seq, transcriptome sequencing, loss-of-function experiments in NB cells, in vivo experiments Neuro-oncology Medium 38864832
2025 IRF2BP2 functions as a transcriptional repressor of adipocyte lipolysis by directly repressing lipolysis-related genes including LIPE (hormone-sensitive lipase). Adipocyte-selective deletion of Irf2bp2 in mice increased Lipe expression and free fatty acid levels, resulting in adipose tissue inflammation and glucose intolerance. ChIP-seq, RNA-seq, adipocyte-specific KO mice, primary human adipocyte deletion and overexpression, free fatty acid measurement Science advances High 39752494
2025 In ven/aza-resistant AML, MCL1 binds IRF2BP2 (identified by co-IP of MCL1 coupled with mass spectrometry), resulting in cytoplasmic sequestration of IRF2BP2 and loss of its transcriptional repression. This de-represses ACSL1 (a rate-limiting enzyme for fatty acid oxidation), promoting ven/aza resistance in leukemic stem cells. Co-immunoprecipitation of MCL1 + mass spectrometry, subcellular fractionation, ACSL1 inhibition functional assays, gene expression in LSCs bioRxivpreprint Medium 40475530
2025 IRF2BP2 cooperates with TRIM28 and DNMT1 to epigenetically silence transposable elements (particularly HERV-K/LTR5_Hs) in AML. Loss of IRF2BP2 induced differentiation and apoptosis linked to TE transcriptional activation; CRISPR activation of HERV-K recapitulated IRF2BP2 loss phenotypes, and targeted re-silencing of HERV-K partially rescued these effects. Single-cell Perturb-seq screen, CRISPR activation, ChIP/chromatin analyses for TRIM28/DNMT1 co-occupancy, rescue experiments bioRxivpreprint Medium bio_10.1101_2025.11.12.688028
2026 An IRF2BP2::JAK2 fusion protein confers cytokine-independent growth in Ba/F3 cells, localizes to the cytoplasm, and drives constitutive JAK-STAT signaling. Both type I (ruxolitinib) and type II (CHZ868) JAK inhibitors potently inhibit the fusion. CRISPR-Cas9 engineering of Irf2bp2::Jak2 in Ba/F3 cells, cytokine-independent growth assay, subcellular localization, JAK inhibitor treatment Genes, chromosomes & cancer Medium 41711169
2024 Variants in the C-terminal RING finger domain of IRF2BP2 caused irregular aggregate formation and cytoplasmic distribution rather than the expected nuclear localization, and impaired nuclear translocation of IRF2 and NFκB1 (p50), as shown in HEK293 cells expressing EGFP-fused mutants. Confocal fluorescence microscopy, immunoblotting, overexpression of EGFP-fused mutants, luciferase reporter for NFκB1 Clinical immunology Medium 39059757
2036 IRF2BP2 patient-derived mutant constructs showed impaired repression of NFAT activation compared to wild-type, as demonstrated by NFAT luciferase reporter assay in Jurkat cells. Mutant IRF2BP2 constructs also showed higher TNF-α transcript levels compared to wild-type IRF2BP2. NFAT luciferase reporter assay in Jurkat cells, quantitative cDNA determination The Journal of allergy and clinical immunology Medium 40090425
2023 IRF2BP2 promotes lymph node metastasis in oral squamous cell carcinoma by enhancing mitochondrial fission through contributing to Drp1 S616 phosphorylation and mitochondrial localization, which upregulates CPT1A expression and fatty acid oxidation. CPT1A overexpression rescued invasion in IRF2BP2-silenced cells. Confocal microscopy, transmission electron microscopy, immunofluorescence, western blot for Drp1 phosphorylation, CPT1A rescue experiment, in vivo xenograft model Molecular carcinogenesis Medium 37737489
2023 Agmatine binds directly to IRF2BP2 (identified by protein microarray). This competitive binding releases IRF2, allowing free IRF2 to translocate to the BV2 microglia nucleus and activate KLF4 transcription, increasing CD206-positive (M2) microglial polarization. Protein microarray, immunofluorescence/nuclear translocation assay, flow cytometry for CD206 Inflammation research Low 37314519

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 75 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 47 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 26 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
2024 Super-enhancer-driven IRF2BP2 enhances ALK activity and promotes neuroblastoma cell proliferation. Neuro-oncology 14 38864832
2022 OIP5-AS1 Inhibits Oxidative Stress and Inflammation in Ischemic Stroke Through miR-155-5p/IRF2BP2 Axis. Neurochemical research 14 36460840
2024 miR‑155 promotes an inflammatory response in HaCaT cells via the IRF2BP2/KLF2/NF‑κB pathway in psoriasis. International journal of molecular medicine 12 39219281
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
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) 8 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
2025 Transcriptional regulation of adipocyte lipolysis by IRF2BP2. Science advances 5 39752494
2023 Case Report: A novel IRF2BP2 mutation in an IEI patient with recurrent infections and autoimmune disorders. Frontiers in immunology 5 37350971
2023 IRF2BP2 drives lymphatic metastasis in OSCC cells by elevating mitochondrial fission-dependent fatty acid oxidation. Molecular carcinogenesis 5 37737489
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 IRF2BP2 deficiency: An important form of common variable immunodeficiency with inflammation. The Journal of allergy and clinical immunology 4 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 4 40246117
2024 Novel hypermorphic variants in IRF2BP2 identified in patients with common variable immunodeficiency and autoimmunity. Clinical immunology (Orlando, Fla.) 4 39059757
2021 IRF2BP2 3'UTR Polymorphism Increases Coronary Artery Calcification in Men. Frontiers in cardiovascular medicine 4 34760935
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

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