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Showing HIVEP2 — MIBP1 is a alias.

HIVEP2

Transcription factor HIVEP2 · UniProt P31629

Length
2446 aa
Mass
269.1 kDa
Annotated
2026-06-10
40 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

HIVEP2 (Schnurri-2/MIBP1) is a large zinc-finger transcription factor that governs cell fate and survival decisions by acting as a context-dependent transcriptional repressor and a signal-responsive cofactor (PMID:2022670, PMID:15699073). Through its C2H2 zinc-finger DNA-binding domain it engages specific sequence elements, including the HIV-1 enhancer and an intronic site in c-myc (PMID:2022670, PMID:7838722), and it represses transcription by binding κB/NF-κB motifs in direct competition with p50 NF-κB, thereby globally dampening NF-κB-driven gene expression (PMID:15699073, PMID:22294689); this repression is attenuated by O-GlcNAcylation catalyzed by its binding partner OGT (PMID:22294689). Its repressor functions extend to silencing c-myc, where it acts through physical interaction with the Ski-interacting protein SKIP via its acidic region (PMID:11872163), and it can also partner with RFX1 to bind viral negative-regulatory elements (PMID:8709229, PMID:9018153). HIVEP2 additionally serves as a nuclear signal integrator: upon BMP-2 stimulation it translocates to the nucleus and cooperates with Smad1/4 and C/EBPα on the PPARγ2 promoter to drive adipogenesis and bone remodeling (PMID:16580992, PMID:17311925), and upon TGF-β stimulation it forms a cytoplasmic complex with CLIC4 that co-translocates to the nucleus to sustain phospho-Smad2/3 signaling (PMID:19448624). In the immune system, Schnurri-2 enables positive selection of thymocytes by dampening TCR-induced Bax activation and the mitochondrial death pathway (PMID:21475200), suppresses Th2 differentiation and supports memory T-cell survival through NF-κB repression (PMID:15699073, PMID:17404274), and is required for NK-cell cytotoxic effector function (PMID:21936769). In the nervous system it regulates immediate-early and neurotransmitter-related gene programs, influencing stress behavior and contributing to neuropathic pain through control of excitatory glutamate receptor subunit expression (PMID:16836985, PMID:35218885).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1991 Medium

    Established HIVEP2 as a large metal/zinc-finger DNA-binding protein, defining its modular architecture and its inducibility in activated T cells.

    Evidence cDNA cloning, domain analysis, and DNA-binding characterization on the HIV-1 enhancer in Jurkat T cells

    PMID:2022670

    Open questions at the time
    • No in vivo function established
    • Target genes beyond the HIV-1 enhancer not defined
    • Mechanism of transcriptional effect (activation vs repression) unresolved
  2. 1994 Medium

    Demonstrated sequence-specific DNA recognition by the zinc fingers at a defined c-myc intronic element, linking HIVEP2 to a specific cellular target gene.

    Evidence In vitro DNA-binding assay with bacterially expressed fusion protein on rat c-myc intron 1

    PMID:7838722

    Open questions at the time
    • Functional transcriptional consequence not yet shown
    • No cellular validation of binding
    • Cofactor requirements unknown
  3. 1996 Medium

    Showed HIVEP2 partners with RFX1 to occupy viral regulatory elements and confer silencer activity, introducing a cofactor-dependent repression mechanism.

    Evidence Supershift and reporter assays on the HBV enhancer EP element

    PMID:8709229 PMID:9018153

    Open questions at the time
    • Stoichiometry and heterodimer interface not defined
    • Generality beyond viral promoters unclear
    • Cellular targets not identified
  4. 1999 Medium

    Revealed that HIVEP2 can also act as a transcriptional activator at a cellular promoter, indicating context-dependent regulatory output.

    Evidence DNA binding, co-activation reporter assay with SEF-2, and in situ hybridization for SSTR-2 in brain

    PMID:10207097

    Open questions at the time
    • Switch between activation and repression not mechanistically explained
    • No in vivo validation of SSTR-2 regulation
  5. 2002 High

    Identified SKIP as a direct repression cofactor binding the acidic region, providing a molecular basis for c-myc silencing.

    Evidence Yeast two-hybrid, in vitro pull-down, reciprocal Co-IP, and reporter assay; in situ hybridization in neurons

    PMID:11872163

    Open questions at the time
    • Whether SKIP recruitment generalizes to other repressed genes unknown
    • Structural basis of the acidic-region/SKIP interaction undefined
  6. 2001 High

    Established an essential in vivo role: HIVEP2 is required for positive selection of thymocytes downstream of TCR engagement.

    Evidence Schnurri-2 knockout mouse with thymocyte flow cytometry

    PMID:11668343

    Open questions at the time
    • Molecular mechanism of the survival signal not yet defined at this stage
  7. 2005 High

    Defined the core repressive mechanism in immunity: HIVEP2 competes with p50 NF-κB for the κB motif to restrain NF-κB-driven Th2 differentiation.

    Evidence KO mouse, in vitro Th differentiation, NF-κB binding competition and promoter reporter assays

    PMID:15699073

    Open questions at the time
    • Genome-wide scope of NF-κB target repression not assessed here
    • Regulation of HIVEP2 occupancy in response to signals unclear
  8. 2006 High

    Established HIVEP2 as a BMP-2-responsive nuclear cofactor that cooperates with Smad1/4 and C/EBPα to induce PPARγ2 and drive adipogenesis.

    Evidence KO mouse, MEF differentiation, nuclear translocation imaging, Co-IP, and ChIP on the PPARγ2 promoter

    PMID:16580992

    Open questions at the time
    • Signal that triggers nuclear entry mechanistically undefined
    • How the same factor switches between NF-κB repression and Smad coactivation unresolved
  9. 2006 Medium

    Extended HIVEP2 function to the nervous system, linking it to immediate-early gene (c-Fos) regulation and stress behavior.

    Evidence KO mouse behavioral testing, corticosterone measurement, and c-Fos immunohistochemistry

    PMID:16836985

    Open questions at the time
    • Direct transcriptional targets in neurons not identified
    • Link between c-Fos changes and behavior correlative
  10. 2007 High

    Showed bidirectional control of bone remodeling, positioning HIVEP2 as a positive regulator of osteoblastic and osteoclastic transcription programs.

    Evidence KO mouse, bone histomorphometry, in vitro mineralization, and osteocalcin promoter reporter with overexpression

    PMID:17311925

    Open questions at the time
    • Direct versus indirect effects on osteoclast genes not separated
    • Relationship to BMP/Smad cooperation in bone not fully resolved
  11. 2007 High

    Connected NF-κB repression to T-cell survival, showing HIVEP2 controls FasL expression to permit memory T-cell formation.

    Evidence KO mouse, adoptive transfer, apoptosis assays, and p65 NF-κB overexpression epistasis

    PMID:17404274

    Open questions at the time
    • Whether FasL is a direct HIVEP2/NF-κB target gene not shown directly
  12. 2009 High

    Defined a cytoplasmic-to-nuclear signaling role: HIVEP2 chaperones CLIC4 to the nucleus to protect phospho-Smad2/3 and sustain TGF-β signaling.

    Evidence Reciprocal Co-IP, nuclear fractionation, siRNA knockdown, nuclear-targeting rescue, and phospho-Smad protection assays

    PMID:19448624

    Open questions at the time
    • How TGF-β triggers the cytoplasmic CLIC4-HIVEP2 complex unclear
    • Relationship between this TGF-β role and the BMP/Smad1/4 role not integrated
  13. 2011 High

    Resolved the mechanism of positive selection: HIVEP2 dampens TCR-induced Bax activation and the mitochondrial death pathway in thymocytes.

    Evidence KO mouse with genetic epistasis (death-pathway ablation rescue), Bax activation assay, and in vivo/in vitro selection assays

    PMID:21475200

    Open questions at the time
    • Transcriptional targets mediating Bax restraint not identified
    • Link to NF-κB repression in this context not established
  14. 2011 Medium

    Extended HIVEP2 immune function to NK cells, linking its loss to cytotoxic defects, altered STAT/NF-κB signaling, and lymphomagenesis.

    Evidence KO mouse cytotoxicity assays, perforin/granzyme-B immunoblot, and phospho-STAT/flow cytometry

    PMID:21936769

    Open questions at the time
    • Direct transcriptional targets in NK cells undefined
    • Causal chain from signaling changes to lymphoma not established
  15. 2012 High

    Established genome-wide NF-κB repression and uncovered O-GlcNAcylation by OGT as a regulatory switch attenuating that repression.

    Evidence Microarray/GSEA with overexpression and knockdown, NF-κB reporter, Co-IP/mass spectrometry of OGT, and deletion mutagenesis mapping the OGT-binding region

    PMID:22294689

    Open questions at the time
    • Specific O-GlcNAc-modified residues not mapped
    • Whether O-GlcNAcylation alters DNA binding or cofactor recruitment unresolved
  16. 2019 Low

    Linked HIVEP2 to dopaminergic neuron gene regulation through activation of the SLC6A3 (DAT) gene.

    Evidence Immunofluorescence localization and transcriptional targeting of an SLC6A3 intronic sequence

    PMID:31586043

    Open questions at the time
    • Method of demonstrating activation not specified
    • Direct binding versus indirect effect not distinguished
    • Single lab, limited mechanistic dissection
  17. 2022 Medium

    Implicated HIVEP2 in neuropathic pain by showing it promotes excitatory glutamate receptor subunit expression in spinal cord.

    Evidence Spared nerve injury model with lentiviral Shn-2 knockdown, GluN2D/GluR1 immunoblot, and mechanical allodynia testing

    PMID:35218885

    Open questions at the time
    • Direct transcriptional regulation of GluN2D/GluR1 not shown
    • Cell-type specificity in spinal cord undefined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single factor toggles between NF-κB/SKIP-mediated repression and Smad/C/EBPα-mediated activation, and how post-translational modification and partner availability direct this switch across tissues, remains unresolved.
  • No structural model of the DNA-binding or acidic regions
  • Direct genome-wide target maps in neurons and bone lacking
  • Mechanism coordinating cytoplasmic CLIC4 complex versus nuclear repressor pools unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 4 GO:0140110 transcription regulator activity 4 GO:0098772 molecular function regulator activity 2
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 2
Pathway
R-HSA-168256 Immune System 4 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-1266738 Developmental Biology 2 R-HSA-162582 Signal Transduction 2 R-HSA-5357801 Programmed Cell Death 2
Partners
CEBPACLIC4NFKB1OGTRFX1SKIPSMAD1SMAD4

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1991 HIV-EP2 (HIVEP2) protein was identified as a large metal-finger transcription factor (1,833 aa, MW ~211 kDa) that binds to the HIV-1 enhancer with a DNA-binding domain consisting of a metal-finger structure, similar to HIV-EP1. The protein contains a nuclear localization signal followed by a Ser/Thr-rich region, a metal-finger DNA-binding domain, and a cluster of acidic amino acids. Expression of HIV-EP2 mRNA is greatly induced by mitogen and phorbol ester treatment of Jurkat T cells. cDNA cloning, cross-hybridization, protein domain analysis, Northern blotting, DNA-binding characterization The Journal of biological chemistry Medium 2022670
1994 MIBP1 (rat ortholog of HIVEP2/MBP-2) binds sequence-specifically to a 9-bp sequence in rat c-myc intron 1 via its zinc finger regions, demonstrated by expression of a fusion protein in E. coli. The protein has two widely separated zinc finger regions each carrying C2H2 motifs. cDNA cloning, in vitro DNA-binding assay with bacterially expressed fusion protein, Northern blotting Nucleic acids research Medium 7838722
1996 MIBP1 (HIVEP2) and RFX1 associate in vivo to form a complex that binds to the EP element within hepatitis B virus enhancer I. The EP site alone can repress transcription of the SV40 promoter in a position- and orientation-independent manner, suggesting silencer function. Supershift assay with polyclonal antisera, DNA-protein complex analysis, transcriptional reporter assay Journal of virology Medium 8709229
1997 MIBP1 (HIVEP2) and RFX1 can bind simultaneously, most likely as a heterodimer, to the NRE gamma subregion of the hepatitis B virus core promoter negative regulatory element, and this binding is required for the gene-suppressive activity of NRE gamma. DNA binding assay, mutagenesis of NRE gamma, gel mobility shift assay with RFX1 and MIBP1 Virology Medium 9018153
1999 MIBP1 (HIVEP2) interacts specifically with a TC-rich enhancer element in the SSTR-2 promoter and with the SEF-2 initiator-binding protein to enhance transcription from the basal SSTR-2 promoter. MIBP1 mRNA expression overlaps precisely with SSTR-2 expression in the frontal cortex and hippocampus. cDNA library screening, DNA binding assay, transcriptional co-activation assay, in situ hybridization, Northern blotting Molecular and cellular biology Medium 10207097
2000 MIBP1 (HIVEP2) and RFX1 are induced during retinoic acid-mediated granulocytic differentiation of HL60 cells. Both proteins are absent from undifferentiated HL60 cells and their induction is inversely correlated with down-regulation of c-myc levels, supporting a role for MIBP1 in silencing c-myc during differentiation. Immunoblot, gel mobility shift assay, retinoic acid differentiation assay, time-course analysis The Biochemical journal Low 10642512
2001 Shn-2 (HIVEP2) knockout mice exhibit severely defective positive selection of CD4+ and CD8+ T cells in the thymus, establishing that Shn-2 is required for the survival signals initiated by T cell receptor engagement during positive selection. Shn-2 knockout mouse model, flow cytometry of thymocyte populations Nature immunology High 11668343
2002 MIBP1 (HIVEP2) represses c-myc transcription from the major promoter P2. MIBP1 physically interacts with the Ski-interacting protein (SKIP), confirmed by yeast two-hybrid, in vitro pull-down assay, and co-immunoprecipitation. The acidic region of MIBP1 interacts with the N-terminal half of SKIP. MIBP1 is highly expressed in post-mitotic neurons but not in immature neuroepithelium. Transcriptional reporter assay, yeast two-hybrid, in vitro pull-down, co-immunoprecipitation, in situ hybridization Journal of biochemistry High 11872163
2005 Shn-2 (HIVEP2)-deficient mice show dramatically enhanced differentiation of naive T cells into Th2 cells with constitutive activation of NF-κB and enhanced GATA3 induction. Shn-2 competes with p50 NF-κB for binding to a consensus NF-κB motif and inhibits NF-κB-driven promoter activity, establishing Shn-2 as a negative regulator of Th2 differentiation via NF-κB repression. Shn-2 KO mouse, in vitro Th1/Th2 differentiation assay, NF-κB binding competition assay, promoter reporter assay, flow cytometry The Journal of experimental medicine High 15699073
2006 Shn-2 (HIVEP2) KO mice have reduced white adipose tissue and Shn-2-deficient mouse embryonic fibroblasts cannot efficiently differentiate into adipocytes. Shn-2 enters the nucleus upon BMP-2 stimulation and, in cooperation with Smad1/4 and C/EBPalpha, induces PPARgamma2 expression. Shn-2 directly interacts with both Smad1/4 and C/EBPalpha on the PPARgamma2 promoter. Shn-2 KO mouse, MEF differentiation assay, nuclear translocation imaging, co-immunoprecipitation, chromatin immunoprecipitation, reporter assay Developmental cell High 16580992
2006 Shn-2 (HIVEP2) KO mice exhibit hypersensitivity to stress, increased anxiety-like behavior, hyperactivity, and elevated stress-induced corticosterone levels. Basal and stress-induced c-Fos expression are decreased in Shn-2 KO mice, indicating a role for Shn-2 in regulating neuronal immediate-early gene expression and stress responses. Shn-2 KO mouse, behavioral testing, corticosterone measurement, immunohistochemistry for c-Fos Brain research Medium 16836985
2007 Shn-2 (HIVEP2) deficiency suppresses osteoblastic bone formation (reduced osterix, osteocalcin, mineralization) and osteoclastic bone resorption (reduced Nfatc1, c-fos, TRAP-positive cells). Shn-2 overexpression enhances osteocalcin promoter activity and BMP-dependent osteoblastic differentiation, placing Shn-2 as a positive regulator of transcription factors required for bone remodeling. Shn-2 KO mouse, bone histomorphometry, in vitro mineralization assay, promoter reporter assay, bone marrow cell culture The Journal of biological chemistry High 17311925
2007 Shn-2 (HIVEP2)-deficient effector Th1/Th2 cells have increased susceptibility to apoptosis associated with increased FasL expression, leading to failure in memory T cell generation. Shn-2 repression of NF-κB controls FasL expression and is required for cell survival during memory T cell formation. Shn-2 KO mouse, adoptive transfer, BrdU incorporation, apoptosis assay, CD69/FasL measurement, p65 NF-κB overexpression experiment Journal of immunology High 17404274
2009 CLIC4 interacts with Schnurri-2 (HIVEP2) in the cytoplasm upon TGF-beta stimulation, and they co-translocate to the nucleus. In the nucleus, CLIC4 associates with phospho-Smad2 and phospho-Smad3, protecting them from dephosphorylation by nuclear phosphatases. In the absence of Schnurri-2, TGF-beta signaling is abrogated; direct nuclear targeting of CLIC4 rescues signaling and removes the requirement for Schnurri-2. Co-immunoprecipitation, nuclear fractionation, TGF-beta signaling assays, siRNA knockdown, nuclear targeting constructs, phospho-Smad immunoblot Nature cell biology High 19448624
2011 Shn-2 (HIVEP2) functions downstream of TCR proximal signaling to dampen Bax activation and the mitochondrial death pathway in double-positive thymocytes. Shn-2-deficient DP thymocytes inappropriately undergo negative selection in response to positive-selecting signals. Shn-2 levels increase after TCR stimulation. Genetic ablation of TCR-induced death rescues positive selection in Shn-2-deficient mice. Shn-2 KO mouse, genetic epistasis (death pathway ablation cross), Bax activation assay, in vitro TCR stimulation, in vivo selection assays, flow cytometry Nature High 21475200
2011 Shn-2 (HIVEP2) deficiency in NK cells leads to decreased perforin and granzyme-B expression, reduced STAT5 phosphorylation, enhanced STAT3 phosphorylation and NF-κB p65 expression, and decreased surface activation markers (CD27, CD69, CD122), resulting in impaired NK cell cytotoxicity and spontaneous CD3-positive lymphoma development. Shn-2 KO mouse, cytotoxicity assay, immunoblot for perforin/granzyme-B, phospho-STAT analysis, flow cytometry Leukemia & lymphoma Medium 21936769
2012 MIBP1 (HIVEP2) globally represses NF-κB target gene expression. MIBP1 binds to the NF-κB binding site and represses NF-κB-responsive promoter activity in reporter assays. Knockdown of endogenous MIBP1 upregulates NF-κB pathway genes. O-GlcNAc transferase (OGT) is a prominent MIBP1 binding partner identified by co-immunoprecipitation and mass spectrometry; a 154-amino acid region of MIBP1 is required for OGT binding and O-GlcNAcylation of MIBP1. O-GlcNAcylation attenuates MIBP1-mediated NF-κB repression. Microarray with GSEA, MIBP1 overexpression and knockdown, NF-κB reporter assay, Co-IP with mass spectrometry, deletion mutagenesis, luciferase assay The Journal of biological chemistry High 22294689
2019 HIVEP2 is expressed in both the cytoplasm and nuclei of dopaminergic neurons and can target the intronic sequence GTGGCTTTCT of SLC6A3 (DAT), thereby activating the SLC6A3 gene. Immunofluorescence localization, chromatin binding/transcriptional activation assay for SLC6A3 intronic target Translational psychiatry Low 31586043
2022 Shn-2 (HIVEP2) is upregulated in the L4-L6 spinal cord segments following spared nerve injury. Knockdown of Shn-2 using lentivirus decreases GluN2D subunit and GluR1 levels in the spinal cord and alleviates mechanical allodynia, indicating Shn-2 promotes expression of excitatory glutamate receptor subunits and contributes to neuropathic pain. Spared nerve injury mouse model, lentiviral knockdown of Shn-2, immunoblot for GluN2D and GluR1, mechanical allodynia testing Neuroscience Medium 35218885

Source papers

Stage 0 corpus · 40 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Schnurri-2 controls BMP-dependent adipogenesis via interaction with Smad proteins. Developmental cell 147 16580992
2013 Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 143 23389689
2009 TGF-beta signalling is regulated by Schnurri-2-dependent nuclear translocation of CLIC4 and consequent stabilization of phospho-Smad2 and 3. Nature cell biology 88 19448624
2001 Murine Schnurri-2 is required for positive selection of thymocytes. Nature immunology 63 11668343
1991 HIV-EP2, a new member of the gene family encoding the human immunodeficiency virus type 1 enhancer-binding protein. Comparison with HIV-EP1/PRDII-BF1/MBP-1. The Journal of biological chemistry 55 2022670
2005 Regulation of T helper type 2 cell differentiation by murine Schnurri-2. The Journal of experimental medicine 45 15699073
2015 Loss-of-function variants in HIVEP2 are a cause of intellectual disability. European journal of human genetics : EJHG 40 26153216
1999 Activation of somatostatin receptor II expression by transcription factors MIBP1 and SEF-2 in the murine brain. Molecular and cellular biology 39 10207097
2016 Mutations in HIVEP2 are associated with developmental delay, intellectual disability, and dysmorphic features. Neurogenetics 37 27003583
2011 Dampening of death pathways by schnurri-2 is essential for T-cell development. Nature 34 21475200
2001 Structure of the human zinc finger protein HIVEP3: molecular cloning, expression, exon-intron structure, and comparison with paralogous genes HIVEP1 and HIVEP2. Genomics 30 11161801
2019 HIV-1 infection increases microRNAs that inhibit Dicer1, HRB and HIV-EP2, thereby reducing viral replication. PloS one 28 30682089
2007 Lack of Schnurri-2 expression associates with reduced bone remodeling and osteopenia. The Journal of biological chemistry 28 17311925
1994 Cloning and characterization of a c-myc intron binding protein (MIBP1). Nucleic acids research 25 7838722
2006 Schnurri-2 mutant mice are hypersensitive to stress and hyperactive. Brain research 24 16836985
2002 Characterization of the biological functions of a transcription factor, c-myc intron binding protein 1 (MIBP1). Journal of biochemistry 22 11872163
2000 Induction of Myc-intron-binding polypeptides MIBP1 and RFX1 during retinoic acid-mediated differentiation of haemopoietic cells. The Biochemical journal 22 10642512
2007 Schnurri-2 controls memory Th1 and Th2 cell numbers in vivo. Journal of immunology (Baltimore, Md. : 1950) 21 17404274
1997 Interaction of transcription factors RFX1 and MIBP1 with the gamma motif of the negative regulatory element of the hepatitis B virus core promoter. Virology 21 9018153
2017 Immature morphological properties in subcellular-scale structures in the dentate gyrus of Schnurri-2 knockout mice: a model for schizophrenia and intellectual disability. Molecular brain 20 29233179
2010 CLIC4 and Schnurri-2: a dynamic duo in TGF-beta signaling with broader implications in cellular homeostasis and disease. Nucleus (Austin, Tex.) 19 20617112
2010 Uncoupling of growth plate maturation and bone formation in mice lacking both Schnurri-2 and Schnurri-3. Proceedings of the National Academy of Sciences of the United States of America 18 20404140
1996 Interactions of the transcription factors MIBP1 and RFX1 with the EP element of the hepatitis B virus enhancer. Journal of virology 16 8709229
2012 Genome-wide repression of NF-κB target genes by transcription factor MIBP1 and its modulation by O-linked β-N-acetylglucosamine (O-GlcNAc) transferase. The Journal of biological chemistry 15 22294689
2010 Memory Th1/Th2 cell generation controlled by Schnurri-2. Advances in experimental medicine and biology 13 20795536
2007 Schnurri-2 regulates Th2-dependent airway inflammation and airway hyperresponsiveness. International immunology 10 17493960
2019 Identification of HIVEP2 as a dopaminergic transcription factor related to substance use disorders in rats and humans. Translational psychiatry 9 31586043
2019 Novel HIVEP2 Variants in Patients with Intellectual Disability. Molecular syndromology 9 31602191
2005 Frequent down-regulation of HIVEP2 in human breast cancer. Breast cancer research and treatment 9 15868437
2015 Combined behavioral studies and in vivo imaging of inflammatory response and expression of mGlu5 receptors in schnurri-2 knockout mice. Neuroscience letters 8 26483320
2019 Expanding the phenotype of intellectual disability caused by HIVEP2 variants. American journal of medical genetics. Part A 6 31207095
1992 Mapping of the human gene for the human immunodeficiency virus type 1 enhancer binding protein HIV-EP2 to chromosome 6q23-q24. Genomics 6 1733857
2019 Novel HIVEP2 Variant p.Q1248* is Associated with Developmental Delay: A Case Report. Journal of pediatric genetics 4 31406623
2011 Murine Schnurri-2 controls natural killer cell function and lymphoma development. Leukemia & lymphoma 4 21936769
2013 Identification and characterization of human MIBP1 gene in glioma cell differentiation. Journal of molecular neuroscience : MN 3 24158731
2011 Schnurri-2 deficiency counteracts against bone loss induced by ovariectomy. Journal of cellular physiology 3 21069746
2022 Schnurri-2 Promotes the Expression of Excitatory Glutamate Receptors and Contributes to Neuropathic Pain. Neuroscience 2 35218885
2026 Single-gene knockout of RNLS or HIVEP2 are insufficient to protect β-cell spheroids from allo- and xeno-rejection. Frontiers in immunology 0 41710881
2026 Dynamic changes in the corpus callosum in a case of HIVEP2-related disorder: a case report and literature review. BMC pediatrics 0 41808101
2023 Parental gonadossomatic mosaicism in HIVEP2-related intellectual disability and impact on genetic counseling-case report. Frontiers in genetics 0 37441550

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