Affinage

ARHGEF28

Rho guanine nucleotide exchange factor 28 · UniProt Q8N1W1

Length
1705 aa
Mass
191.9 kDa
Annotated
2026-06-09
31 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ARHGEF28 (RGNEF/p190RhoGEF) is a bifunctional 190 kDa protein that couples RhoA-specific guanine nucleotide exchange to RNA binding, integrating cytoskeletal signaling at focal adhesions with post-transcriptional control in neurons (PMID:11058585, PMID:11435431). Its tandem DH/PH module catalyzes RhoA-specific GDP release in vitro while sparing Rac1 and Cdc42, and the full-length protein is autoinhibited until binding partners unmask activity (PMID:11058585); crystallography shows that activated RhoA·GTP and Rac1·GTP dock onto the same hydrophobic surface of its PH domain to recruit the enzyme to substrate RhoA·GDP, generating both positive feedback and Rac→Rho cross-talk (PMID:29196061). Downstream of integrins and GPCRs, ARHGEF28 forms a scaffold with FAK through its C-terminal coiled-coil binding the FAK FAT domain (PMID:12702722, PMID:21224360), and genetic knockout establishes it as essential for RhoA activation, focal adhesion formation, and migration after fibronectin stimulation (PMID:22649559); this scaffolding role promotes FAK-Y397 autophosphorylation and peripheral adhesion assembly in a PH-domain-dependent but GEF-activity-independent manner, whereas its GEF activity separately drives paxillin-Y118 phosphorylation (PMID:24006257). It is an effector of Gα13 downstream of gastrin/CCK2 receptor signaling (PMID:25922072) and supports NF-κB-dependent transcriptional programs in tumor and bone contexts (PMID:31308489, PMID:41571890). As an RNA-binding protein, its C-terminal domain binds the destabilizing element of NF-L mRNA to extend its half-life, a site also engaged by BC1 RNA (PMID:11435431, PMID:12215442). The protein additionally engages TDP-43 RNA-recognition motifs through an N-terminal IPT/TIG-containing fragment, and ARHGEF28 and TDP-43 act antagonistically to regulate splicing of long introns in axon-guidance genes (PMID:38739752, PMID:39360635).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 2000 High

    Established the catalytic identity and substrate specificity of the protein, defining it as a RhoA-selective GEF and revealing an autoinhibited full-length state.

    Evidence In vitro GDP-release and protein-binding assays with domain dissection plus microtubule binding in vitro and in vivo

    PMID:11058585

    Open questions at the time
    • Identity of the partner(s) that relieve autoinhibition in vivo not defined
    • Functional role of microtubule binding not characterized
  2. 2001 High

    Identified the protein as a sequence-specific RNA-binding factor, linking it to neurofilament mRNA stability and revealing a function distinct from its GEF activity.

    Evidence GST-pulldown, Northwestern, gel-shift, RNA cross-linkage, and mRNA half-life measurement in stable neuronal transfectants

    PMID:11435431

    Open questions at the time
    • Mechanism by which binding stabilizes NF-L mRNA unknown
    • Connection between RNA-binding and GEF functions unresolved
  3. 2001 High

    Mapped phosphorylation-independent 14-3-3 binding and showed it regulates the protein's cytoplasmic aggregation, hinting at scaffold/localization control.

    Evidence Yeast two-hybrid, co-IP, co-localization, and deletion mutagenesis mapping the I1370QAIQNL site

    PMID:11533041

    Open questions at the time
    • Functional consequence of 14-3-3 binding for GEF or RNA activity not established
  4. 2002 Medium

    Showed the noncoding BC1 RNA competes for the same C-terminal RNA-binding site as NF-L, implying regulatory competition among RNA ligands.

    Evidence GST-fusion affinity chromatography and cross-competition gel-shift assays

    PMID:12215442

    Open questions at the time
    • In vitro only; cellular relevance of competition not demonstrated
    • Single lab
  5. 2003 High

    Defined the direct FAK–ARHGEF28 interaction and placed the protein downstream of integrin and growth-factor receptor signaling driving RhoA activation.

    Evidence Reciprocal co-IP, yeast two-hybrid with FAT domain mutagenesis, and RhoA GTP-loading assay in neuronal cells/brain extract

    PMID:12702722

    Open questions at the time
    • Whether interaction governs GEF activity directly not shown
    • Tyrosine phosphorylation sites on the GEF not mapped
  6. 2003 Medium

    Localized anti-apoptotic activity to cytoplasmic retention sequences overlapping JIP-1/14-3-3 sites, linking subcellular retention to survival function.

    Evidence EGFP-tagged deletion constructs with apoptosis and microscopy readouts in Neuro 2a cells

    PMID:14499478

    Open questions at the time
    • No in vitro reconstitution
    • Mechanism of anti-apoptotic effect undefined
    • Single lab
  7. 2003 Medium

    Connected the protein to immune-receptor signaling, showing CD40-induced expression drives RhoA-dependent NF-κB activation in B cells.

    Evidence 2D-gel identification, overexpression with dominant-negative RhoA and GEF constructs, NF-κB reporter assay

    PMID:12496377

    Open questions at the time
    • Direct biochemical link from GEF to NF-κB not shown
    • Single lab
  8. 2008 Medium

    Revealed density-dependent competition between ARHGEF28 and E-cadherin for delta-catenin, modulating RhoA activity with cell contact.

    Evidence Co-IP, immunofluorescence, RhoA activity assay, and ectopic E-cadherin expression in MEFs

    PMID:18930028

    Open questions at the time
    • Direct vs indirect delta-catenin binding not fully resolved
    • Single lab
  9. 2010 Medium

    Extended the RNA-binding function to human RGNEF and tied NFL mRNA interaction to ALS pathology.

    Evidence In vitro gel-shift and IP-RT-PCR in ALS patient vs control tissue lysates

    PMID:19488899

    Open questions at the time
    • Disease-specific interaction correlative, not causal
    • Single lab
  10. 2011 High

    Demonstrated the Rgnef–FAK complex is required for FAK adhesion targeting, paxillin phosphorylation, invasion, and tumor growth, establishing oncogenic relevance.

    Evidence shRNA knockdown, dominant-negative C-terminal competition with binding-site deletion, phosphorylation assays, orthotopic tumor implantation

    PMID:21224360

    Open questions at the time
    • Did not separate GEF-dependent from scaffold-dependent contributions
  11. 2012 High

    Genetic knockout established the protein as essential for integrin-stimulated RhoA activation, focal adhesion formation, and migration.

    Evidence Conditional Rgnef knockout MEFs with haptotaxis, wound closure, focal adhesion quantification, RhoA assay, and rescue by re-expression

    PMID:22649559

    Open questions at the time
    • Did not dissect which molecular function (GEF vs scaffold) drives each phenotype
  12. 2013 High

    Separated the scaffold and catalytic functions, showing PH-dependent GEF-independent FAK-Y397 activation versus GEF-dependent paxillin-Y118 phosphorylation.

    Evidence Rgnef-null MEFs with PH-domain and GEF-inactive mutant rescue, immunofluorescence, phosphotyrosine immunoblotting

    PMID:24006257

    Open questions at the time
    • How the PH domain promotes FAK activation mechanistically not resolved
  13. 2015 High

    Identified the protein as a selective Gα13 effector downstream of gastrin/CCK2 receptor, linking GPCR signaling to FAK/paxillin phosphorylation.

    Evidence Reciprocal co-IP with constitutively active Gα mutants, point mutagenesis, SRE-luciferase reporter, shRNA epistasis, RhoA assay

    PMID:25922072

    Open questions at the time
    • Structural basis of Gα13 selectivity not defined
  14. 2017 High

    Provided structural mechanism for GEF recruitment, showing both RhoA·GTP and Rac1·GTP bind the PH domain to localize the enzyme, enabling feedback and cross-talk.

    Evidence X-ray crystallography of PH-domain complexes plus in vitro nucleotide exchange assays

    PMID:29196061

    Open questions at the time
    • Cellular validation of Rac→Rho cross-talk through this surface not shown
  15. 2017 Medium

    Linked the protein to stress survival and injury responses in neurons and to Staufen1 RNA granules rather than canonical stress granules.

    Evidence In vivo sciatic nerve injury model, stress survival assays with deletion constructs, immunofluorescence co-localization

    PMID:28495450

    Open questions at the time
    • Mechanism of N-terminal protective effect undefined
    • Single lab
  16. 2018 Medium

    Defined an NLS/NES within the PH domain controlling nucleocytoplasmic shuttling via exportin-1, providing a basis for nuclear functions.

    Evidence NLS/NES mutagenesis, fusion-protein microscopy, Leptomycin B inhibition

    PMID:30482479

    Open questions at the time
    • Nuclear function of the shuttling not established
    • Single lab
  17. 2019 Medium

    Showed the protein is required for ovarian tumor growth by sustaining an NF-κB-driven antioxidant gene program.

    Evidence Rgnef knockout mouse models, spheroid assays, RNA-seq, antioxidant rescue, NF-κB pathway analysis

    PMID:31308489

    Open questions at the time
    • Direct link from GEF activity to NF-κB antioxidant signature not biochemically defined
    • Single lab
  18. 2024 High

    Established a direct ARHGEF28–TDP-43 interaction whose N-terminal fragment is neuroprotective in two ALS models, defining a therapeutic mechanism.

    Evidence Direct protein interaction with IPT/TIG domain mapping, Drosophila genetic epistasis, AAV9/NF242 delivery in rNLS8 mice

    PMID:38739752

    Open questions at the time
    • Whether endogenous full-length protein performs this function not addressed
  19. 2024 Medium

    Revealed that ARHGEF28 and TDP-43 antagonistically regulate long-intron splicing of axon-guidance genes, defining a shared post-transcriptional mechanism.

    Evidence Comparative RNA-seq of TDP-43- and RGNEF-depleted neuronal cells with long-intron processivity analysis

    PMID:39360635

    Open questions at the time
    • Direct splicing-factor activity vs indirect effect not distinguished
    • Single lab
  20. 2026 Medium

    Demonstrated an in vivo role in bone remodeling, with Rgnef driving osteoclastogenesis via RhoA/Rac1 and NF-κB/MAPK/AKT signaling.

    Evidence Rgnef-deficient and transgenic mice, differentiation assays, GTPase activity assays, in vivo bone loss models

    PMID:41571890

    Open questions at the time
    • Direct effectors linking GTPase activation to bone-cell transcription not defined
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the dual GEF and RNA-binding/splicing activities are coordinated within a single protein, and what governs the switch between cytoskeletal and post-transcriptional roles, remains unresolved.
  • No unified model linking GEF, scaffold, and RNA-regulatory functions
  • Endogenous regulation of nucleocytoplasmic shuttling and its functional output undefined
  • Whether RNA binding and exchange activity are mutually exclusive not tested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 4 GO:0060090 molecular adaptor activity 3 GO:0008092 cytoskeletal protein binding 1 GO:0098772 molecular function regulator activity 1
Localization
GO:0005829 cytosol 3 GO:0005634 nucleus 1 GO:0005856 cytoskeleton 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-1474244 Extracellular matrix organization 2 R-HSA-8953854 Metabolism of RNA 2
Partners
CTNND2GNA13PTK2/FAKRAC1RHOATARDBPYWHAEYWHAH
Complex memberships
Rgnef-FAK scaffold complex

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 The isolated tandem DH/PH domain of p190RhoGEF activates RhoA in vitro (GDP release and protein binding assays), but not Rac1 or Cdc42, establishing RhoA-specific GEF activity. Full-length p190RhoGEF fails to activate RhoA in vitro, suggesting autoinhibition requiring unknown binding partners to unmask exchange activity in vivo. p190RhoGEF directly interacts with microtubules via its C-terminal region adjacent to the DH/PH domain, shown by in vitro and in vivo binding experiments. In vitro GDP release assay, protein binding assay, immunofluorescence, in vitro and in vivo microtubule binding experiments The Journal of biological chemistry High 11058585
2003 FAK directly interacts with p190RhoGEF in neuronal cells and brain tissue extracts. The FAK C-terminal focal adhesion targeting (FAT) domain binds the C-terminal coiled-coil domain of p190RhoGEF, identified by two-hybrid assay and deletion mutagenesis. A FAK FAT domain mutation (Leu-1034 to Ser) disrupts this interaction. FAK activity promotes p190RhoGEF tyrosine phosphorylation and RhoA GTP loading downstream of laminin/integrin and IGF-1 receptor stimulation. Co-immunoprecipitation, co-localization, yeast two-hybrid, deletion mutagenesis, dominant-negative inhibition (FRNK), RhoA GTP-loading assay The Journal of biological chemistry High 12702722
2001 14-3-3η and 14-3-3ε are binding partners of p190RhoGEF, identified by yeast two-hybrid screen and confirmed biochemically by co-immunoprecipitation and co-localization. A phosphorylation-independent binding site (I1370QAIQNL) in p190RhoGEF was mapped; deletion of this site abolishes 14-3-3η interaction in vitro and prevents 14-3-3η-mediated alteration of p190RhoGEF cytoplasmic aggregation in cells. Yeast two-hybrid, co-immunoprecipitation, co-localization with fluorescent fusion proteins, deletion mutagenesis The Journal of biological chemistry High 11533041
2001 p190RhoGEF binds directly and specifically to the 68-nucleotide destabilizing element in the 3' UTR of NF-L (neurofilament light) mRNA via its C-terminal domain (clone 39), demonstrated by Northwestern blot, gel-shift, and cross-linkage assays. Expression of p190RhoGEF in stably transfected neuronal cells increased the half-life of wild-type NF-L mRNA but not of a mutant lacking the destabilizing element, establishing a functional role in NF-L mRNA stability. GST-fusion pulldown, Northwestern blot, gel-shift assay, RNA cross-linkage, stable transfection with mRNA half-life measurement The Journal of biological chemistry High 11435431
2002 BC1 RNA (a neuronally expressed non-coding RNA) binds to the same C-terminal site of p190RhoGEF as NF-L mRNA and competes with NF-L mRNA for p190RhoGEF binding, identified by affinity chromatography and cross-competition experiments using a GST-p190RhoGEF C-terminal fusion protein. GST-fusion affinity chromatography, gel-shift, cross-competition binding assay The Journal of biological chemistry Medium 12215442
2003 Anti-apoptotic activity of p190RhoGEF is localized to two cytoplasmic retention sequences (CRS-1 and CRS-2) in its C-terminal region that overlap with the JIP-1 and 14-3-3 binding sites. Deleting both CRS sequences abolishes cytoplasmic retention and anti-apoptotic activity of EGFP-tagged p190RhoGEF in Neuro 2a cells; restoring either CRS-1 or CRS-2 rescues both properties. Transfection of EGFP-tagged deletion constructs, apoptosis assay, fluorescence microscopy in Neuro 2a cells Brain research. Molecular brain research Medium 14499478
2003 p190RhoGEF expression is induced by CD40 stimulation in WEHI 231 B cells. Overexpression of p190RhoGEF mimics CD40-stimulated cellular structure changes and NF-κB activation through RhoA; these effects are blocked by dominant-negative RhoA (T19N) or dominant-negative p190RhoGEF (Y1003A). 2D gel electrophoresis identification, overexpression with dominant-negative constructs, NF-κB reporter assay Journal of immunology Medium 12496377
2008 delta-Catenin interacts with p190RhoGEF in the cytoplasm at low cell density, reducing RhoA activity. At high cell density, E-cadherin outcompetes p190RhoGEF for delta-catenin binding, shifting delta-catenin to the plasma membrane and restoring RhoA activity. Ectopic E-cadherin expression in mouse embryonic fibroblasts decreased delta-catenin's effect on RhoA activity reduction. Co-immunoprecipitation, immunofluorescence, RhoA activity assay, ectopic E-cadherin expression Biochemical and biophysical research communications Medium 18930028
2010 Human RGNEF (the human homologue of p190RhoGEF) directly interacts with human NFL mRNA in vitro by gel-shift assay. In tissue lysates, RGNEF-NFL mRNA interaction was detected by IP-RT-PCR only in ALS patient samples, not in neuropathologically normal controls. Gel-shift assay (in vitro), IP-RT-PCR (in tissue lysates) Amyotrophic lateral sclerosis Medium 19488899
2011 Rgnef forms a complex with FAK in human colon carcinoma cells. Upon gastrin stimulation, Rgnef-FAK interaction is required for FAK translocation to focal adhesions, paxillin tyrosine phosphorylation, cell motility, and invadopodia formation. Overexpression of the Rgnef C-terminal region (aa 1279–1582) disrupts endogenous Rgnef-FAK interaction and blocks these events; a version lacking the FAK binding site (aa 1302–1582) does not. Rgnef-C-expressing cells form smaller, less invasive tumors in vivo. shRNA knockdown, co-immunoprecipitation, dominant-negative C-terminal fragment competition, phosphorylation assays, orthotopic tumor implantation Cancer research High 21224360
2012 Genetic knockout of Rgnef in mouse embryo fibroblasts (Rgnef-/- MEFs) significantly inhibits haptotaxis migration, wound closure motility, focal adhesion number, and RhoA GTPase activation after fibronectin-integrin stimulation. These phenotypes are rescued by epitope-tagged Rgnef re-expression, establishing Rgnef as essential for RhoA regulation downstream of integrins. Conditional knockout (floxed Rgnef × CMV-Cre), primary MEF isolation, haptotaxis assay, wound closure assay, focal adhesion quantification, RhoA GTP-loading assay, rescue by re-expression PloS one High 22649559
2013 Rgnef plays a non-canonical, upstream scaffolding role in promoting FAK localization to peripheral adhesions and FAK-Y397 activation upon fibronectin binding, independent of its GEF catalytic activity. A PH domain mutation in Rgnef blocks adhesion formation, FAK localization, and FAK/paxillin phosphorylation without disrupting the Rgnef-FAK interaction. A GEF-inactive Rgnef mutant rescues FAK-Y397 phosphorylation and adhesion localization but not paxillin-Y118 phosphorylation, indicating paxillin-pY118 requires Rgnef GEF activity through a distinct mechanism. Rgnef-null MEFs, site-directed mutagenesis (PH domain and GEF-inactive mutants), immunofluorescence, phosphotyrosine immunoblotting, rescue experiments Journal of cell science High 24006257
2015 Rgnef is a new effector for Gα13 downstream of gastrin and the CCK2 receptor in DLD-1 colon carcinoma cells. Rgnef co-immunoprecipitates with activated Gα13Q226L but not Gα12Q229L; the Rgnef C-terminal region (aa 1279–1582) is sufficient for this interaction and its exogenous expression blocks Gα13-stimulated SRE activity. Point mutations in the Rgnef C-terminal region disrupt Gα13 association but not Gαq association. Gα13 depletion reduces gastrin-induced FAK-pY397 and paxillin-pY31. Co-immunoprecipitation, shRNA depletion of Gα13, SRE-luciferase reporter assay, point mutagenesis of Rgnef C-terminus, RhoA GTP-binding assay The Journal of biological chemistry High 25922072
2017 Crystal structures reveal that activated Rac1·GTP and RhoA·GTP use their effector-binding surfaces to associate with the same hydrophobic surface on the p190RhoGEF PH domain. Both activated RhoA and Rac1 stimulate nucleotide exchange on RhoA·GDP by p190RhoGEF in vitro, localizing it to its substrate. This demonstrates a positive feedback (activated RhoA) and a cross-talk mechanism (activated Rac1 directly stimulates RhoA activation through p190RhoGEF). X-ray crystallography, in vitro nucleotide exchange assay Journal of structural biology High 29196061
2017 RGNEF expression is upregulated in murine spinal motor neurons following distal sciatic nerve injury. Under cellular stress (sodium arsenite or sorbitol), RGNEF expression confers a survival benefit in HEK293T cells; the NH2-terminus domain is essential for this protective effect. Under stress, RGNEF associates with Staufen1-positive granules but not TIA-1-positive stress granules. In vivo nerve injury model, in vitro stress assay with deletion constructs, immunofluorescence co-localization Molecular and cellular neurosciences Medium 28495450
2018 A 23-amino acid bipartite nuclear localization signal (NLS) within the Pleckstrin Homology (PH) domain of RGNEF controls its nuclear localization; deletion or mutation of this region abolishes nuclear localization. Within this NLS, an overlapping nuclear export signal (NES) promotes nuclear export in an exportin-1-dependent manner (confirmed by Leptomycin B treatment). The PH domain alone is sufficient to translocate a 160 kDa fusion protein to the nucleus. Deletion and point mutagenesis of NLS/NES, fluorescence microscopy of fusion proteins, Leptomycin B inhibition European journal of cell biology Medium 30482479
2019 Rgnef is essential for ovarian tumor spheroid formation in vitro and tumor growth in vivo using transgenic and transplantable Rgnef knockout mouse models. Rgnef supports an NF-κB-mediated antioxidant gene signature (including Gpx4, Nqo1, Gsta4); antioxidant treatment rescues growth of Rgnef-knockout spheroids, and Rgnef re-expression facilitates NF-κB-dependent tumorsphere survival. Rgnef knockout mouse model, spheroid formation assay, RNA-sequencing, antioxidant rescue experiment, NF-κB reporter/pathway analysis Oncogene Medium 31308489
2024 An N-terminal fragment of RGNEF (NF242) directly interacts with the RNA recognition motifs (RRMs) of TDP-43, competing with RNA binding. The IPT/TIG domain of NF242 is essential for this interaction. In a Drosophila ALS model overexpressing TDP-43, genetic expression of NF242 suppressed neuropathological phenotypes (increased lifespan, abolished motor defects, prevented neurodegeneration). Intracerebroventricular injection of AAV9/NF242 in a murine TDP-43 model (rNLS8) improved lifespan and motor phenotype and decreased neuroinflammation markers. Direct protein-protein interaction assay, domain deletion (IPT/TIG), Drosophila genetic epistasis model, murine AAV9 intracerebroventricular injection Brain : a journal of neurology High 38739752
2024 RGNEF and TDP-43 act predominantly in an antagonistic manner to regulate expression of axon guidance genes in neuronal cells. Mechanistically, both factors affect the processivity of long intron removal (splicing), explaining their mode of transcriptomic action upon depletion. Comparative transcriptomics (RNA-seq) of TDP-43- and RGNEF-depleted neuronal cells, long intron processivity analysis FASEB journal Medium 39360635
2026 Rgnef promotes osteoclastogenesis and attenuates osteoblastogenesis through activation of RhoA and Rac1, leading to enhanced NF-κB, MAPK, and AKT signaling. Rgnef-deficient mice show increased bone mass due to reduced osteolysis and increased osteogenesis, while Rgnef-overexpressing mice show the opposite. Rgnef-deficient mice are protected from bone loss in LPS-induced inflammation and ovariectomy models. Rgnef-deficient and transgenic overexpressing mice, osteoclast/osteoblast differentiation assays, RhoA/Rac1 activity assay, NF-κB/MAPK/AKT pathway analysis, in vivo bone loss models Experimental & molecular medicine Medium 41571890

Source papers

Stage 0 corpus · 31 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 Direct interaction of focal adhesion kinase with p190RhoGEF. The Journal of biological chemistry 156 12702722
2000 Characterization of p190RhoGEF, a RhoA-specific guanine nucleotide exchange factor that interacts with microtubules. The Journal of biological chemistry 138 11058585
2001 Identification of a novel interaction of 14-3-3 with p190RhoGEF. The Journal of biological chemistry 76 11533041
2011 p190RhoGEF (Rgnef) promotes colon carcinoma tumor progression via interaction with focal adhesion kinase. Cancer research 51 21224360
2001 p190RhoGEF Binds to a destabilizing element in the 3' untranslated region of light neurofilament subunit mRNA and alters the stability of the transcript. The Journal of biological chemistry 46 11435431
2013 Detection of a novel frameshift mutation and regions with homozygosis within ARHGEF28 gene in familial amyotrophic lateral sclerosis. Amyotrophic lateral sclerosis & frontotemporal degeneration 33 23286752
2019 Rgnef promotes ovarian tumor progression and confers protection from oxidative stress. Oncogene 30 31308489
2012 Rgnef (p190RhoGEF) knockout inhibits RhoA activity, focal adhesion establishment, and cell motility downstream of integrins. PloS one 29 22649559
2013 A non-canonical role for Rgnef in promoting integrin-stimulated focal adhesion kinase activation. Journal of cell science 26 24006257
2010 Human low molecular weight neurofilament (NFL) mRNA interacts with a predicted p190RhoGEF homologue (RGNEF) in humans. Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases 25 19488899
2014 RhoGEFs in cell motility: novel links between Rgnef and focal adhesion kinase. Current molecular medicine 22 24467206
2008 E-Cadherin negatively modulates delta-catenin-induced morphological changes and RhoA activity reduction by competing with p190RhoGEF for delta-catenin. Biochemical and biophysical research communications 21 18930028
2015 Gastrin-stimulated Gα13 Activation of Rgnef Protein (ArhGEF28) in DLD-1 Colon Carcinoma Cells. The Journal of biological chemistry 19 25922072
2014 ARHGEF28 gene exon 6/intron 6 junction mutations in Chinese amyotrophic lateral sclerosis cohort. Amyotrophic lateral sclerosis & frontotemporal degeneration 19 24712971
2003 Cutting edge: induced expression of a RhoA-specific guanine nucleotide exchange factor, p190RhoGEF, following CD40 stimulation and WEHI 231 B cell activation. Journal of immunology (Baltimore, Md. : 1950) 18 12496377
2002 Binding of p190RhoGEF to a destabilizing element on the light neurofilament mRNA is competed by BC1 RNA. The Journal of biological chemistry 16 12215442
2019 Rare, low-frequency and common coding variants of ARHGEF28 gene and their association with sporadic amyotrophic lateral sclerosis. Neurobiology of aging 12 31060816
2017 Direct regulation of p190RhoGEF by activated Rho and Rac GTPases. Journal of structural biology 12 29196061
2024 Mitigation of TDP-43 toxic phenotype by an RGNEF fragment in amyotrophic lateral sclerosis models. Brain : a journal of neurology 11 38739752
2017 Rho guanine nucleotide exchange factor (RGNEF) is a prosurvival factor under stress conditions. Molecular and cellular neurosciences 11 28495450
2012 Increased p190RhoGEF expression in activated B cells correlates with the induction of the plasma cell differentiation. Experimental & molecular medicine 9 22113105
2012 Over-expression of a RhoA-specific guanine nucleotide exchange factor, p190RhoGEF, in mouse dendritic cells negatively regulates cellular responses to bacterial lipopolysaccharide. Molecules and cells 9 22814846
2003 Cytoplasmic retention sites in p190RhoGEF confer anti-apoptotic activity to an EGFP-tagged protein. Brain research. Molecular brain research 9 14499478
2022 Expression of a RhoA-Specific Guanine Nucleotide Exchange Factor, p190RhoGEF, in Mouse Macrophages Negatively Affects M1 Polarization and Inflammatory Responses. Frontiers in immunology 7 35422804
2020 Inclusion Formation and Toxicity of the ALS Protein RGNEF and Its Association with the Microtubule Network. International journal of molecular sciences 7 32764283
2018 A novel overlapping NLS/NES region within the PH domain of Rho Guanine Nucleotide Exchange Factor (RGNEF) regulates its nuclear-cytoplasmic localization. European journal of cell biology 7 30482479
2019 Over-expression of p190RhoGEF enhances B-cell activation and germinal center formation in T-cell-dependent humoral immune responses. Immunology and cell biology 5 31361349
2023 Over-Expression of p190RhoGEF Regulates the Formation of Atherosclerotic Plaques in the Aorta of ApoE-/- Mice via Macrophage Polarization. International journal of molecular sciences 3 37628966
2024 Circular RNA circ_ARHGEF28 inhibits MST1/2 dimerization to suppress Hippo pathway to induce cisplatin resistance in ovarian cancer. Cancer cell international 2 39034401
2024 Axon guidance genes are regulated by TDP-43 and RGNEF through long-intron removal. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2 39360635
2026 Rgnef regulates bone mass through the activation of RhoA and Rac1. Experimental & molecular medicine 1 41571890

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