Affinage

ARHGEF3

Rho guanine nucleotide exchange factor 3 · UniProt Q9NR81

Length
526 aa
Mass
59.8 kDa
Annotated
2026-06-09
30 papers in source corpus 17 papers cited in narrative 17 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

ARHGEF3 (XPLN) is a DH-PH domain guanine nucleotide exchange factor that selectively activates RhoA and RhoB to drive actin cytoskeletal remodeling, stress fiber and focal adhesion assembly through Rho kinase, while also executing GEF-independent regulatory functions (PMID:12221096, PMID:23192023). Its enzymatic specificity is intrinsic: ARHGEF3 catalyzes GDP-to-GTP exchange on RhoA and RhoB but not RhoC, a discrimination set by isoleucine 43 of RhoC, and its tandem DH-PH module undergoes PH-domain rearrangement upon RhoA engagement (PMID:12221096, PMID:23192023). Through this RhoA/ROCK axis ARHGEF3 governs diverse programs in vivo: it restrains skeletal muscle mass, fiber size, and regeneration by blocking autophagy flux, an activity that requires GEF function and is recapitulated in dystrophic mdx muscle (PMID:33406419, PMID:37311604); it supports erythroid transferrin/iron uptake upstream of RhoA (PMID:21715309); and it shapes P-cadherin gradients and placode cell fate during hair follicle morphogenesis (PMID:41490244). ARHGEF3 carries a separable, GEF-independent activity through its N-terminal 125-amino-acid domain that binds mTORC2 via rictor and inhibits its kinase activity toward Akt Ser473, thereby negatively regulating myoblast differentiation and the mTORC2-SPARC axis (PMID:24043828, PMID:28315487). In a further non-canonical role, ARHGEF3 stabilizes ATP-citrate lyase by reducing its acetylation and blocking NEDD4-mediated degradation to promote tumor cell proliferation (PMID:36241648). Additional context-specific roles in AML macrophage differentiation, adipocyte hypertrophy, antiviral restriction, and tumor microenvironment remodeling have been described (PMID:25494542, PMID:40216078, PMID:36016278, PMID:42023986).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2002 High

    Establishing whether ARHGEF3 is a functional GEF and which Rho GTPases it acts on defined its core biochemical identity and the structural basis of its selectivity.

    Evidence In vitro nucleotide exchange and binding assays with mutagenesis (Ile43), plus cell overexpression with dominant-negative Rho kinase

    PMID:12221096

    Open questions at the time
    • Did not establish physiological contexts where RhoA vs RhoB activation matters
    • Did not address GEF-independent functions
  2. 2011 Medium

    Linking ARHGEF3 to erythroid iron handling showed that its Rho-GEF activity has a tissue-specific physiological output beyond cytoskeletal assembly.

    Evidence Morpholino knockdown in zebrafish with iron rescue, siRNA and transferrin uptake assay in K562 cells

    PMID:21715309

    Open questions at the time
    • Molecular link between RhoA activity and transferrin uptake machinery undefined
    • Single lab across two model systems
  3. 2012 High

    Solving the tandem DH-PH structure provided the structural rationale for substrate engagement and conformational change upon RhoA binding.

    Evidence X-ray crystallography at 1.79 Å by MAD phasing

    PMID:23192023

    Open questions at the time
    • No co-crystal with RhoA/RhoB to confirm the inferred PH rearrangement
    • N-terminal mTORC2-binding region not in the construct
  4. 2013 High

    Discovery that ARHGEF3 binds and inhibits mTORC2 independently of its GEF activity revealed it as a bifunctional protein with a separable N-terminal regulatory module.

    Evidence Yeast two-hybrid, reciprocal Co-IP, in vitro mTORC2 kinase assay with purified XPLN, and domain deletion mapping to N-terminal 125 aa

    PMID:24043828

    Open questions at the time
    • Structural basis of rictor/mTORC2 binding unresolved
    • How GEF and mTORC2-inhibitory activities are coordinated unknown
  5. 2014 Medium

    Knockdown transcriptomics placed ARHGEF3/RhoA upstream of bone-cell gene-expression programs, extending its reach to transcriptional outputs.

    Evidence siRNA knockdown with microarray and qRT-PCR validation in osteoblast- and osteoclast-like lines

    PMID:24840563

    Open questions at the time
    • No direct enzymatic or binding assay connecting ARHGEF3 to the transcriptional changes
    • Mechanism of gene regulation unmapped
  6. 2015 Medium

    Showing nuclear-to-cytoplasmic relocation upon HDAC inhibition coupled ARHGEF3 localization to RhoA/ROCK-driven myeloid differentiation, indicating regulated subcellular activity.

    Evidence siRNA, fractionation/immunofluorescence, GTP-RhoA pulldown, and pharmacological inhibitors in U937 AML cells

    PMID:25494542

    Open questions at the time
    • Mechanism of nuclear retention and HDACi-triggered export unknown
    • Single cell line
  7. 2017 Medium

    Demonstrating that ARHGEF3 negatively regulates the mTORC2-SPARC axis and is itself suppressed by TGF-β1/Smad reinforced its mTORC2-inhibitory role and revealed an upstream control input.

    Evidence siRNA knockdown, western blot/qRT-PCR for SPARC and pAkt, TGF-β1/Smad and HDACi treatments in lung fibroblasts

    PMID:28315487

    Open questions at the time
    • No in vitro reconstitution of the SPARC link
    • Single lab
  8. 2021 High

    An ARHGEF3 KO mouse demonstrated that its GEF activity restrains skeletal muscle regeneration by blocking autophagy, separating the GEF function from Akt signaling in vivo.

    Evidence KO mouse, acute injury model, GEF-inactive mutant, ROCK inhibitor, and autophagy flux assays across ages

    PMID:33406419

    Open questions at the time
    • How RhoA/ROCK suppresses autophagy mechanistically not defined
    • Relevant muscle cell type for the effect not fully resolved
  9. 2022 Medium

    Identification of ACLY stabilization showed a second GEF-independent function in which ARHGEF3 controls protein stability via acetylation.

    Evidence siRNA/overexpression, xenografts, ACLY-NEDD4 Co-IP, acetylation site mapping (K17/K86), and GEF-inactive mutant in NSCLC

    PMID:36241648

    Open questions at the time
    • How ARHGEF3 reduces ACLY acetylation enzymatically unknown
    • Whether ARHGEF3 acts directly on ACLY or via an intermediary unresolved
  10. 2022 Medium

    An overexpression screen revealed antiviral restriction against Flaviviridae, expanding ARHGEF3's functional repertoire to host defense.

    Evidence Lentiviral overexpression with HCV replicons and full-length HCV, plus YFV/ZIKV replication assays; conserved in rhesus ARHGEF3

    PMID:36016278

    Open questions at the time
    • Molecular mechanism of antiviral action undefined
    • Whether GEF activity is required not tested
  11. 2023 High

    Genetic and pharmacological dissection in mdx muscle confirmed that the ARHGEF3/ROCK pathway impairs muscle quality by blocking autophagy flux, validating the autophagy mechanism in a disease setting.

    Evidence Arhgef3 KO in mdx mice, 3D-engineered muscle, ROCK inhibitor, GEF-inactive mutant, chloroquine autophagy epistasis, force measurements

    PMID:37311604

    Open questions at the time
    • Upstream signals elevating ARHGEF3 in dystrophic muscle unknown
    • Molecular link from ROCK to autophagy machinery not detailed
  12. 2024 Medium

    miR-451a was shown to directly target the ARHGEF3 3'-UTR, identifying a post-transcriptional control point governing its erythroid role.

    Evidence Dual-luciferase 3'-UTR reporter, siRNA knockdown, and erythroid differentiation assays in K562 cells

    PMID:38801936

    Open questions at the time
    • Downstream effector mechanism in erythroid maturation not defined
    • Single lab
  13. 2025 Medium

    ARHGEF3 was placed in an adipogenic loop coupling RhoA-dependent YAP nuclear translocation with PPARγ activity, linking it to metabolic tissue expansion.

    Evidence KO mice on HFD, in vitro adipogenesis, ChIP for YAP-RhoA promoter binding, Co-IP, PPARγ luciferase reporter, YAP immunostaining

    PMID:40216078

    Open questions at the time
    • YAP-RhoA promoter binding needs independent replication
    • Direct molecular partner connecting ARHGEF3 to YAP unclear
  14. 2026 Medium

    A RHOA-ROCK-PTEN-AKT cascade was shown to remodel the tumor microenvironment via IRF1-driven chemokines and FASN suppression, connecting ARHGEF3 GEF signaling to anti-tumor immunity.

    Evidence Gain/loss-of-function, RhoA activity assay, pathway inhibitors, CXCL10/11 and FASN readouts, in vivo tumor models

    PMID:42023986

    Open questions at the time
    • Single lab, novel pathway not independently replicated
    • Mechanistic link from ROCK to PTEN not detailed
  15. 2026 Medium

    A KO embryo study established that ARHGEF3 patterns P-cadherin gradients and restricts placode fate, demonstrating a developmental morphogenesis role tied to cytoskeletal control.

    Evidence Arhgef3 KO mouse embryos, P-/E-cadherin immunostaining, hair follicle morphometry, F-actin culture models

    PMID:41490244

    Open questions at the time
    • How ARHGEF3 selectively controls P- but not E-cadherin unknown
    • Link between RhoA activity and cadherin gradient unmapped

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how ARHGEF3's GEF-dependent (RhoA/RhoB/ROCK) and GEF-independent (mTORC2 inhibition, ACLY stabilization) activities are integrated, regulated, and partitioned across the diverse tissue contexts in which it acts.
  • No unified model coordinating the two functional modes
  • No structure of full-length ARHGEF3 with its N-terminal mTORC2-binding region
  • Tissue-specific regulation of ARHGEF3 expression and localization incompletely defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 2 GO:0098772 molecular function regulator activity 2 GO:0140096 catalytic activity, acting on a protein 2
Localization
GO:0005856 cytoskeleton 2 GO:0005634 nucleus 1 GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-9612973 Autophagy 2 R-HSA-1266738 Developmental Biology 1
Partners
ACLYRHOARHOBRICTOR

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 XPLN (ARHGEF3) is a guanine nucleotide exchange factor that stimulates GDP-to-GTP exchange on RhoA and RhoB but not RhoC, RhoG, Rac1, or Cdc42 in vitro, and the selectivity against RhoC is determined by isoleucine 43 in RhoC (valine in RhoA/RhoB). XPLN preferentially associates with RhoA and RhoB, and when expressed in cells stimulates stress fiber and focal adhesion assembly in a Rho kinase-dependent manner. In vitro nucleotide exchange assay, co-precipitation/binding assay, cell overexpression with dominant-negative Rho kinase and active RhoA mutants, focus formation assay The Journal of biological chemistry High 12221096
2012 Crystal structure of the tandem DH-PH domains of mouse XPLN (ARHGEF3) was determined at 1.79 Å resolution by multiwavelength anomalous dispersion. The structure revealed an α4-α5 loop in the DH domain that is flexible and intramolecular DH-PH interactions, suggesting PH-domain rearrangement occurs upon RhoA binding. High structural similarity to other RhoGEFs (NET1, PDZ-RhoGEF, LARG, ITSN1/2) was observed. X-ray crystallography (MAD phasing, 1.79 Å resolution) Acta crystallographica. Section F, Structural biology and crystallization communications High 23192023
2013 XPLN (ARHGEF3) interacts with mTORC2 (but not mTORC1) in a rictor-dependent manner and acts as an endogenous inhibitor of mTORC2 kinase activity toward Akt. Knockdown of XPLN enhances Akt Ser473 phosphorylation; overexpression suppresses it. Purified XPLN inhibits mTORC2 kinase activity in vitro without affecting mTORC1. The GEF activity of XPLN is dispensable for mTORC2 inhibition, whereas the N-terminal 125-amino-acid fragment is necessary and sufficient for mTORC2 inhibition and for negative regulation of myoblast differentiation. Yeast two-hybrid screen, co-immunoprecipitation, siRNA knockdown, overexpression, in vitro mTORC2 kinase assay with purified components, domain deletion analysis Proceedings of the National Academy of Sciences of the United States of America High 24043828
2015 In AML cells (U937), ARHGEF3 protein is primarily nuclear but undergoes cytoplasmic translocation upon HDACi (MS275) treatment. Cytoplasmic ARHGEF3 activates the RhoA/ROCK pathway, leading to SAPK/JNK phosphorylation and Elk1 activation. ARHGEF3 silencing prevents RhoA activation, reduces SAPK/JNK phosphorylation and Elk1 activity, and blocks CD68 macrophage differentiation marker expression. siRNA knockdown, immunofluorescence/subcellular fractionation for localization, Rho activation assay (GTP-RhoA pulldown), western blotting for pathway components, pharmacological inhibitors (C3 transferase, Y27632) Epigenetics Medium 25494542
2011 Silencing of arhgef3 in zebrafish causes microcytic hypochromic anemia rescued by intracellular iron supplementation, demonstrating that ARHGEF3 regulates transferrin/iron uptake in erythroid cells. Silencing of RhoA phenocopies arhgef3 loss. In K562 cells, ARHGEF3 knockdown severely impairs transferrin uptake, placing ARHGEF3 upstream of RhoA in an iron-uptake pathway. Morpholino knockdown in zebrafish, rescue by iron injection, siRNA knockdown in K562 cells, transferrin uptake assay Blood Medium 21715309
2021 ARHGEF3 KO mice show enhanced skeletal muscle mass, fiber size, and function after acute injury. This effect requires the GEF activity of ARHGEF3 (not Akt signaling) and operates via the RhoA/ROCK pathway. ARHGEF3 KO promotes autophagy, and autophagy activation is required for the enhanced regeneration phenotype. Overexpression of ARHGEF3 inhibits muscle regeneration in a ROCK-dependent manner. In aged mice, ARHGEF3 depletion prevents muscle weakness by restoring autophagy. Knockout mouse model (ARHGEF3-KO), acute muscle injury model, GEF-inactive mutant overexpression, ROCK inhibitor treatment, autophagy flux assays, muscle function measurements Cell reports High 33406419
2017 XPLN (ARHGEF3) knockdown in human lung fibroblasts stimulates SPARC expression and Akt Ser473 phosphorylation. TGF-β1 downregulates XPLN via Smad2/3. HDACi treatment upregulates XPLN mRNA and reverses TGF-β1-induced SPARC expression, establishing XPLN as a negative regulator of the mTORC2-SPARC axis. siRNA knockdown, western blotting and qRT-PCR for SPARC and pAkt, TGF-β1/Smad pathway analysis, HDAC inhibitor treatment Pulmonary pharmacology & therapeutics Medium 28315487
2014 ARHGEF3 knockdown in osteoblast-like cells causes downregulation of TNFRSF11B (osteoprotegerin). RHOA knockdown in osteoblast-like cells downregulates ACTA2 (alpha-2 actin) and upregulates PTH1R, and in osteoclast-like cells downregulates ARHGDIA and ACTA2, placing ARHGEF3/RhoA upstream of these bone-cell gene-expression programs. siRNA knockdown, microarray followed by qRT-PCR validation in multiple human osteoblast-like and osteoclast-like cell lines PloS one Medium 24840563
2022 ARHGEF3 overexpression inhibits HCV subgenomic replicon RNA replication and full-length HCV replication, as well as replication of yellow fever virus and Zika virus (Flaviviridae), in cell-based systems. This antiviral activity is conserved between human and rhesus macaque ARHGEF3. Lentiviral overexpression screen with luciferase-expressing HCV replicons, independent validation with full-length HCV infection assay and flavivirus replication assays Viruses Medium 36016278
2022 ARHGEF3 promotes NSCLC cell proliferation in vitro and in vivo by stabilizing ATP-citrate lyase (ACLY) protein: ARHGEF3 reduces acetylation of ACLY on Lys17 and Lys86, preventing ACLY interaction with its E3 ubiquitin ligase NEDD4 and subsequent degradation. This function is independent of ARHGEF3's GEF activity. siRNA knockdown and overexpression, xenograft model, co-immunoprecipitation (ACLY-NEDD4 interaction), acetylation site mapping, GEF-inactive mutant Cell death & disease Medium 36241648
2023 ARHGEF3 is elevated in dystrophic mdx muscles and drives RhoA/ROCK activation. ARHGEF3 KO in mdx mice restores muscle quality (force production) and morphology without affecting regeneration. ARHGEF3 overexpression further compromises mdx muscle quality in a GEF activity- and ROCK-dependent manner. The ARHGEF3/ROCK pathway impairs muscle function by blocking autophagy flux, as chloroquine-mediated autophagy inhibition abolishes the benefit of ARHGEF3/ROCK inhibition. Arhgef3 KO in mdx mice, 3D-engineered mdx muscle model, ROCK inhibitor (Y-27632), GEF-inactive mutant overexpression, autophagy flux assay with chloroquine, muscle force measurements Journal of cachexia, sarcopenia and muscle High 37311604
2025 ARHGEF3 promotes adipocyte hypertrophy and differentiation through two coordinated mechanisms: (1) RhoA-dependent facilitation of YAP nuclear translocation and YAP binding to the RhoA promoter, and (2) enhancement of PPARγ transcriptional activity, establishing a reciprocal activation loop. ARHGEF3-deficient mice on a high-fat diet show reduced weight gain and smaller adipocyte size correlated with decreased RhoA expression and altered cytoskeletal dynamics. ARHGEF3-KO mice on HFD, in vitro adipogenesis (C3H10T1/2 cells), ChIP for YAP-RhoA promoter binding, co-immunoprecipitation, luciferase reporter for PPARγ activity, immunostaining for YAP localization Journal of advanced research Medium 40216078
2026 Tumor-intrinsic ARHGEF3 activates the RHOA-ROCK-PTEN cascade to inhibit AKT signaling, which upregulates IRF1-dependent chemokines CXCL10 and CXCL11 (promoting T-cell infiltration) and suppresses FASN-mediated fatty acid synthesis (limiting myeloid immunosuppression). These dual effects reshape the tumor microenvironment toward T-cell inflammation. Cell-based gain/loss-of-function, RhoA activity assay, pathway inhibitors, CXCL10/11 measurement, FASN activity assay, in vivo tumor models Advanced science Medium 42023986
2026 ARHGEF3 restricts placode cell fate acquisition and establishes a radial gradient of P-cadherin (but not E-cadherin) across hair follicle placodes during embryonic development. In Arhgef3-KO embryos, placodes are enlarged with elevated P-cadherin at junctions and disrupted gradient, correlating with aberrant epithelial organization and altered hair follicle downgrowth geometry. Arhgef3 KO mouse embryos, immunostaining for P-cadherin and E-cadherin, hair follicle morphometry, cell culture models for F-actin accumulation PLoS biology Medium 41490244
2024 miR-451a directly binds the 3'-UTR of ARHGEF3 mRNA (confirmed by dual-luciferase reporter assay), and knockdown of ARHGEF3 in K562 cells reverses hydroquinone-induced suppression of erythroid differentiation, placing ARHGEF3 as a downstream effector of the miR-451a/c-Jun axis in erythroid maturation. Dual-luciferase 3'-UTR reporter assay, siRNA knockdown, erythroid differentiation assays in K562 cells Toxicology Medium 38801936
2025 Inhibition of miR-512-3p in Moyamoya disease endothelial colony-forming cells increases ARHGEF3 expression and downstream RhoA GTPase activity, leading to enhanced tubule formation (angiogenesis rescue). Bioinformatics and functional data identify ARHGEF3 as a direct target of miR-512-3p. miR-512-3p inhibition in primary ECFCs, GTPase activity assay, tubule formation assay, western blotting for ARHGEF3/RhoA Scientific reports Low 40634490
2024 ARHGEF3 promotes F-actin accumulation at the cell cortex and P-cadherin enrichment at cell-cell junctions in culture models, consistent with its role in hair placode morphogenesis. Cell culture overexpression, phalloidin staining for F-actin, immunostaining for P-cadherin bioRxivpreprint Low 39314354

Source papers

Stage 0 corpus · 30 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 XPLN, a guanine nucleotide exchange factor for RhoA and RhoB, but not RhoC. The Journal of biological chemistry 119 12221096
2013 XPLN is an endogenous inhibitor of mTORC2. Proceedings of the National Academy of Sciences of the United States of America 40 24043828
2021 ARHGEF3 Regulates Skeletal Muscle Regeneration and Strength through Autophagy. Cell reports 30 33406419
2015 ARHGEF3 controls HDACi-induced differentiation via RhoA-dependent pathways in acute myeloid leukemias. Epigenetics 30 25494542
2000 Isolation of two novel human RhoGEFs, ARHGEF3 and ARHGEF4, in 3p13-21 and 2q22. Biochemical and biophysical research communications 30 10873612
2014 The Rho-GEF Gef3 interacts with the septin complex and activates the GTPase Rho4 during fission yeast cytokinesis. Molecular biology of the cell 29 25411334
2008 Identification of a role for the ARHGEF3 gene in postmenopausal osteoporosis. American journal of human genetics 29 18499081
2011 Silencing of RhoA nucleotide exchange factor, ARHGEF3, reveals its unexpected role in iron uptake. Blood 28 21715309
2017 SNP in human ARHGEF3 promoter is associated with DNase hypersensitivity, transcript level and platelet function, and Arhgef3 KO mice have increased mean platelet volume. PloS one 22 28542600
2014 Influence of ARHGEF3 and RHOA knockdown on ACTA2 and other genes in osteoblasts and osteoclasts. PloS one 21 24840563
2016 The putative tumor activator ARHGEF3 promotes nasopharyngeal carcinoma cell pathogenesis by inhibiting cellular apoptosis. Oncotarget 19 27028992
2022 ARHGEF3 regulates the stability of ACLY to promote the proliferation of lung cancer. Cell death & disease 17 36241648
1992 Secretion of the STA3 heat-stable enterotoxin of Escherichia coli: extracellular delivery of Pro-STA is accomplished by either Pro or STA. Molecular microbiology 17 1474896
2017 XPLN is modulated by HDAC inhibitors and negatively regulates SPARC expression by targeting mTORC2 in human lung fibroblasts. Pulmonary pharmacology & therapeutics 16 28315487
2021 Disrupting RhoA activity by blocking Arhgef3 expression mitigates microglia-induced neuroinflammation post spinal cord contusion. Journal of neuroimmunology 13 34390950
2023 RhoA/ROCK signalling activated by ARHGEF3 promotes muscle weakness via autophagy in dystrophic mdx mice. Journal of cachexia, sarcopenia and muscle 11 37311604
2009 Common variants in FLNB/CRTAP, not ARHGEF3 at 3p, are associated with osteoporosis in southern Chinese women. Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA 11 19727905
2020 Genetic variants in RET, ARHGEF3 and CTNNAL1, and relevant interaction networks, contribute to the risk of Hirschsprung disease. Aging 9 32139661
2022 Role of ARHGEF3 as a GEF and mTORC2 Regulator. Frontiers in cell and developmental biology 8 35174167
2021 ARHGEF3 Associated with Invasion, Metastasis, and Proliferation in Human Osteosarcoma. BioMed research international 6 34350290
2024 c-Jun targets miR-451a to regulate HQ-induced inhibition of erythroid differentiation via the BATF/SETD5/ARHGEF3 axis. Toxicology 5 38801936
2022 A Human and Rhesus Macaque Interferon-Stimulated Gene Screen Shows That Over-Expression of ARHGEF3/XPLN Inhibits Replication of Hepatitis C Virus and Other Flavivirids. Viruses 4 36016278
2020 Prostate Cancer Growth Inhibition by 1-(3,5-Dimethylphenyl)-6-methyl-1H-pyrazolo[4,3-c]pyridin-4(5H)-one via Down-regulation of Phosphorylation PI3K/AKT and STA3/JAK2. Doklady. Biochemistry and biophysics 4 33368049
2025 ARHGEF3 coordinates adipocyte hypertrophy and differentiation through dual YAP-RhoA and PPARγ activation. Journal of advanced research 3 40216078
2012 Structure of the Rho-specific guanine nucleotide-exchange factor Xpln. Acta crystallographica. Section F, Structural biology and crystallization communications 3 23192023
2025 Plasma extracellular vesicle-associated miR-512-3p modulates angiogenesis in pediatric Moyamoya disease by targeting ARHGEF3. Scientific reports 1 40634490
2026 The Rho GTPase regulator ARHGEF3 orchestrates hair placode budding by coordinating cell fate and P-cadherin patterning in mice. PLoS biology 0 41490244
2026 Tumor-Intrinsic ARHGEF3 Enhances Antitumor Immunity by Promoting T-Cell Infiltration and Limiting Myeloid Cell-Mediated Immunosuppression. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 0 42023986
2026 Selected ARHGEF3 Gene Polymorphisms Associated With Platelet Hyperaggregability in Patients With Venous Thromboembolism. Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis 0 42142076
2024 ARHGEF3 Regulates Hair Follicle Morphogenesis. bioRxiv : the preprint server for biology 0 39314354

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