Affinage

ARHGAP5

Rho GTPase-activating protein 5 · UniProt Q13017

Length
1502 aa
Mass
172.5 kDa
Annotated
2026-04-28
30 papers in source corpus 21 papers cited in narrative 23 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ARHGAP5 (p190-B RhoGAP) is a GTPase-activating protein that inactivates Rho family GTPases—principally RhoA and RhoB, but also Rac1 and CDC42—to control actin cytoskeleton dynamics, cell spreading, migration, epithelial-mesenchymal transition, and tissue barrier integrity (PMID:8537347, PMID:18996642, PMID:29097442). Through its RhoGAP activity, ARHGAP5 regulates mammary ductal morphogenesis by modulating the IGF/IRS signaling axis, and controls hematopoietic stem cell self-renewal by suppressing p16(Ink4a) and normalizing TGF-β1/p38MAPK signaling (PMID:12637587, PMID:19713466, PMID:28176763). ARHGAP5 is recruited to integrin adhesion sites at the plasma membrane, and its expression is regulated transcriptionally by CREB1 and c-JUN/SIRT1, and post-transcriptionally through m6A modification (METTL3/YTHDF1), pseudouridylation (DKC1), and miR-486-5p targeting (PMID:8537347, PMID:32483433, PMID:30250020, PMID:31097692, PMID:23474761, PMID:39368791). In dermal microvascular endothelial cells, a patient-derived point mutation in ARHGAP5 impairs RhoB inactivation and disrupts capillary barrier recovery after TNF stimulation (PMID:29097442).

Mechanistic history

Synthesis pass · year-by-year structured walk · 8 steps
  1. 1995 High

    Establishing the core biochemical identity of ARHGAP5: its recombinant GAP domain directly stimulates GTP hydrolysis by RhoA, Rac1, and CDC42, and the protein is recruited to integrin adhesion sites, linking extracellular matrix signaling to Rho GTPase regulation.

    Evidence In vitro GAP assay with recombinant C-terminal domain, co-immunoprecipitation, immunofluorescence at fibronectin bead binding sites

    PMID:8537347

    Open questions at the time
    • Relative specificity among Rho substrates in vivo not determined
    • Structural basis of GAP-substrate recognition unknown
    • Regulation of GAP activity (e.g., phosphorylation) not addressed
  2. 2003 High

    Genetic loss-of-function in mice revealed that ARHGAP5 is required for mammary ductal morphogenesis and acts upstream of IRS-1/IRS-2 in the IGF signaling axis, converting ARHGAP5 from a biochemical RhoGAP to a developmental regulator of tissue patterning.

    Evidence p190-B knockout and heterozygous mice, mammary transplantation into cleared fat pads, IRS-1/IRS-2 western blotting; complemented by gain-of-function transgenic overexpression (2006) and embryonic mammary bud analysis with IGF-1R/IRS double-KO epistasis (2007)

    PMID:12637587 PMID:16469769 PMID:17662267

    Open questions at the time
    • Direct biochemical mechanism linking RhoGAP activity to IRS protein expression not defined
    • Relevant Rho substrate in mammary epithelium not identified
  3. 2009 High

    ARHGAP5 was shown to limit hematopoietic stem cell self-renewal: its loss enhanced long-term engraftment by repressing p16(Ink4a), and separately, p190-B deletion disrupted the mesenchymal niche via impaired Wnt signaling in MSCs, establishing both cell-autonomous and non-cell-autonomous roles.

    Evidence p190-B KO mouse serial transplantation, p16(Ink4a) transcriptional analysis (2009); MSC coculture, CFU assays, Wnt signaling analysis (2013); TGF-β1/p38MAPK measurement and single-HSPC fate tracking (2017)

    PMID:19713466 PMID:23563238 PMID:28176763

    Open questions at the time
    • Specific Rho GTPase substrate responsible for HSC phenotype not identified
    • How p190-B couples Rho inactivation to p16(Ink4a) transcription is unknown
    • MSC-intrinsic versus paracrine effects not fully separated
  4. 2013 High

    miR-486-5p was shown to directly target the ARHGAP5 3ʹ-UTR, establishing that ARHGAP5 expression in cancer is regulated post-transcriptionally and that ARHGAP5 promotes lung cancer cell migration and invasion downstream of this miRNA.

    Evidence Luciferase 3ʹ-UTR reporter assay, miR-486-5p overexpression/silencing, ARHGAP5 siRNA knockdown, in vivo metastasis model

    PMID:23474761

    Open questions at the time
    • Whether miR-486-5p regulation operates in non-cancer contexts unknown
    • Contribution of ARHGAP5 relative to other miR-486-5p targets not delineated
  5. 2017 High

    A patient-derived point mutation in the ARHGAP5 GAP domain was shown to impair RhoB (not just RhoA) inactivation in endothelial cells, establishing ARHGAP5 as a physiological regulator of capillary barrier function through RhoB.

    Evidence Patient-derived dermal microvascular endothelial cells, TNF stimulation, TEER measurement, RhoB activation assay, phenocopy by siRNA knockdown in normal ECs

    PMID:29097442

    Open questions at the time
    • Whether the barrier phenotype extends to other vascular beds not tested
    • In vivo vascular permeability phenotype in knockout mice not reported
  6. 2018 High

    Transcriptional control of ARHGAP5 was elucidated: SIRT1 deacetylates c-JUN to suppress ARHGAP5 transcription, while CREB1 activates it, defining two independent transcription-factor-level inputs governing ARHGAP5 abundance in cancer contexts.

    Evidence Co-IP of SIRT1–c-JUN, deacetylation assay, ARHGAP5 knockdown rescue (2018); ChIP of CREB1 on ARHGAP5 promoter (2020)

    PMID:30250020 PMID:32483433

    Open questions at the time
    • Whether SIRT1/c-JUN and CREB1 cooperate or compete on the ARHGAP5 promoter unknown
    • Chromatin-level regulation and enhancer landscape not mapped
  7. 2019 Medium

    Epitranscriptomic regulation of ARHGAP5 was uncovered: METTL3-mediated m6A modification of ARHGAP5 mRNA (read by YTHDF1) and pseudouridylation by DKC1 both modulate ARHGAP5 mRNA stability, adding RNA-modification-level control to the multi-layered regulation of ARHGAP5 expression.

    Evidence ChIP, RIP, m6A detection, METTL3 recruitment by lncRNA ARHGAP5-AS1 (2019); ADAR1/METTL3/YTHDF1 axis in breast cancer (2022); DKC1 enzymatic assay and pseudouridylation detection in ovarian cancer (2024)

    PMID:31097692 PMID:36077054 PMID:39368791

    Open questions at the time
    • Relative contributions of m6A versus pseudouridylation to ARHGAP5 mRNA half-life not compared
    • Whether epitranscriptomic regulation operates in non-cancer tissues unknown
    • Each axis reported by single labs
  8. 2016 Medium

    Multiple cancer contexts established ARHGAP5 as a mediator of RhoA inactivation downstream of various upstream signals (CD147 in HCC, ANGPTL4 at the BBB), reinforcing its role as a convergence point for RhoA regulation in disease.

    Evidence FRET-based RhoA biosensor, p190-B knockdown epistasis in HCC (2016); ARHGAP5 knockdown with RhoA/MYL5 pathway in brain endothelium (2019)

    PMID:27601938 PMID:31766605

    Open questions at the time
    • Direct physical interaction between CD147 or ANGPTL4 and ARHGAP5 not shown
    • Upstream signaling mechanism from CD147 to ARHGAP5 transcription not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • Major unresolved questions include: which Rho substrate(s) are the physiologically relevant targets in each tissue context, whether the synthetic lethality of ARHGAP5/ARHGAP35 double loss is therapeutically exploitable, and whether ARHGAP5 GAP domain variants are causative for human disease such as idiopathic hypogonadotropic hypogonadism.
  • No structural model of ARHGAP5 GAP domain bound to any Rho substrate
  • Synthetic lethality with ARHGAP35 observed only in one endometrial cancer line (preprint)
  • IHH disease association not confirmed by zebrafish modeling

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0003924 GTPase activity 1
Localization
GO:0005856 cytoskeleton 2 GO:0005886 plasma membrane 1
Pathway
R-HSA-162582 Signal Transduction 8 R-HSA-1266738 Developmental Biology 3 R-HSA-168256 Immune System 3
Partners
ARVCFCDC42METTL3RAC1RHOARHOBSIRT1YTHDF1

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 p190-B (ARHGAP5) was cloned and its recombinant C-terminal Rho GAP domain was shown in vitro to have GAP activity for RhoA, Rac1, and CDC42Hs/G25K. The N-terminal portion contains a GTPase domain. p190-B co-localizes with α5β1 integrin and is recruited to the plasma membrane beneath fibronectin-coated bead binding sites, along with Rho, establishing a transmembrane link between integrins and p190-B/Rho signaling. Recombinant protein in vitro GAP assay, immunoprecipitation, immunofluorescence, integrin antibody-coated bead recruitment assay The Journal of biological chemistry High 8537347
2000 Transient transfection of a p190-B expression construct into MCF-10A human mammary epithelial cells resulted in disruption of the actin cytoskeleton, demonstrating a direct role for p190-B in regulating signaling pathways influencing cell migration and invasion. Transient transfection with p190-B expression construct, actin cytoskeleton imaging Cell growth & differentiation Medium 10939588
2003 p190-B RhoGAP (ARHGAP5) is required for mammary ductal morphogenesis: p190-B heterozygous and null mice show decreased ductal outgrowth due to decreased proliferation in cap cells of terminal end buds, phenotypically similar to IGF-I receptor null mammary epithelium, and decreased expression of insulin receptor substrates IRS-1 and IRS-2, indicating p190-B regulates ductal morphogenesis partly by modulating the IGF signaling axis. p190-B knockout/heterozygous mouse model, mammary transplantation into cleared fat pad, IRS-1/2 western blotting Molecular endocrinology High 12637587
2006 Overexpression of p190-B RhoGAP in the developing mammary gland disrupts ductal morphogenesis—causing abnormal terminal end buds with aberrant budding, increased branching, delayed ductal elongation, and hyperplastic lesions during pregnancy—accompanied by altered IGF pathway signaling, discontinuous myoepithelial layer, increased collagen, and macrophage infiltration in the stroma. Tetracycline-regulatable p190-B transgenic mouse model, histology, IHC, IGF signaling analysis Molecular endocrinology High 16469769
2007 p190-B RhoGAP is required for embryonic mammary bud development; p190-B-deficient embryos show smaller buds with impaired mesenchymal proliferation and differentiation, phenocopied by IRS-1/2 double knockout embryos, establishing that IGF signaling through p190-B and IRS proteins is critical for mammary bud morphogenesis and epithelial-mesenchymal interactions. p190-B knockout mouse embryos, IGF-1R knockout comparison, IRS-1/2 double knockout comparison, histology, proliferation assay Developmental biology High 17662267
2008 ARHGAP5 (p190-B RhoGAP) promotes cell spreading and migration by negatively regulating RhoA activity in Huh-7 hepatocellular carcinoma cells; ARHGAP5 was identified as a target of amplification at chromosomal region 14q12 in hepatocellular carcinoma. High-density oligonucleotide microarray for copy number, RhoA activity assay, functional cell spreading/migration assays Cancer letters Medium 18996642
2009 Loss of p190-B RhoGAP enhances hematopoietic stem cell (HSC) long-term engraftment and self-renewal during serial transplantation. p190-B deficiency represses upregulation of p16(Ink4a) in HSCs, providing a mechanistic basis for p190-B-mediated HSC self-renewal activity. p190-B knockout mouse, serial transplantation, ex vivo culture, transcriptional analysis of p16(Ink4a) Blood High 19713466
2013 p190-B RhoGAP deletion in mice causes hematopoietic failure due to non-cell-autonomous defects in the mesenchymal microenvironment. p190-B loss impairs Wnt signaling in mesenchymal stem cells (MSCs), alters MSC lineage fate specification to osteoblast and adipocyte lineages, and disrupts bone marrow niche composition. p190-B knockout mouse, coculture of MSCs with wild-type bone marrow cells, colony-forming unit assays (CFU-fibroblast, CFU-adipocyte, CFU-osteoblast), Wnt signaling analysis Leukemia High 23563238
2013 miR-486-5p directly binds the 3'-UTR of ARHGAP5 mRNA to suppress its expression, and ARHGAP5 knockdown inhibits lung cancer cell migration and invasion, establishing ARHGAP5 as a downstream effector of miR-486-5p in NSCLC metastasis. Luciferase 3'-UTR reporter assay, miR-486-5p overexpression/silencing, ARHGAP5 siRNA knockdown, migration/invasion assays in vitro, in vivo metastasis model Oncogene High 23474761
2017 A point mutation in p190B RhoGAP impairs RhoB inactivation in dermal microvascular endothelial cells, leading to prolonged RhoB activation after TNF stimulation, impaired recovery of barrier function, and increased endothelial permeability. siRNA knockdown of p190B in normal ECs recapitulates the mutant phenotype, establishing p190B as a regulator of capillary endothelial barrier function via RhoB inactivation. Patient-derived endothelial cells with p190B point mutation, TNF stimulation, transendothelial electrical resistance (TEER) measurement, siRNA knockdown in normal ECs, RhoB activation assay The Journal of experimental medicine High 29097442
2017 Loss of p190-B RhoGAP normalizes bioactive TGF-β1 levels and p38MAPK activity in hematopoietic stem and progenitor cells (HSPCs), reduces asymmetric fate choice, and promotes symmetric retention of multi-lineage capacity. This establishes a p190-B RhoGAP–ROS–TGF-β–p38MAPK signaling network balancing HSPC self-renewal and differentiation. p190-B knockout mouse, transplantation, single HSPC culture, p38MAPK activity assay, TGF-β1 measurement, asymmetric distribution analysis Nature communications High 28176763
2018 SIRT1 suppresses ARHGAP5 expression by physically associating with transcription factor c-JUN and deacetylating it to inhibit its transcriptional activity on the ARHGAP5 promoter. Silencing of ARHGAP5 inhibits gastric cancer cell migration and invasion, and ARHGAP5 mediates SIRT1-dependent suppression of GC metastasis. mRNA microarray, co-immunoprecipitation (SIRT1–c-JUN interaction), deacetylation assay, ARHGAP5 knockdown, in vitro migration/invasion assays, in vivo metastasis model Cell death & disease High 30250020
2019 lncRNA ARHGAP5-AS1 activates ARHGAP5 transcription in the nucleus by directly interacting with the ARHGAP5 promoter, and also stabilizes ARHGAP5 mRNA in the cytoplasm by recruiting METTL3 to stimulate m6A modification of ARHGAP5 mRNA. Impaired autophagic degradation of ARHGAP5-AS1 (dependent on SQSTM1 transport to autophagosomes) leads to ARHGAP5 upregulation and chemoresistance in gastric cancer. ChIP assay, RNA immunoprecipitation, METTL3 recruitment assay, m6A modification detection, autophagy inhibition, SQSTM1 knockdown, ARHGAP5-AS1 knockdown/overexpression Cell death & disease High 31097692
2019 Meningitic E. coli-induced ANGPTL4 in brain microvascular endothelial cells disrupts blood-brain barrier via ARHGAP5/RhoA/MYL5 signaling cascade: ANGPTL4 increases MYL5 expression through RhoA pathway activation (by downregulating ARHGAP5, a negative regulator of RhoA), leading to increased BBB permeability without affecting tight junction proteins. ANGPTL4 recombinant protein treatment, in vitro and in vivo permeability assay, RhoA activity measurement, MYL5 expression analysis, ARHGAP5 knockdown Pathogens Medium 31766605
2020 ARHGAP5 promotes colorectal cancer cell epithelial-mesenchymal transition by negatively regulating RhoA activity. CREB1 transcriptionally upregulates ARHGAP5 expression, and decreased miR-137 contributes to ARHGAP5 mRNA stability in CRC. RNAi, ChIP assay (CREB1 binding to ARHGAP5 promoter), RhoA activity assay, EMT markers, in vitro migration/invasion, xenograft models Theranostics High 32483433
2022 ADAR1 interacts with METTL3 and edits METTL3 mRNA to change its miR-532-5p binding site, leading to increased METTL3 protein levels. METTL3 then m6A-modifies ARHGAP5 mRNA, which is recognized by YTHDF1, promoting breast cancer proliferation, migration, and invasion. This establishes ADAR1/METTL3/ARHGAP5/YTHDF1 as an oncogenic axis. Co-immunoprecipitation (ADAR1–METTL3), m6A sequencing/detection, luciferase assay, YTHDF1 RIP, ADAR1 knockdown in vivo xenograft International journal of molecular sciences Medium 36077054
2022 ARHGAP5 GAP domain variants identified in patients with idiopathic hypogonadotropic hypogonadism were shown by in vitro GAP activity assay to have decreased activity; however, arhgap5 zebrafish morphants did not display significant GnRH3-GFP+ neuronal abnormalities, making ARHGAP5 a candidate rather than confirmed gene for IHH. In vitro GAP activity assay, zebrafish gnrh3:egfp neuronal area phenotype assessment, exome sequencing Genetics in medicine Low 36178483
2022 lncRNA ARHGAP5-AS1 interacts with SMAD7 protein via its PY motif and prevents SMAD7 ubiquitination and degradation by blocking interaction between SMAD7 and E3 ligases SMURF1/SMURF2, thereby suppressing TGF-β signaling and inhibiting breast cancer cell migration. RNA pulldown assay, RNA immunoprecipitation, co-immunoprecipitation (SMAD7–SMURF1/2), dual luciferase reporter (TGF-β signaling), F-actin staining, transwell migration assay Breast cancer research and treatment Medium 34370213
2023 circARHGAP5 (derived from exons 2-3 of ARHGAP5) directly binds AUF1 RNA-binding protein and prevents AUF1 from degrading BIM mRNA, thereby promoting BIM expression and sensitizing cervical squamous cell carcinoma cells to cisplatin-induced apoptosis. RNA pulldown, RIP, circARHGAP5 overexpression/knockdown, BIM mRNA stability assay, in vitro and in vivo cisplatin apoptosis assays Cancer science Medium 36632741
2024 lncRNA ZFHX2-AS1 interacts with pseudouridine synthase DKC1 and attenuates its enzymatic activity, thereby reducing pseudouridylation of ARHGAP5 mRNA and stabilizing it. ARHGAP5 in turn promotes epithelial-mesenchymal transition by regulating Rho GTPase activities in ovarian cancer. RIP, DKC1 enzymatic activity assay, pseudouridylation detection, ARHGAP5 mRNA stability assay, ZFHX2-AS1 overexpression/knockdown, in vitro and in vivo functional assays, Rho GTPase activity assay Cellular signalling Medium 39368791
2016 CD147 upregulates p190-B RhoGAP (ARHGAP5) at both mRNA and protein levels in hepatocellular carcinoma cells. p190-B mediates CD147-induced RhoA deactivation, as silencing p190-B rescues stress fiber and focal adhesion formation and blunts the CD147 overexpression effect on cell movement. qRT-PCR, western blot, RhoA biosensor (FRET), siRNA knockdown, immunofluorescence, wound-healing assay, IHC in HCC tissues Cancer cell international Medium 27601938
2025 In hepatocytes, N-cadherin maintains hepatic polarity by facilitating RhoA inactivation through ARVCF (p120-catenin family member) and its partner p190B/ARHGAP5, while E-cadherin promotes RhoA activation and bile canaliculi elongation via a distinct pathway, establishing dual opposing roles of cadherins in controlling RhoA activity through ARHGAP5. Live imaging, RhoA activity assay, CRISPR/gene knockdown, localization studies in hepatocyte models bioRxivpreprint Medium
2025 CRISPR/Cas9 knockout of p190B (ARHGAP5) in HEC-1-A endometrial cancer cells leads to actin remodeling with formation of Cross-Linked Actin Networks (CLANs) dependent on the Rho/ROCK pathway. Loss of p190A (ARHGAP35) causes a similar phenotype, and simultaneous loss of both paralogs is synthetically lethal in endometrial cancer cells. CRISPR/Cas9 KO, actin cytoskeleton imaging, ROCK inhibitor treatment, proteomic analysis bioRxivpreprint Medium

Source papers

Stage 0 corpus · 30 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 Downregulation of miR-486-5p contributes to tumor progression and metastasis by targeting protumorigenic ARHGAP5 in lung cancer. Oncogene 208 23474761
2019 Impaired autophagic degradation of lncRNA ARHGAP5-AS1 promotes chemoresistance in gastric cancer. Cell death & disease 158 31097692
1995 p190-B, a new member of the Rho GAP family, and Rho are induced to cluster after integrin cross-linking. The Journal of biological chemistry 112 8537347
2018 SIRT1 suppresses the migration and invasion of gastric cancer by regulating ARHGAP5 expression. Cell death & disease 52 30250020
2015 MiR-744 functions as a proto-oncogene in nasopharyngeal carcinoma progression and metastasis via transcriptional control of ARHGAP5. Oncotarget 44 25961434
2003 p190-B RhoGAP regulates mammary ductal morphogenesis. Molecular endocrinology (Baltimore, Md.) 42 12637587
2022 N6 -methyladenosine-modified lncRNA ARHGAP5-AS1 stabilises CSDE1 and coordinates oncogenic RNA regulons in hepatocellular carcinoma. Clinical and translational medicine 40 36354136
2008 A novel amplification target, ARHGAP5, promotes cell spreading and migration by negatively regulating RhoA in Huh-7 hepatocellular carcinoma cells. Cancer letters 39 18996642
2006 P190-B Rho GTPase-activating protein overexpression disrupts ductal morphogenesis and induces hyperplastic lesions in the developing mammary gland. Molecular endocrinology (Baltimore, Md.) 39 16469769
2017 p190-B RhoGAP and intracellular cytokine signals balance hematopoietic stem and progenitor cell self-renewal and differentiation. Nature communications 36 28176763
2022 RNA Editing Enzyme ADAR1 Regulates METTL3 in an Editing Dependent Manner to Promote Breast Cancer Progression via METTL3/ARHGAP5/YTHDF1 Axis. International journal of molecular sciences 35 36077054
2000 P190-B, a Rho-GTPase-activating protein, is differentially expressed in terminal end buds and breast cancer. Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 35 10939588
2007 Crosstalk between the p190-B RhoGAP and IGF signaling pathways is required for embryonic mammary bud development. Developmental biology 34 17662267
2018 Lactic acid induced microRNA-744 enhances motility of SiHa cervical cancer cells through targeting ARHGAP5. Chemico-biological interactions 30 30423314
2021 High-throughput sequencing identified circular RNA circUBE2K mediating RhoA associated bladder cancer phenotype via regulation of miR-516b-5p/ARHGAP5 axis. Cell death & disease 23 34285193
2020 Investigation of the role and mechanism of ARHGAP5-mediated colorectal cancer metastasis. Theranostics 23 32483433
2017 A p190BRhoGAP mutation and prolonged RhoB activation in fatal systemic capillary leak syndrome. The Journal of experimental medicine 21 29097442
2009 Loss of the Rho GTPase activating protein p190-B enhances hematopoietic stem cell engraftment potential. Blood 19 19713466
2021 Long non-coding RNA ARHGAP5-AS1 inhibits migration of breast cancer cell via stabilizing SMAD7 protein. Breast cancer research and treatment 16 34370213
1998 Cloning, genomic organization and chromosomal assignment of the mouse p190-B gene. Biochimica et biophysica acta 16 9838117
2022 miR-486-5p inhibits invasion and migration of HTR8/SVneo trophoblast cells by down-regulating ARHGAP5. Placenta 15 35477045
2019 Meningitic Escherichia coli Induction of ANGPTL4 in Brain Microvascular Endothelial Cells Contributes to Blood-Brain Barrier Disruption via ARHGAP5/RhoA/MYL5 Signaling Cascade. Pathogens (Basel, Switzerland) 14 31766605
2022 Exosomes derived from human umbilical cord mesenchymal stem cells reduce tendon injuries via the miR-27b-3p/ARHGAP5/RhoA signaling pathway. Acta biochimica et biophysica Sinica 12 35130628
2023 Circular RNA ARHGAP5 inhibits cisplatin resistance in cervical squamous cell carcinoma by interacting with AUF1. Cancer science 9 36632741
2016 CD147 promotes cell motility via upregulation of p190-B RhoGAP in hepatocellular carcinoma. Cancer cell international 7 27601938
2013 p190-B RhoGAP regulates the functional composition of the mesenchymal microenvironment. Leukemia 7 23563238
2023 Silencing of the circ-Arhgap5 RNA protects neuronal PC12 cells against injury and depends on the miR-29a-3p/Rock1 axis. Metabolic brain disease 4 36790698
2022 The p190 RhoGAPs, ARHGAP35, and ARHGAP5 are implicated in GnRH neuronal development: Evidence from patients with idiopathic hypogonadotropic hypogonadism, zebrafish, and in vitro GAP activity assay. Genetics in medicine : official journal of the American College of Medical Genetics 4 36178483
2024 ZFHX2-AS1 interacts with DKC1 to regulate ARHGAP5 pseudouridylation and suppress ovarian cancer progression. Cellular signalling 3 39368791
2024 Exposure to BaA inhibits trophoblast cell invasion and induces miscarriage by regulating the DEC1/ARHGAP5 axis and promoting ubiquitination-mediated degradation of MMP2. Journal of hazardous materials 2 39191013