Affinage

ARHGAP35

Rho GTPase-activating protein 35 · UniProt Q9NRY4

Length
1499 aa
Mass
170.5 kDa
Annotated
2026-04-28
100 papers in source corpus 46 papers cited in narrative 46 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ARHGAP35 (p190RhoGAP-A) is the principal GTPase-activating protein for RhoA, integrating signals from integrins, cadherins, and growth factor receptors to locally suppress RhoA-GTP and coordinate cytoskeletal remodeling, cell adhesion, migration, and cytokinesis. Its activation requires Src-family or Arg kinase-mediated phosphorylation at Y1105, which promotes high-affinity binding to the p120RasGAP SH2 domains and recruitment to the plasma membrane, adherens junctions, or lipid rafts where it exerts its GAP activity (PMID:15084284, PMID:31891593, PMID:16971514); an intramolecular autoinhibitory interaction between the protrusion-localization sequence (PLS) and the GAP domain, along with inhibitory phosphorylation by Rho-kinase (S1150), GSK-3β, and ERK, provides multilayered negative regulation (PMID:36516886, PMID:19103606, PMID:18502760, PMID:20439493). A polybasic region adjacent to the GAP domain, regulated by PKC phosphorylation and acidic phospholipids, switches substrate preference between RhoA and Rac1 (PMID:19673492, PMID:23499677). During mitosis, ARHGAP35 localizes to the cleavage furrow where it antagonizes the RhoGEF ECT2 and complexes with anillin to fine-tune contractility, and its timely proteasomal degradation via an N-terminal degron is essential for successful cytokinesis; in neurons it maintains dendritic spine stability downstream of Arg kinase, it is required for primary ciliogenesis at the basal body, and it suppresses tumorigenesis by activating the Hippo–LATS–YAP pathway in cooperation with p120RasGAP and ZO-2 (PMID:25359885, PMID:20534586, PMID:17928439, PMID:26859289, PMID:32641858, PMID:37995182).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 1995 High

    Establishing c-Src as the upstream kinase linking growth factor signaling to p190RhoGAP activation resolved how receptor tyrosine kinase signals reach Rho-family GTPases through a cytoplasmic GAP.

    Evidence Dominant-negative/wild-type c-Src overexpression with immunofluorescence and phosphotyrosine analysis in EGF-stimulated fibroblasts

    PMID:7542246

    Open questions at the time
    • Specific tyrosine site(s) phosphorylated by c-Src not yet mapped
    • Whether Src phosphorylation directly stimulates GAP catalytic activity or acts via recruitment not distinguished
  2. 1998 High

    Demonstrating that integrin α6β1 activates p190RhoGAP and that blocking p190RhoGAP inhibits matrix invasion established it as a critical effector linking integrin engagement to Rho suppression during cell motility.

    Evidence Integrin stimulation, tyrosine phosphorylation assays, anti-p190RhoGAP antibody microinjection, and invasion assays in melanoma cells

    PMID:9417037

    Open questions at the time
    • Identity of the kinase mediating integrin-induced p190RhoGAP phosphorylation unresolved
    • In vivo relevance to metastasis not tested
  3. 2001 High

    Using dominant-negative p190RhoGAP to show that it is required for integrin-dependent RhoA inactivation, cell spreading, and polarity establishment placed it as the central RhoA-inactivating mechanism during adhesion.

    Evidence Dominant-negative and wild-type overexpression with RhoA activity assays, cell spreading, and migration assays in fibroblasts

    PMID:11553710

    Open questions at the time
    • Genetic loss-of-function not yet performed
    • Contribution of p190B paralog not assessed
  4. 2003 High

    Two discoveries—cadherin-induced Src-dependent phosphorylation promoting p120RasGAP binding, and cell-cycle-regulated proteasomal degradation during mitosis—revealed that p190RhoGAP operates in both adhesion signaling and cytokinesis under distinct regulatory modes.

    Evidence RhoA affinity pulldown, co-IP, PP2 inhibition for cadherin axis; conditional overexpression, ubiquitination assays, proteasome inhibition for mitotic degradation

    PMID:12606561 PMID:14610059

    Open questions at the time
    • E3 ligase mediating mitotic degradation not identified
    • Whether cadherin and integrin pathways converge on the same phospho-site unclear
  5. 2004 High

    Identification of Y1105 as the specific Arg kinase phosphorylation site that triggers p120RasGAP binding and GAP activation provided the first defined molecular switch controlling p190RhoGAP activity.

    Evidence In vitro kinase assay, Y1105 site-directed mutagenesis, co-IP, RhoA activity assay in arg−/− fibroblasts and neurons

    PMID:15084284

    Open questions at the time
    • Whether other kinases also target Y1105 not yet shown
    • Structural basis for how pY1105 engages p120RasGAP SH2 domain unknown
  6. 2006 High

    Three studies collectively established that p120RasGAP binding serves primarily as a membrane recruitment mechanism rather than an allosteric activator, and that p190RhoGAP translocation to adherens junctions via p120-catenin mediates Rac/Rho antagonism.

    Evidence arg−/− fibroblasts with fractionation and in vitro GAP assay; p120-catenin co-IP and PDGFR signaling in epithelial cells; tTG/Src epistasis experiments

    PMID:16452636 PMID:16971514 PMID:17129786

    Open questions at the time
    • Whether p120-catenin and p120RasGAP compete for p190RhoGAP binding not resolved
    • How p190RhoGAP distinguishes RhoA from Rac1 at junctions unclear
  7. 2007 High

    Work in arg−/− neurons showed that p190RhoGAP localizes to dendritic spines and is essential for spine maturation and synapse stability via RhoA–ROCKII suppression, extending its function to postmitotic neuronal physiology.

    Evidence arg−/− mouse genetics with ROCKII heterozygosity epistasis, immunolocalization in hippocampal neurons, RhoA activity assay

    PMID:17227794 PMID:17652459 PMID:17928439

    Open questions at the time
    • Spine-specific activating kinase not confirmed in vivo
    • Whether p190RhoGAP loss contributes to neurodegenerative disease not tested
  8. 2008 High

    Multiple inhibitory phosphorylation events were discovered—Rho-kinase at S1150 (feedback loop), Brk at Y1105 (dual Ras/Rho modulation), and syndecan-4/PKCα-mediated membrane redistribution—revealing that p190RhoGAP is a multi-input signaling integrator.

    Evidence In vitro kinase assays with phosphomutants, Rnd binding assays in VSMCs, PKCα mutants with membrane fractionation, and Brk in vitro kinase assay in breast cancer cells

    PMID:18541700 PMID:18829532 PMID:19103606

    Open questions at the time
    • Relative contributions of activating vs. inhibiting kinases in a single cell type not quantified
    • No structural model of how S1150 phosphorylation disrupts Rnd binding
  9. 2009 High

    A cluster of discoveries established additional regulatory layers: GSK-3β C-terminal phosphorylation inhibits GAP activity, PKC phosphorylation at S1221/T1226 switches substrate preference from Rac to Rho via polybasic region–lipid interactions, SHP2 controls basal phosphorylation state, and p190RhoGAP antagonizes ECT2 at the cleavage furrow.

    Evidence In vitro GAP/RacGAP assays with liposomes and PKC; GSK-3β phosphomutants with migration assays; SHP2 siRNA with RhoA assays in VSMCs; FRET RhoA biosensor at the furrow with ECT2 co-IP

    PMID:18502760 PMID:18642445 PMID:19254711 PMID:19393245 PMID:19673492 PMID:19692654 PMID:19803801

    Open questions at the time
    • How PKC-mediated substrate switching operates in vivo not demonstrated
    • Whether SHP2 directly dephosphorylates Y1105 not confirmed
  10. 2010 High

    Mapping the minimal N-terminal degron (four residues in GBDS1) sufficient for mitotic ubiquitination, and showing ERK phosphorylation reduces peripheral localization, completed the picture of how p190RhoGAP is temporally and spatially silenced during mitosis and adhesion maturation.

    Evidence RNAi reconstitution with degradation-resistant mutants and domain mapping; MEK/ERK inhibitors with phospho-site mutants and focal adhesion quantification

    PMID:20439493 PMID:20534586

    Open questions at the time
    • Identity of the E3 ligase recognizing the N-terminal degron still unknown
    • How ERK phosphorylation reduces membrane association mechanistically unclear
  11. 2013 High

    Mapping the minimal p120-catenin CRAD region (residues 820–843) required for p190RhoGAP membrane targeting at junctions, and demonstrating cellular RacGAP activity requiring the polybasic region, established p190RhoGAP as a dual-specificity GAP whose substrate selectivity depends on membrane context.

    Evidence p120-catenin truncation mutants with membrane fractionation and barrier assays; cellular Rac/Rho activity assays with polybasic region mutants

    PMID:23499677 PMID:23653363

    Open questions at the time
    • Structural basis for polybasic region-mediated substrate switching not determined
    • Whether RacGAP activity is physiologically relevant in vivo untested
  12. 2014 High

    Discovery that p190RhoGAP forms a complex with anillin at the cleavage furrow and that both anillin binding and GAP activity are required for cytokinesis defined the molecular scaffold through which p190RhoGAP tunes contractility during cell division.

    Evidence Depletion/rescue with anillin-binding and GAP-dead mutants, RhoA-GTP measurement, blebbistatin rescue

    PMID:25359885

    Open questions at the time
    • How anillin recruits p190RhoGAP to the furrow structurally unknown
    • Whether anillin interaction is direct or via a bridging factor not fully resolved
  13. 2016 High

    Identification of the PLS as a protrusion-targeting sequence that binds cortactin and also functions as an intramolecular autoinhibitory domain, together with the finding that a GAP-domain mutation causes ciliogenesis failure and glomerulocystic kidneys, revealed new regulatory and physiological dimensions of p190RhoGAP.

    Evidence Truncation mutagenesis with co-IP of cortactin and localization/RhoA assays; ENU mutagenesis screen with L1396Q in vitro GAP assay and ROCK inhibitor rescue in mouse kidneys

    PMID:26859289 PMID:27646271

    Open questions at the time
    • Structural basis for PLS autoinhibition not determined at atomic resolution
    • Whether ciliogenesis role is GAP-dependent or scaffolding-dependent not fully dissected
  14. 2018 High

    Crystal structure of the N-terminal pseudoGTPase domain bound to GTP revealed six structural inserts that prevent catalysis and regulator binding, establishing a third pseudoGTPase in p190RhoGAP and suggesting a structural/scaffolding rather than catalytic role for this domain.

    Evidence X-ray crystallography at 2.8 Å with GTP hydrolysis assay, mutagenesis, and nucleotide exchange assays

    PMID:30174148

    Open questions at the time
    • Cellular function of constitutive GTP binding unknown
    • Whether pseudoGTPase domain mediates protein–protein interactions not tested
  15. 2019 High

    Co-crystal structure of the p120RasGAP N-SH2 domain with pY1105 peptide at 1.6 Å defined the atomic basis for the central activating interaction, while in vivo studies showed p190RhoGAP controls motor axon guidance via both GAP-dependent and GAP-independent mechanisms.

    Evidence X-ray crystallography with ITC (Kd ~0.3 µM) and mutagenesis; mouse mutagenesis screen with GAP-dead mutant axon guidance phenotyping

    PMID:30902550 PMID:31332286 PMID:31891593

    Open questions at the time
    • Full-length p190RhoGAP–p120RasGAP complex structure unavailable
    • Molecular basis of GAP-independent axon guidance function unknown
  16. 2020 High

    Demonstrating that p190RhoGAP cooperates with E-cadherin to activate LATS kinases and phosphorylate YAP revealed a direct mechanism for tumor suppression beyond Rho inactivation, linking p190RhoGAP to Hippo pathway regulation.

    Evidence Xenograft mouse model, LATS kinase assay, YAP phosphorylation, cancer mutant analysis, contact inhibition assays

    PMID:32641858

    Open questions at the time
    • Whether p190RhoGAP activates LATS directly or via an intermediary not resolved
    • Mechanism by which p190RhoGAP induces E-cadherin expression unknown
  17. 2022 High

    Demonstrating that the PLS autoinhibits the GAP domain via an intramolecular interaction, and that cancer-associated PLS mutations (S866F, Δ865–870) abolish autoinhibition, provided a structural explanation for how somatic mutations constitutively activate p190RhoGAP in tumors.

    Evidence Two-hybrid screen, co-IP, cancer mutation analysis, cellular RhoA activity assays

    PMID:36516886

    Open questions at the time
    • Atomic-resolution structure of PLS–GAP interaction not available
    • Whether constitutive GAP activation is oncogenic or tumor-suppressive in different contexts not clarified
  18. 2023 High

    Identification of ZO-2 as a required partner in a tripartite p190RhoGAP–p120RasGAP–ZO-2 complex for Hippo pathway activation established the tight junction as a signaling platform for p190RhoGAP-mediated tumor suppression and contact inhibition.

    Evidence Co-IP, LATS kinase assay, tumorigenesis assays, siRNA knockdown of ZO-2 and RasGAP

    PMID:37995182

    Open questions at the time
    • How ZO-2 connects p190RhoGAP to LATS mechanistically not determined
    • Whether other tight junction proteins participate not tested
  19. 2024 High

    Discovery that the CPLANE protein Fuzzy recruits ARHGAP35 to the basal body for ciliogenesis, confirmed by genetic interaction, identified the upstream targeting mechanism for p190RhoGAP's ciliary function.

    Evidence Co-IP of Fuzzy and ARHGAP35, immunolocalization at basal body, Fuzzy−/− mouse genetics, genetic interaction assay

    PMID:38546045

    Open questions at the time
    • Whether Fuzzy directly binds ARHGAP35 or via a bridging protein not resolved
    • Structural basis of basal body targeting unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • A full-length structural model of p190RhoGAP, the mechanism by which it activates LATS kinases in the Hippo pathway, and the identity of the E3 ubiquitin ligase responsible for mitotic degradation via the N-terminal degron remain unresolved.
  • No full-length structure or cryo-EM model exists
  • E3 ligase for mitotic N-terminal degron unidentified
  • How PLS autoinhibition is relieved by upstream signals is structurally undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 10 GO:0140096 catalytic activity, acting on a protein 6 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005886 plasma membrane 6 GO:0005856 cytoskeleton 3 GO:0005815 microtubule organizing center 2 GO:0005829 cytosol 2 GO:0005929 cilium 2
Pathway
R-HSA-162582 Signal Transduction 9 R-HSA-1640170 Cell Cycle 5 R-HSA-1500931 Cell-Cell communication 3 R-HSA-1266738 Developmental Biology 2 R-HSA-1852241 Organelle biogenesis and maintenance 2
Partners
ABL2ANLNCTNND1CTTNECT2FUZRASA1TJP2
Complex memberships
p190RhoGAP–anillin (cytokinesis)p190RhoGAP–p120RasGAPp190RhoGAP–p120RasGAP–ZO-2 (Hippo activation)

Evidence

Reading pass · 46 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 p190RhoGAP (ARHGAP35) inactivates RhoA downstream of integrin engagement to promote cell spreading, membrane protrusion, and directional migration in fibroblasts; dominant-negative p190RhoGAP elevates RhoA activity, impairs spreading, and blocks polarity establishment Dominant-negative and wild-type overexpression, RhoA activity assays, cell spreading/migration assays Molecular biology of the cell High 11553710
1995 c-Src phosphorylates p190RhoGAP on tyrosine residues; this phosphorylation correlates with EGF-induced actin cytoskeleton remodeling (stress fiber disassembly/reassembly) and p190RhoGAP redistribution into cytoplasmic arc-like structures Dominant-negative/wild-type c-Src overexpression, immunofluorescence confocal microscopy, phosphotyrosine analysis The Journal of cell biology High 7542246
2006 Rac1 activation causes translocation of p190RhoGAP to adherens junctions where it binds p120-catenin; this p120-p190RhoGAP interaction is required for adherens junction assembly and locally inhibits RhoA to coordinate Rac/Rho antagonism downstream of PDGFR Co-immunoprecipitation, knockdown, PDGFR signaling assays, cell fractionation Cell High 17129786
1998 Activation of alpha6beta1 integrin in melanoma cells induces tyrosine phosphorylation of p190RhoGAP and promotes membrane-protrusive activities at invadopodia; microinjection of anti-p190RhoGAP antibodies blocks matrix degradation and invasion Integrin stimulation, tyrosine phosphorylation assays, microinjection of blocking antibodies, invasion assays The Journal of biological chemistry High 9417037
2003 Cadherin engagement induces tyrosine phosphorylation of p190RhoGAP (requiring Src family kinases) and increases its binding to p120RasGAP, leading to RhoA inactivation; dominant-negative p190RhoGAP blocks cadherin-induced RhoA inhibition Active RhoA affinity pulldown to isolate activated GAPs, co-immunoprecipitation, PP2 inhibitor, dominant-negative expression The Journal of biological chemistry High 12606561
2005 Focal adhesion kinase (FAK) associates with and directly phosphorylates p190RhoGAP in vitro, suppressing RhoA activity; FAK-mediated p190RhoGAP activation is required for endothelial barrier restoration after thrombin-induced permeability increase In vitro kinase assay (recombinant FAK phosphorylating p190RhoGAP), co-immunoprecipitation, dominant-negative FAK (FRNK) adenoviral expression, RhoA activity assay The Journal of biological chemistry High 16308318
2004 The Arg (Abl-related gene) tyrosine kinase phosphorylates p190RhoGAP at Y1105 in vitro and in vivo; this phosphorylation promotes p190RhoGAP association with p120RasGAP, stimulates p190RhoGAP RhoGAP activity, and is required for adhesion-dependent RhoA inhibition and neuritogenesis In vitro kinase assay, site-directed mutagenesis (Y1105), co-immunoprecipitation, arg-/- fibroblasts/neurons, Rho activity assay Current biology : CB High 15084284
2006 Integrin signaling through the Arg kinase activates p190RhoGAP by promoting its association with p120RasGAP, which recruits p190RhoGAP to the cell periphery; p120 binding is required for in vivo but not in vitro p190RhoGAP activation, demonstrating that membrane recruitment is the critical activation mechanism arg-/- fibroblasts, dominant-negative p120 fragment, cell fractionation, in vitro GAP assay, co-immunoprecipitation Molecular biology of the cell High 16971514
2007 Arg kinase acts through p190RhoGAP to suppress RhoA activity, attenuate actomyosin contractility, and regulate focal adhesion dynamics; the Arg N-terminal kinase domain suffices to reduce stress fibers via p190RhoGAP, while full focal adhesion inhibition also requires the Arg C-terminal cytoskeleton-binding domain arg-/- fibroblasts, Arg domain mutant re-expression, myosin activity assays, focal adhesion quantification Molecular biology of the cell High 17652459
2007 p190RhoGAP localizes to dendritic spines in hippocampal neurons; its activity is reduced in arg-/- mice, causing elevated RhoA activity and failure of dendritic spine maturation, with subsequent synapse and dendrite loss; reducing ROCKII gene dosage suppresses dendritic regression in arg-/- mice (epistasis) arg-/- mouse genetics, ROCKII heterozygosity epistasis, immunolocalization, RhoA activity assay The Journal of neuroscience High 17928439
2009 FAK promotes formation of a FAK-p120RasGAP-p190RhoGAP complex at leading-edge focal adhesions via fibronectin-integrin signaling; FAK Y397 phosphorylation mediates SH2-dependent binding of p120RasGAP, facilitating p190RhoGAP tyrosine phosphorylation and RhoA inhibition required for cell polarity during migration Wound healing/Golgi reorientation polarity assays, co-immunoprecipitation, FAK Y397 mutant, Pyk2-FAK chimera reconstitution, p120RasGAP knockdown Journal of cell science High 19435801
2008 alpha5beta1 integrin engagement triggers Src-dependent tyrosine phosphorylation of p190RhoGAP, while syndecan-4 engagement causes PKC-alpha-dependent redistribution of phosphorylated p190RhoGAP to the membrane; both pathways must converge on p190RhoGAP for efficient RhoA suppression and focal adhesion formation Integrin/syndecan-4 engagement experiments, cell fractionation, PKC-alpha mutants, siRNA knockdown, RhoA activity assay The Journal of cell biology High 18541700
2008 Rho-kinase phosphorylates p190A RhoGAP at Ser1150, impairing its GAP activity by disrupting Rnd binding; this creates a positive feedback loop sustaining RhoA activation in response to high-dose endothelin-1 in vascular smooth muscle cells In vitro kinase assay, phosphomimetic and phosphoresistant mutants, Rnd binding assays, RhoA activity assay in VSMCs The Journal of biological chemistry High 19103606
2008 Breast tumor kinase (Brk) phosphorylates p190RhoGAP-A at Y1105 in vitro and in vivo, promoting its association with p120RasGAP; this simultaneously activates p190RhoGAP (inactivating RhoA) and attenuates p120RasGAP (activating Ras), driving breast cancer proliferation and invasion In vitro kinase assay, Y1105 mutagenesis, co-immunoprecipitation, RhoA/Ras activity assays, invasion/migration/transformation assays Cancer research High 18829532
2003 p190RhoGAP is cell cycle-regulated: endogenous protein levels decrease in late mitosis via ubiquitin-mediated proteasomal degradation requiring the N-terminal GTP-binding region; overexpression causes abnormal cleavage furrow positioning and cytokinesis failure in a GAP-domain-dependent manner Conditional/transient overexpression, confocal localization during cytokinesis, proteasome inhibition, ubiquitination assays The Journal of cell biology High 14610059
2009 p190RhoGAP localizes to the cleavage furrow and reduces RhoA-GTP levels there in a dose-dependent manner as measured by FRET biosensor; overexpression causes multiple cycles of abnormal furrow site selection and ingression/regression, while ECT2 (RhoGEF) and p190RhoGAP colocalize at the furrow and physically interact to antagonistically regulate RhoA-GTP FRET-based RhoA biosensor, time-lapse microscopy, co-immunoprecipitation of ECT2 and p190RhoGAP Experimental cell research High 18642445 19254711
2010 Mitotic reduction of p190RhoGAP levels is required for successful cytokinesis; a degradation-resistant p190RhoGAP mutant causes cytokinesis failure dependent on GAP activity; the N-terminal GBDS1 region (four residues) is necessary and sufficient for mitotic ubiquitination and degradation RNAi reconstitution with degradation-resistant mutant, domain mapping, cytokinesis assays The Journal of biological chemistry High 20534586
2014 p190RhoGAP-A forms a complex with the cytokinetic organizer anillin; p190RhoGAP-A depletion causes excess RhoA-GTP at the furrow and cytokinesis failure; mutants unable to bind anillin or lacking GAP activity fail to rescue; excess contractility is the proximate cause (rescued by myosin II inhibitor blebbistatin) Depletion/rescue with anillin-binding and GAP-dead mutants, RhoA-GTP measurement, blebbistatin rescue Journal of cell science High 25359885
2009 GSK-3beta phosphorylates p190A RhoGAP in a priming-dependent manner at C-terminal tail residues, inhibiting p190A GAP activity in vitro and in vivo; p190A-deficient fibroblasts show directional migration defects, and this requires GSK-3beta-mediated phosphorylation In vitro GAP activity assay with GSK-3beta phosphorylation, p190A-deficient fibroblasts, phospho-site mutagenesis, directional migration assays The Journal of biological chemistry High 18502760
2009 Acidic phospholipids inhibit p190A RhoGAP activity toward Rho and promote its RacGAP activity; PKC phosphorylation at Ser1221 and Thr1226 within a polybasic region prevents phospholipid binding, thereby reversing this substrate preference switch In vitro GAP/RacGAP activity assays, liposome binding assays, PKC phosphorylation, site-directed mutagenesis Biochemistry High 19673492
2013 p190RhoGAP has cellular RacGAP activity that requires an intact polybasic region adjacent to the GAP domain; this same region inhibits RhoGAP activity in cells, enabling p190RhoGAP to alternately suppress Rac or Rho depending on polybasic region status Cellular Rac/Rho activity assays with polybasic region mutants Cellular signalling Medium 23499677
2007 Actin cytoskeleton rearrangements during cell spreading suppress RhoA by promoting accumulation of p190RhoGAP in lipid rafts; the cytoskeletal protein filamin controls this p190RhoGAP redistribution, as cells lacking filamin (or expressing calpain-resistant filamin) fail to accumulate p190RhoGAP in rafts Lipid raft fractionation, siRNA knockdown of p190RhoGAP, filamin knockout/mutant cells, RhoA activity assay Journal of cell science High 17227794
2011 Caveolin-1 deficiency leads to eNOS activation and peroxynitrite generation, which selectively nitrates p190RhoGAP-A at Tyr1105, impairing its GAP activity and activating RhoA, causing adherens junction disassembly and endothelial hyperpermeability; thrombin similarly induces nitration of p120-catenin-associated p190RhoGAP-A Cav-1-/- endothelial cells, nitrotyrosine immunoprecipitation, eNOS inhibition, in vitro GAP activity assay with nitrated protein The Journal of cell biology High 21624953
2009 SHP2 phosphatase maintains p190A RhoGAP basally phosphorylated and active (via c-Abl); angiotensin II AT1R activation induces SHP2-mediated dephosphorylation of p190A, inactivating it and enabling RhoA activation; phosphomimetic p190A mutants block ANG II-induced RhoA activation siRNA knockdown of p190A and SHP2, phospho-mutant overexpression (phosphoresistant, phosphomimetic), RhoA-kinase activity assays in VSMCs American journal of physiology. Cell physiology High 19692654
2010 ERK activity is required for fibronectin-stimulated RhoA-GTP loading; ERK phosphorylates the C-terminus of p190A RhoGAP to reduce its peripheral localization and GAP activity, thereby promoting Rho-dependent focal adhesion maturation MEK/ERK inhibitors, phospho-site mapping of p190A C-terminus, localization assays, focal adhesion quantification, RhoA activity assay Molecular and cellular biology High 20439493
2006 Cell surface transglutaminase (tTG) activates RhoA by clustering integrins, which inhibits Src kinase activity and decreases Src-mediated activation of p190RhoGAP; pharmacological Src inhibition reproduces the RhoA activation, placing tTG upstream of Src-p190RhoGAP tTG overexpression, integrin cross-linking, Src inhibitor (PP2), p190RhoGAP activation measurement, RhoA activity assay Molecular biology of the cell Medium 16452636
2016 p190A RhoGAP contains a protrusion localization sequence (PLS) that is necessary and sufficient for targeting to leading-edge actin protrusions; cortactin binds the PLS and is required for p190A recruitment to protrusions; the PLS also negatively regulates GAP activity; cancer-associated PLS mutations disrupt both localization and function Truncation mutagenesis, co-immunoprecipitation with cortactin, subcellular localization assays, RhoA activity assays, cancer mutation analysis The Journal of cell biology High 27646271
2022 The PLS of p190A RhoGAP acts as an autoinhibitory domain that masks the GAP domain; the PLS interacts with a region adjacent to the GAP domain in cis (intramolecular interaction); cancer-associated PLS mutations (S866F, Δ865-870) abolish this autoinhibitory interaction, constitutively activating GAP function Two-hybrid screen, co-immunoprecipitation, cancer mutation analysis, cellular RhoA activity assays The Journal of biological chemistry High 36516886
2013 p190RhoGAP interacts with a 23-amino-acid stretch (residues 820-843, CRAD) in the C-terminal domain of p120-catenin; this interaction is required for membrane targeting of p190RhoGAP and activation of its GAP activity at cell-cell junctions, reciprocally suppressing RhoA and activating Rac1 to protect endothelial barrier function p120-catenin truncation mutants, p190RhoGAP membrane fractionation, RhoA/Rac1 activity assays, barrier permeability assays The Journal of biological chemistry High 23653363
2018 Crystal structure of the N-terminal GTPase domain of p190RhoGAP-A co-purified with GTP reveals an unusual GTP-Mg2+ binding pocket with six inserts that prevent catalytic activity and interactions with canonical GTPase regulators; mutational analysis shows GTP/Mg2+ binding stabilizes the domain; this establishes N-GTPase as a third pseudoGTPase domain in p190RhoGAP X-ray crystallography (2.8 Å), biochemical GTP hydrolysis assay, mutagenesis, nucleotide exchange assays Structure High 30174148
2019 The p120RasGAP N-terminal SH2 domain binds the phosphorylated Y1105-containing peptide of p190RhoGAP (EEENI[pY]SVPHDST) via the conserved FLVR arginine (R207); crystal structure at 1.6 Å reveals peptide binding stabilizes the βE-βF loop and specific arginine conformations; dissociation constant ~0.3 μM X-ray crystallography (1.75 and 1.6 Å co-crystal), isothermal titration calorimetry, site-directed mutagenesis, native gel shift PloS one High 31891593
2009 NMR structure of the first FF domain of p190A RhoGAP (RhoGAPFF1) reveals a non-canonical α1-α2-α3-α4 topology; Y308 is buried in the hydrophobic core and inaccessible to kinases in the folded state; phosphorylation by PDGFR-alpha requires prior domain unfolding and causes irreversible destabilization, providing a mechanism for inhibition of TFII-I interaction NMR spectroscopy, thermal unfolding assays, in vitro phosphorylation at different temperatures Journal of molecular biology High 19393245
2021 HNRNPL facilitates back-splicing of ARHGAP35 exons 2-3 to produce circARHGAP35, which is translated via an m6A-modified start codon into a truncated protein containing four FF domains but lacking the RhoGAP domain; this truncated protein promotes cancer progression by interacting with TFII-I in the nucleus circRNA identification, m6A sequencing, ORF translation assay, co-immunoprecipitation with TFII-I, HNRNPL knockdown Advanced science Medium 34258149
2016 p190A RhoGAP is required for primary cilium formation in renal nephrons; a GAP-domain mutation (L1396Q) reduces GAP activity toward RhoA and Rac1, causes glomerulocystic kidneys in mice; p190A localizes to the base of cilia; ROCK inhibition or F-actin polymerization blockade rescues ciliogenesis defects ENU mutagenesis, in vitro GAP activity assay with L1396Q mutant, immunolocalization, ROCK/F-actin inhibitor rescue, kidney phenotype analysis PLoS genetics High 26859289
2020 Polycystin-1 (PC1) regulates ARHGAP35 localization at centrosomes; PKD1-null cystic cells show decreased centrosomal ARHGAP35 associated with increased centrosomal active RhoA and ROCK signaling; ROCK inhibition reduces cyst expansion in vitro and in Pkd1 mouse models Centrosome-targeted proximity ligation assay, dual immunofluorescence, cilia length as phenotypic readout, ROCK inhibitor in 3D cyst assay and mouse model JCI insight Medium 32663194
2019 The E3 ubiquitin ligase TRIM65 directly ubiquitinates and promotes proteasomal degradation of ARHGAP35; TRIM65 overexpression elevates RhoA GTPase activity and enhances CRC metastasis; forced ARHGAP35 expression rescues TRIM65-induced migration phenotypes Co-immunoprecipitation, ubiquitination assay, rescue experiments, in vivo metastasis mouse model Oncogene High 31332286
2020 p190A RhoGAP promotes mesenchymal-to-epithelial transition, induces CDH1/E-cadherin expression, and cooperates with E-cadherin to activate LATS kinases and phosphorylate YAP, suppressing tumor growth; p190A is obligatory for E-cadherin to activate LATS kinases; cancer-associated p190A mutants lack these activities Xenograft mouse model, LATS kinase assay, YAP phosphorylation assay, cancer mutant functional analysis, contact inhibition assays Oncogene High 32641858
2023 p190A RhoGAP activates the Hippo pathway via a complex requiring both p120 RasGAP and the tight junction protein ZO-2; ZO-2 interaction with p190A is dependent on RasGAP; RasGAP and ZO-2 are both necessary for p190A-mediated LATS kinase activation, MET, contact inhibition, and tumor suppression Co-immunoprecipitation, LATS kinase assay, tumorigenesis assays, siRNA knockdown of ZO-2 and RasGAP Cell reports High 37995182
2016 p190A interacts with all 13 eIF3 subunits and other translational preinitiation factors via its first FF motif (FF1) and the winged helix/PCI domain of eIF3A; the interaction is phosphorylation-dependent (S296 in FF1), serum-stimulated, and the p190A/eIF3 complex is distinct from eIF3-S6K1 or eIF3-mTOR complexes Tandem mass spectrometry of endogenous p190A complex, co-immunoprecipitation, site-directed mutagenesis (S296A, Y308), phosphatase treatment The Journal of biological chemistry Medium 28007963
2019 p190RhoGAP acts as a critical regulator of motor axon guidance in mice via two mechanisms: a GAP-independent mode that transiently suppresses attraction to Netrin-1 while axons exit the spinal cord, and a GAP-dependent mode that enables RhoA inhibition for targeting specific muscles; identified by mouse mutagenesis screen Mouse mutagenesis screen, GAP-dead mutant analysis, motor axon guidance phenotyping Neuron High 30902550
2024 The CPLANE protein Fuzzy interacts with ARHGAP35 (p190A RhoGAP) and recruits it to the basal body of primary cilia; loss of Fuzzy reduces ARHGAP35 at the basal body, increases RhoA activity and actin polymerization there, and impairs ciliogenesis; genetic interaction between Fuzzy and Arhgap35 alleles confirmed Co-immunoprecipitation of Fuzzy and ARHGAP35, immunolocalization at basal body, Fuzzy-/- mouse genetics, genetic interaction assay Development High 38546045
2018 In IPF fibroblasts, Rnd3 expression and p190RhoGAP activity are both suppressed; restoration of Rnd3 levels increases p190RhoGAP activity and decreases RhoA activity, reducing the fibrotic phenotype; the IPF drugs nintedanib and pirfenidone decrease fibrosis through upregulation of Rnd3 and p190RhoGAP activity Rnd3 restoration in IPF fibroblasts, p190RhoGAP GAP activity assay, RhoA activity assay, pharmacological treatment Molecular biology of the cell Medium 29995590
2009 p190RhoGAP and ECT2 (RhoGEF) physically associate (co-immunoprecipitation) and colocalize at the cleavage furrow; ECT2 rescues p190-induced multinucleation in a dose-dependent manner; their opposing activities on RhoA-GTP together determine cytokinesis outcome Co-immunoprecipitation, colocalization, Rho pull-down assay, multinucleation rescue assay Cell cycle Medium 18642445
2014 HPV16 E7 protein binds p190RhoGAP via conserved region 3 (CR3) of E7 and the middle domain of p190RhoGAP; E7 proteins from multiple HPV types bind p190RhoGAP; this interaction dysregulates p190RhoGAP GAP activity, alters the actin cytoskeleton, and negatively regulates cell spreading on fibronectin Mass spectrometry identification, co-immunoprecipitation, CR3 mutagenesis, domain mapping, cell spreading assay Journal of virology Medium 24403595
2018 p190RhoGAP depletion causes multipolar spindle formation and prolonged mitotic arrest; p190RhoGAP-depleted multipolar cells localize Aurora A to all poles but activate it only at centriolar poles; Eg5 inhibitor rescue indicates excess Eg5-generated forces underlie the multipolar spindle; defining a role for p190RhoGAP in spindle pole integrity independent of RhoA siRNA depletion, Aurora A activation assay, Eg5 inhibitor rescue, spindle pole analysis by microscopy Chromosoma Medium 29656322
2023 p120RasGAP SH2 domains interact with three doubly phosphorylated partners with distinct binding modes: p190RhoGAP binding engages both SH2 domains with high affinity (~μM), EphB4 binds with ~100-fold lower affinity via single SH2 domain; SAXS reveals distinct conformational states; none of these interactions affect RasGAP catalytic activity Isothermal titration calorimetry, small-angle X-ray scattering (SAXS), in vitro GAP activity assay The Journal of biological chemistry High 37507023

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2001 RhoA inactivation by p190RhoGAP regulates cell spreading and migration by promoting membrane protrusion and polarity. Molecular biology of the cell 388 11553710
2006 p120-catenin and p190RhoGAP regulate cell-cell adhesion by coordinating antagonism between Rac and Rho. Cell 338 17129786
1995 c-Src regulates the simultaneous rearrangement of actin cytoskeleton, p190RhoGAP, and p120RasGAP following epidermal growth factor stimulation. The Journal of cell biology 224 7542246
1998 Activation of beta1 integrin signaling stimulates tyrosine phosphorylation of p190RhoGAP and membrane-protrusive activities at invadopodia. The Journal of biological chemistry 170 9417037
2003 Cadherin engagement inhibits RhoA via p190RhoGAP. The Journal of biological chemistry 143 12606561
2005 Suppression of RhoA activity by focal adhesion kinase-induced activation of p190RhoGAP: role in regulation of endothelial permeability. The Journal of biological chemistry 131 16308318
2009 A FAK-p120RasGAP-p190RhoGAP complex regulates polarity in migrating cells. Journal of cell science 120 19435801
2021 HNRNPL Circularizes ARHGAP35 to Produce an Oncogenic Protein. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 108 34258149
2007 Inhibition of Rho via Arg and p190RhoGAP in the postnatal mouse hippocampus regulates dendritic spine maturation, synapse and dendrite stability, and behavior. The Journal of neuroscience : the official journal of the Society for Neuroscience 103 17928439
2006 Integrin signaling through Arg activates p190RhoGAP by promoting its binding to p120RasGAP and recruitment to the membrane. Molecular biology of the cell 103 16971514
2006 Cell surface transglutaminase promotes RhoA activation via integrin clustering and suppression of the Src-p190RhoGAP signaling pathway. Molecular biology of the cell 102 16452636
2008 p190RhoGAP is the convergence point of adhesion signals from alpha 5 beta 1 integrin and syndecan-4. The Journal of cell biology 91 18541700
2007 Filamin links cell shape and cytoskeletal structure to Rho regulation by controlling accumulation of p190RhoGAP in lipid rafts. Journal of cell science 84 17227794
2004 Adhesion-dependent regulation of p190RhoGAP in the developing brain by the Abl-related gene tyrosine kinase. Current biology : CB 83 15084284
1985 Structural requirements for the activation of rat anterior pituitary adenylate cyclase by growth hormone-releasing factor (GRF): discovery of (N-Ac-Tyr1, D-Arg2)-GRF(1-29)-NH2 as a GRF antagonist on membranes. Endocrinology 83 2994998
2011 Caveolin-1-eNOS signaling promotes p190RhoGAP-A nitration and endothelial permeability. The Journal of cell biology 82 21624953
2003 p190RhoGAP can act to inhibit PDGF-induced gliomas in mice: a putative tumor suppressor encoded on human chromosome 19q13.3. Genes & development 73 12600941
2008 Breast tumor kinase phosphorylates p190RhoGAP to regulate rho and ras and promote breast carcinoma growth, migration, and invasion. Cancer research 71 18829532
2007 The Abl-related gene tyrosine kinase acts through p190RhoGAP to inhibit actomyosin contractility and regulate focal adhesion dynamics upon adhesion to fibronectin. Molecular biology of the cell 71 17652459
2003 p190RhoGAP is cell cycle regulated and affects cytokinesis. The Journal of cell biology 62 14610059
2013 Interaction of p190RhoGAP with C-terminal domain of p120-catenin modulates endothelial cytoskeleton and permeability. The Journal of biological chemistry 59 23653363
2006 PTP-PEST couples membrane protrusion and tail retraction via VAV2 and p190RhoGAP. The Journal of biological chemistry 56 16513648
2019 Exosome-delivered syndecan-1 rescues acute lung injury via a FAK/p190RhoGAP/RhoA/ROCK/NF-κB signaling axis and glycocalyx enhancement. Experimental cell research 55 31487506
2019 Ubiquitin ligase TRIM65 promotes colorectal cancer metastasis by targeting ARHGAP35 for protein degradation. Oncogene 54 31332286
2008 Rho-kinase contributes to sustained RhoA activation through phosphorylation of p190A RhoGAP. The Journal of biological chemistry 53 19103606
2009 Overexpression of E-cadherin on melanoma cells inhibits chemokine-promoted invasion involving p190RhoGAP/p120ctn-dependent inactivation of RhoA. The Journal of biological chemistry 51 19293150
2009 Tks5 recruits AFAP-110, p190RhoGAP, and cortactin for podosome formation. Experimental cell research 51 19540230
2000 p190-A, a human tumor suppressor gene, maps to the chromosomal region 19q13.3 that is reportedly deleted in some gliomas. Gene 48 11054565
2010 p190RhoGAP mediates protective effects of oxidized phospholipids in the models of ventilator-induced lung injury. Experimental cell research 45 21111731
2009 Angiotensin II induces RhoA activation through SHP2-dependent dephosphorylation of the RhoGAP p190A in vascular smooth muscle cells. American journal of physiology. Cell physiology 44 19692654
2009 Regulation of the substrate preference of p190RhoGAP by protein kinase C-mediated phosphorylation of a phospholipid binding site. Biochemistry 41 19673492
2008 p190A RhoGAP is a glycogen synthase kinase-3-beta substrate required for polarized cell migration. The Journal of biological chemistry 40 18502760
2006 p190-RhoGAP as an integral component of the Tiam1/Rac1-induced downregulation of Rho. Biological chemistry 39 16542153
2010 Extracellular signal-regulated kinase promotes Rho-dependent focal adhesion formation by suppressing p190A RhoGAP. Molecular and cellular biology 35 20439493
2010 Neurite outgrowth from PC12 cells by basic fibroblast growth factor (bFGF) is mediated by RhoA inactivation through p190RhoGAP and ARAP3. Journal of cellular physiology 35 20578246
2004 RACK1 regulates Src-mediated Sam68 and p190RhoGAP signaling. Oncogene 34 15184885
2020 Polycystin-1 regulates ARHGAP35-dependent centrosomal RhoA activation and ROCK signaling. JCI insight 33 32663194
2011 Cyclic AMP response element-binding protein prevents endothelial permeability increase through transcriptional controlling p190RhoGAP expression. Blood 33 22049513
2009 p190RhoGAP negatively regulates Rho activity at the cleavage furrow of mitotic cells. Experimental cell research 33 19254711
1998 Rapid recruitment of p120RasGAP and its associated protein, p190RhoGAP, to the cytoskeleton during integrin mediated cell-substrate interaction. Oncogene 33 9690509
2013 RhoA is down-regulated at cell-cell contacts via p190RhoGAP-B in response to tensional homeostasis. Molecular biology of the cell 32 23552690
2010 p190RhoGAP and Rap-dependent RhoGAP (ARAP3) inactivate RhoA in response to nerve growth factor leading to neurite outgrowth from PC12 cells. Experimental & molecular medicine 32 20200473
2010 Neutrophil functions and autoimmune arthritis in the absence of p190RhoGAP: generation and analysis of a novel null mutation in mice. Journal of immunology (Baltimore, Md. : 1950) 32 20675588
2014 A complex of p190RhoGAP-A and anillin modulates RhoA-GTP and the cytokinetic furrow in human cells. Journal of cell science 31 25359885
2012 Folic acid inhibits endothelial cell migration through inhibiting the RhoA activity mediated by activating the folic acid receptor/cSrc/p190RhoGAP-signaling pathway. Biochemical pharmacology 31 23178654
2008 Activated G(alpha)13 impairs cell invasiveness through p190RhoGAP-mediated inhibition of RhoA activity. Cancer research 31 18922893
2001 Role of p190RhoGAP in beta 2 integrin regulation of RhoA in human neutrophils. Journal of immunology (Baltimore, Md. : 1950) 31 11342655
2009 Cdk5-dependent regulation of Rho activity, cytoskeletal contraction, and epithelial cell migration via suppression of Src and p190RhoGAP. Molecular and cellular biology 27 19822667
2008 Opposing roles of p190RhoGAP and Ect2 RhoGEF in regulating cytokinesis. Cell cycle (Georgetown, Tex.) 26 18642445
2016 Cancer-associated mutations in the protrusion-targeting region of p190RhoGAP impact tumor cell migration. The Journal of cell biology 25 27646271
2011 β3 integrin-EGF receptor cross-talk activates p190RhoGAP in mouse mammary gland epithelial cells. Molecular biology of the cell 25 21937717
2020 p190A inactivating mutations cause aberrant RhoA activation and promote malignant transformation via the Hippo-YAP pathway in endometrial cancer. Signal transduction and targeted therapy 23 32457342
2018 A Rnd3/p190RhoGAP pathway regulates RhoA activity in idiopathic pulmonary fibrosis fibroblasts. Molecular biology of the cell 22 29995590
2016 A Point Mutation in p190A RhoGAP Affects Ciliogenesis and Leads to Glomerulocystic Kidney Defects. PLoS genetics 21 26859289
2010 Mitotic down-regulation of p190RhoGAP is required for the successful completion of cytokinesis. The Journal of biological chemistry 21 20534586
2013 p190RhoGAP has cellular RacGAP activity regulated by a polybasic region. Cellular signalling 19 23499677
2016 Symmetry breaking in spreading RAT2 fibroblasts requires the MAPK/ERK pathway scaffold RACK1 that integrates FAK, p190A-RhoGAP and ERK2 signaling. Biochimica et biophysica acta 18 27212270
2011 Interplay between FAK, PKCδ, and p190RhoGAP in the regulation of endothelial barrier function. Microvascular research 18 21549132
2011 P190A RhoGAP is required for mammary gland development. Developmental biology 18 21945077
1984 The effects of long term growth hormone releasing factor (GRF 1-40) administration on growth hormone secretion and synthesis in vitro. Biochemical and biophysical research communications 18 6428404
2013 p190A RhoGAP is involved in EGFR pathways and promotes proliferation, invasion and migration in lung adenocarcinoma cells. International journal of oncology 17 24043274
2019 p190RhoGAP Filters Competing Signals to Resolve Axon Guidance Conflicts. Neuron 16 30902550
2024 The m6A demethylases FTO and ALKBH5 aggravate the malignant progression of nasopharyngeal carcinoma by coregulating ARHGAP35. Cell death discovery 14 38263362
2020 p190A RhoGAP induces CDH1 expression and cooperates with E-cadherin to activate LATS kinases and suppress tumor cell growth. Oncogene 14 32641858
2016 Interaction of p190A RhoGAP with eIF3A and Other Translation Preinitiation Factors Suggests a Role in Protein Biosynthesis. The Journal of biological chemistry 14 28007963
2011 The Tumor Suppressor, p190RhoGAP, Differentially Initiates Apoptosis and Confers Docetaxel Sensitivity to Breast Cancer Cells. Genes & cancer 13 21779478
2014 The human papillomavirus E7 proteins associate with p190RhoGAP and alter its function. Journal of virology 12 24403595
2022 ARHGAP35 is a novel factor disrupted in human developmental eye phenotypes. European journal of human genetics : EJHG 11 36450800
2018 Growth inhibition of KRAS‑ and EGFR‑mutant lung adenocarcinoma by cosuppression of STAT3 and the SRC/ARHGAP35 axis. Oncology reports 11 30015929
2018 The N-Terminal GTPase Domain of p190RhoGAP Proteins Is a PseudoGTPase. Structure (London, England : 1993) 11 30174148
2014 A Blk-p190RhoGAP signaling module downstream of activated Gα13 functionally opposes CXCL12-stimulated RhoA activation and cell invasion. Cellular signalling 11 25025568
2004 A possible role for p190RhoGAP in PKCepsilon-induced morphological effects. Cellular signalling 11 14636894
2019 Crystal structures of p120RasGAP N-terminal SH2 domain in its apo form and in complex with a p190RhoGAP phosphotyrosine peptide. PloS one 10 31891593
2017 Regulation of Rho GTPase activity at the leading edge of migrating cells by p190RhoGAP. Small GTPases 10 28287334
2014 Domain contributions to signaling specificity differences between Ras-guanine nucleotide releasing factor (Ras-GRF) 1 and Ras-GRF2. The Journal of biological chemistry 10 24755227
2009 NMR structural studies on human p190-A RhoGAPFF1 revealed that domain phosphorylation by the PDGF-receptor alpha requires its previous unfolding. Journal of molecular biology 10 19393245
2023 Extracellular matrix stiffness mediates uterine repair via the Rap1a/ARHGAP35/RhoA/F-actin/YAP axis. Cell communication and signaling : CCS 9 36691027
2014 Concise review: Mechanotransduction via p190RhoGAP regulates a switch between cardiomyogenic and endothelial lineages in adult cardiac progenitors. Stem cells (Dayton, Ohio) 9 24710857
2014 Cdc42 and p190RhoGAP activation by CCN2 regulates cell spreading and polarity and induces actin disassembly in migrating keratinocytes. International wound journal 9 25185742
1991 An analogue of growth hormone releasing factor (GRF), (Ac-Try1, D-Phe2)-GRF-(1-29), specifically antagonizes the facilitation of the flexor reflex induced by intrathecal vasoactive intestinal peptide in rat spinal cord. Neuropeptides 9 2067598
2023 Diverse p120RasGAP interactions with doubly phosphorylated partners EphB4, p190RhoGAP, and Dok1. The Journal of biological chemistry 8 37507023
1995 Study of the activation mechanism of human GRF(1-29)NH2 on rat mast cell histamine release. Inflammation research : official journal of the European Histamine Research Society ... [et al.] 8 7544679
2018 PseudoGTPase domains in p190RhoGAP proteins: a mini-review. Biochemical Society transactions 7 30514771
2022 Tumor-derived ARHGAP35 mutations enhance the Gα13-Rho signaling axis in human endometrial cancer. Cancer gene therapy 6 36257976
2024 The CPLANE protein Fuzzy regulates ciliogenesis by suppressing actin polymerization at the base of the primary cilium via p190A RhoGAP. Development (Cambridge, England) 5 38546045
2006 Transforming growth factor beta regulates the expression of the M2 muscarinic receptor in atrial myocytes via an effect on RhoA and p190RhoGAP. The Journal of biological chemistry 5 16707504
1987 Plasma growth hormone (GH) responses to growth hormone releasing factor (hp GRF 1-44) in familial GH deficiency. Acta paediatrica Scandinavica 5 3105240
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
2023 p120 RasGAP and ZO-2 are essential for Hippo signaling and tumor-suppressor function mediated by p190A RhoGAP. Cell reports 3 37995182
1999 Expression of p190A during apoptosis in the regressing rat ventral prostate. Endocrinology 3 10385430
2023 p120 RasGAP and ZO-2 are essential for Hippo signaling and tumor suppressor function mediated by p190A RhoGAP. bioRxiv : the preprint server for biology 2 37292741
2018 P190RhoGAP prevents mitotic spindle fragmentation and is required to activate Aurora A kinase at acentriolar poles. Chromosoma 2 29656322
2023 The Muscarinic Acetylcholine M2 Receptor-Induced Nitration of p190A by eNOS Increases RhoA Activity in Cardiac Myocytes. Cells 1 37887276
2022 Evaluation of a Patient With Non-Myoinvasive Uterine Serous Carcinoma Confined to a Polyp and Positive Peritoneal Washings With Somatic ARHGAP35 and KRAS Mutations. Cureus 1 35949786
2022 Identification of an inhibitory domain in GTPase-activating protein p190RhoGAP responsible for masking its functional GAP domain. The Journal of biological chemistry 1 36516886
2005 Interactions of GRF(1-29)NH2 with plasma proteins and their effects on the release of the peptide from a PLAGA matrix. Journal of controlled release : official journal of the Controlled Release Society 1 15987661
1991 A comparison of the biological activities of authentic rat GRF(1-43)OH with the analogue rat GRF(1-29)NH2. Canadian journal of physiology and pharmacology 1 1829020
2025 A genome-wide screen identified ARHGAP35 as a regulator of regorafenib resistance in liver cancer. Anti-cancer drugs 0 41176659
2025 Loss of p190A RhoGAP induces aneuploidy and enhances bladder cancer cell migration and invasion by modulating actin dynamics. Scientific reports 0 41253923
2024 Backbone 1H, 15N, and 13C resonance assignments of the FF1 domain from P190A RhoGAP in 5 and 8 M urea. Biomolecular NMR assignments 0 39402262