Affinage

ARHGAP35

Rho GTPase-activating protein 35 · UniProt Q9NRY4

Length
1499 aa
Mass
170.5 kDa
Annotated
2026-06-09
100 papers in source corpus 48 papers cited in narrative 48 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ARHGAP35 (p190RhoGAP-A) is a multidomain GTPase-activating protein that functions as a central convergence node for inactivating RhoA downstream of adhesion and growth-factor signaling, thereby controlling actomyosin contractility, cell spreading, migration, and polarity (PMID:11553710, PMID:18541700). Its activation is driven by adhesion-dependent tyrosine phosphorylation—catalyzed by c-Src, the Arg/Abl2 kinase, FAK, and the tumor kinase Brk—primarily at Tyr1105, a modification that creates a phosphopeptide bound with high affinity by the p120RasGAP SH2 domain via the FLVR-motif arginine R207 (PMID:7542246, PMID:15084284, PMID:16308318, PMID:18829532, PMID:31891593). This p190–p120RasGAP association does not directly stimulate catalysis but instead drives recruitment of the complex to the membrane, leading-edge focal adhesions, lipid rafts, and cadherin junctions, where RhoA suppression occurs (PMID:16971514, PMID:19435801, PMID:17227794, PMID:17129786). At adherens junctions p190 couples to the cadherin complex through p120-catenin, which binds a defined C-terminal CRAD segment and is required for membrane translocation, RhoA suppression, and junction assembly (PMID:17129786, PMID:23653363). ARHGAP35 integrates signals from integrins, syndecan-4/PKCα, RTKs, and Rac/Tiam1, acting as the shared point at which these inputs converge to suppress RhoA (PMID:18541700, PMID:16542153). Its output is tuned by an extensive regulatory layer: ROCK-mediated Ser1150 phosphorylation provides feedback inhibition by impairing Rnd binding (PMID:19103606), GSK-3β and ERK phosphorylate the C-terminus to control polarity and localization (PMID:18502760, PMID:20439493), PKC phosphorylation within a polybasic region blocks acidic-phospholipid binding and shifts substrate preference between RhoA and Rac1 (PMID:19673492, PMID:23499677), and eNOS-dependent nitration at Tyr1105 inactivates the GAP and can redirect substrate specificity toward Rac1 (PMID:21624953, PMID:37887276). The protein is also autoinhibited by an intramolecular interaction between its protrusion-localization sequence (PLS) and the GAP domain, an interaction disrupted by cancer-associated mutations (PMID:36516886, PMID:27646271); its N-terminal domain is a pseudoGTPase that constitutively binds GTP without hydrolysis and serves as a protein-interaction platform (PMID:30174148). ARHGAP35 governs cytokinesis by suppressing RhoA at the cleavage furrow in complex with anillin, and its ubiquitin-proteasome-mediated mitotic degradation is required for furrow progression and abscission (PMID:19254711, PMID:25359885, PMID:20534586). Beyond contractility, it promotes ciliogenesis at the basal body—where it is recruited by Fuzzy to restrict actin polymerization—and acts as an upstream activator of the Hippo–LATS–YAP pathway, cooperating with p120RasGAP, ZO-2, and E-cadherin to drive contact inhibition of proliferation and suppress tumorigenesis (PMID:38546045, PMID:26859289, PMID:32457342, PMID:32641858, PMID:37995182).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1995 High

    Established that p190RhoGAP is a tyrosine-phosphorylation substrate linking Src-family kinase activity to actin cytoskeleton remodeling, framing it as a regulated effector rather than a constitutive enzyme.

    Evidence c-Src wild-type/dominant-negative overexpression with imaging of p190/p120RasGAP distribution and phosphotyrosine analysis

    PMID:7542246

    Open questions at the time
    • Did not identify the specific phosphosite or define how phosphorylation alters GAP catalysis
    • Did not establish the RhoA target quantitatively
  2. 2001 High

    Defined the core physiological role: integrin-triggered RhoA inactivation by p190RhoGAP promotes spreading, polarity, and migration, placing it in adhesion signaling.

    Evidence Dominant-negative and overexpression in Rat1 fibroblasts with RhoA activity, spreading, and migration assays on fibronectin

    PMID:11553710

    Open questions at the time
    • Upstream kinase coupling integrins to p190 not identified
    • Membrane recruitment mechanism not addressed
  3. 2004 High

    Identified Tyr1105 as the key adhesion-dependent phosphosite, phosphorylated by Arg kinase, that promotes p120RasGAP binding and stimulates GAP activity — resolving the molecular switch.

    Evidence In vitro kinase assay, arg-/- cells, Y1105 mutagenesis, co-IP, and neuritogenesis assay

    PMID:15084284

    Open questions at the time
    • How p120RasGAP binding converts to RhoA suppression not mechanistically resolved at this stage
  4. 2006 High

    Showed that p120RasGAP binding does not activate the GAP enzymatically in vitro but instead drives membrane recruitment required for in vivo activity, redefining 'activation' as relocalization.

    Evidence arg-/- fibroblasts, dominant-negative p120 fragment, in vitro GAP assays, and localization studies

    PMID:16971514

    Open questions at the time
    • Membrane anchoring partners at the periphery not fully defined
    • Did not address junctional vs. raft recruitment
  5. 2006 High

    Connected p190RhoGAP to adherens junction assembly through a p120-catenin interaction, extending its role from focal adhesions to cell-cell contacts.

    Evidence siRNA of p120 and p190, reciprocal co-IP, and AJ assembly assays in PDGFR-stimulated cells

    PMID:17129786

    Open questions at the time
    • The catenin-binding region on p190 not yet mapped (later defined as CRAD)
  6. 2008 High

    Demonstrated that p190RhoGAP is the convergence point of multiple adhesion receptors (integrin + syndecan-4/PKCα) and is subject to ROCK feedback and GSK-3β/ERK control, establishing a multi-input regulatory architecture.

    Evidence Receptor-blocking antibodies, siRNA, fractionation, in vitro kinase assays with phosphosite mapping and phosphomutants

    PMID:18502760 PMID:18541700 PMID:19103606

    Open questions at the time
    • Quantitative integration of opposing phosphorylation inputs not modeled
    • Crosstalk between distinct phosphosites unresolved
  7. 2009 High

    Defined a polybasic/phospholipid-based mechanism by which PKC phosphorylation toggles substrate preference between RhoA and Rac1, revealing p190 as a dual GAP.

    Evidence In vitro PKC phosphorylation, liposome binding, mutagenesis, and dual-substrate GAP assays

    PMID:19673492 PMID:23499677

    Open questions at the time
    • Physiological triggers selecting Rho vs Rac mode in vivo not fully mapped
  8. 2010 High

    Established that mitotic ubiquitin-proteasome degradation of p190 via its N-terminal region is required for cytokinesis, linking its turnover to cell division.

    Evidence RNAi reconstitution with degradation-resistant mutant, N-terminal deletion mapping, and proteasome inhibitors

    PMID:14610059 PMID:20534586

    Open questions at the time
    • The E3 ligase mediating mitotic degradation not identified here
  9. 2014 High

    Resolved the cytokinetic mechanism: p190 forms a complex with anillin at the furrow and locally suppresses RhoA-GTP to permit abscission.

    Evidence Co-IP, siRNA with anillin-binding and GAP-dead rescue mutants, and blebbistatin rescue

    PMID:19254711 PMID:25359885

    Open questions at the time
    • How anillin binding spatially restricts GAP activity not structurally defined
  10. 2016 High

    Identified the PLS as a dual-function domain that targets p190 to protrusions via cortactin and regulates GAP activity, with cancer mutations disrupting both.

    Evidence Truncation mutants, cortactin co-IP, localization, GAP assays, and cancer-mutation panel

    PMID:27646271

    Open questions at the time
    • Mechanism of GAP regulation by PLS not resolved (later shown autoinhibitory)
  11. 2019 High

    Structurally characterized the regulatory interfaces: the N-terminal domain is a GTP-binding pseudoGTPase and the p120RasGAP SH2 binds pTyr1105 with sub-micromolar affinity via R207.

    Evidence X-ray crystallography of N-GTPase and SH2–phosphopeptide complex, ITC, and mutagenesis

    PMID:30174148 PMID:31891593

    Open questions at the time
    • Full-length architecture and how domains coordinate not solved
    • Interaction partners of the pseudoGTPase platform unidentified
  12. 2019 High

    Identified TRIM65 as an E3 ligase degrading p190A, linking its loss to elevated Rho activity and metastasis in colorectal cancer.

    Evidence Co-IP, ubiquitination assays, TRIM65 perturbation, and in vivo metastasis model

    PMID:31332286

    Open questions at the time
    • Whether TRIM65 mediates the mitotic degradation pathway not addressed
  13. 2020 High

    Revealed a tumor-suppressive role through Hippo signaling: p190A activates LATS and suppresses YAP, requiring E-cadherin, p120RasGAP, and ZO-2, with cancer mutants losing this function.

    Evidence CRISPR KO, cancer-mutant reconstitution, LATS kinase and YAP assays, CDH1 analysis, and xenografts

    PMID:32457342 PMID:32641858 PMID:37995182

    Open questions at the time
    • How GAP activity mechanistically couples to LATS activation not fully defined
    • Direct molecular link between junctional p190 and the Hippo core kinases unresolved
  14. 2024 High

    Established a ciliogenesis role: p190A is recruited to the basal body by Fuzzy to restrict actin polymerization and RhoA, controlling cilium formation.

    Evidence Co-IP, basal-body localization, Fuzzy KO mice, and Fuzzy/Arhgap35 compound mutant epistasis

    PMID:26859289 PMID:32663194 PMID:38546045

    Open questions at the time
    • Centrosomal/ciliary recruitment partners beyond Fuzzy and PC1 not fully mapped

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the many competing phosphorylation, nitration, lipid-binding, autoinhibition, and degradation inputs are quantitatively integrated to set RhoA-vs-Rac1 output in a given cellular context remains unresolved.
  • No full-length structure showing how regulatory domains coordinate
  • No unified model reconciling GAP-dependent and GAP-independent functions
  • Spatiotemporal logic of substrate-preference switching in vivo undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 5 GO:0098772 molecular function regulator activity 4 GO:0060089 molecular transducer activity 2 GO:0003924 GTPase activity 1 GO:0008289 lipid binding 1
Localization
GO:0005815 microtubule organizing center 3 GO:0005886 plasma membrane 3 GO:0005856 cytoskeleton 2 GO:0005929 cilium 2 GO:0005829 cytosol 1
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-162582 Signal Transduction 4 R-HSA-1640170 Cell Cycle 4 R-HSA-1643685 Disease 4 R-HSA-1500931 Cell-Cell communication 2
Partners
ABL2ANLNCTNND1CTTNFUZPTK2RASA1SRC
Complex memberships
eNOS–p190A–RGS3L–caveolin-3 complexp190A–anillin furrow complexp190RhoGAP–p120RasGAP complex

Evidence

Reading pass · 48 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 p190RhoGAP (ARHGAP35) mediates integrin-triggered RhoA inactivation during cell adhesion to fibronectin, promoting membrane protrusion and cell polarity. Dominant negative p190RhoGAP elevated RhoA activity, impaired spreading, and inhibited migration, while overexpression decreased RhoA activity and enhanced motility. Dominant negative and overexpression of p190RhoGAP in Rat1 fibroblasts; RhoA activity assays; cell spreading and migration assays on fibronectin Molecular biology of the cell High 11553710
1995 c-Src regulates EGF-dependent actin cytoskeleton reorganization through tyrosine phosphorylation of p190RhoGAP. The in vivo phosphotyrosine content of p190 varies with c-Src activity, and c-Src variants modulate the rate and extent of p190/RasGAP arc formation and actin stress fiber dynamics. Overexpression of wild-type and dominant negative c-Src variants; confocal immunofluorescence of p190, actin, and p120RasGAP distribution; phosphotyrosine analysis The Journal of cell biology High 7542246
1998 Beta1 integrin activation by laminin peptides induces tyrosine phosphorylation of p190RhoGAP and localizes phospho-p190 with F-actin specifically at invadopodia. Microinjection of antibodies against p190RhoGAP blocked invadopodial membrane-protrusive and matrix-degradative activities. Integrin activation with laminin G peptides and antibodies; immunofluorescence; tyrosine kinase inhibitors; microinjection of anti-p190 antibodies The Journal of biological chemistry High 9417037
2003 Cadherin engagement induces tyrosine phosphorylation of p190RhoGAP and increases its binding to p120RasGAP in a Src-family-kinase-dependent manner. Dominant negative p190RhoGAP antagonized cadherin-induced RhoA inactivation, establishing p190RhoGAP as a required downstream effector of cadherin-mediated RhoA suppression. Constitutively active RhoA pulldown to isolate active GAPs; dominant negative p190RhoGAP expression; PP2 Src kinase inhibitor; co-immunoprecipitation The Journal of biological chemistry High 12606561
2005 FAK directly phosphorylates p190RhoGAP in vitro and associates with p190RhoGAP; this FAK-induced phosphorylation is required for suppression of RhoA activity and restoration of endothelial barrier function after thrombin treatment. Dominant negative FAK (FRNK) prevented p190RhoGAP phosphorylation, increased RhoA activity, and produced irreversible endothelial permeability. In vitro kinase assay with recombinant FAK and p190RhoGAP; adenoviral FRNK expression; RhoA activity assays; endothelial permeability measurements The Journal of biological chemistry High 16308318
2006 Rac activation causes translocation of p190RhoGAP to adherens junctions where it couples to the cadherin complex via interaction with p120-catenin. This p120-p190RhoGAP interaction is required for adherens junction formation, and disruption of either protein prevents junction assembly. siRNA knockdown of p120 and p190RhoGAP; co-immunoprecipitation; immunofluorescence localization; functional AJ assembly assays in NIH3T3 cells stimulated with PDGFR Cell High 17129786
2006 Integrin signaling through the Arg tyrosine kinase activates p190RhoGAP by promoting its association with p120RasGAP and recruiting the p190/p120 complex to the cell periphery. p120 binding does not activate p190RhoGAP activity in vitro; instead, membrane recruitment is required for in vivo activation. arg-/- fibroblasts; dominant-negative p120 fragment; in vitro GAP activity assays; immunofluorescence localization; co-immunoprecipitation Molecular biology of the cell High 16971514
2004 Arg tyrosine kinase phosphorylates p190RhoGAP at Y1105 in vitro and in vivo. This phosphorylation is adhesion-dependent, promotes p190RhoGAP binding to p120RasGAP, stimulates p190RhoGAP GAP activity to inhibit Rho, and induces neuritogenesis in neuroblastoma cells. In vitro kinase assay; arg-/- mouse brain extracts and fibroblasts; site-directed mutagenesis (Y1105); co-immunoprecipitation; neuritogenesis assay Current biology : CB High 15084284
2007 Arg kinase acts through p190RhoGAP to inhibit actomyosin contractility (stress fiber formation) via RhoA suppression upon adhesion to fibronectin. The Arg N-terminal kinase domain is sufficient to act through p190RhoGAP; Arg also requires its C-terminal cytoskeleton-binding half to fully regulate focal adhesion dynamics. arg-/- fibroblasts; Arg re-expression; traction force microscopy; myosin light chain phosphorylation assays; immunofluorescence of stress fibers and focal adhesions Molecular biology of the cell High 17652459
2007 The Arg tyrosine kinase and p190RhoGAP pathway is essential for dendritic spine maturation and synapse/dendrite stability during late postnatal hippocampal development. p190RhoGAP localizes to dendritic spines; p190RhoGAP activity is reduced in arg-/- hippocampus, leading to elevated RhoA. Reducing ROCKII gene dosage suppresses dendritic regression in arg-/- mice. arg-/- mice; genetic epistasis (p190rhogap heterozygous/arg-/- double mutants; ROCKII haploinsufficiency in arg-/- background); immunofluorescence localization; RhoA activity assays; behavioral testing The Journal of neuroscience : the official journal of the Society for Neuroscience High 17928439
2009 FAK forms a complex with p120RasGAP and p190RhoGAP-A (p190A) at leading-edge focal adhesions. Fibronectin-integrin-mediated FAK activation promotes SH2-mediated p120RasGAP binding to FAK, which facilitates FAK-mediated p190A tyrosine phosphorylation. This complex is required for cell polarity during migration; knockdown of p120RasGAP or mutation of FAK Y397 prevents p190A association, tyrosine phosphorylation, and cell polarity. Co-immunoprecipitation; siRNA knockdown; FAK Y397F mutation; wound healing and Golgi reorientation polarity assays; fibronectin-integrin stimulation Journal of cell science High 19435801
2003 p190RhoGAP overexpression induces a multinucleated phenotype dependent on the GAP domain, and endogenous p190RhoGAP localizes to the cleavage furrow of dividing cells. Endogenous p190 protein levels are transiently decreased in late mitosis via ubiquitin-mediated degradation requiring the N-terminal GTP-binding region. Conditional/transient overexpression; GAP domain mutants; confocal immunofluorescence of cleavage furrow localization; ubiquitin-proteasome inhibitors; cell cycle synchronization The Journal of cell biology High 14610059
2006 Cell surface transglutaminase activates RhoA by suppressing the Src-p190RhoGAP regulatory pathway through integrin clustering. tTG-induced integrin aggregation inhibits Src kinase activity, decreasing activation of the Src substrate p190RhoGAP, leading to elevated RhoA-GTP levels. tTG overexpression; Src kinase activity assays; p190RhoGAP phosphorylation measurements; RhoA-GTP pulldown; pharmacological Src inhibition Molecular biology of the cell Medium 16452636
2008 Alpha5beta1 integrin engagement stimulates tyrosine phosphorylation of p190RhoGAP (Src-dependent), while parallel syndecan-4 engagement redistributes tyrosine-phosphorylated p190RhoGAP between membrane and cytosolic fractions via PKCalpha activation. Both pathways must be activated for efficient RhoA suppression and focal adhesion formation; p190RhoGAP is the convergence point of these two adhesion receptor signals. Function-blocking antibodies against alpha5beta1 integrin and syndecan-4; siRNA knockdown; fractionation; phosphotyrosine blotting; RhoA-GTP pulldown; focal adhesion scoring The Journal of cell biology High 18541700
2007 p190RhoGAP accumulates in lipid rafts during early cell spreading, where it exerts Rho inhibitory activity. Filamin controls this accumulation: cells lacking filamin fail to accumulate p190RhoGAP in lipid rafts and maintain high Rho activity even when spread. Calpain-resistant filamin also prevents spreading-induced raft accumulation of p190RhoGAP. siRNA knockdown of p190RhoGAP; filamin-null cell lines; calpain-resistant filamin expression; lipid raft fractionation; RhoA activity assays; cell rounding/spreading assays Journal of cell science High 17227794
2008 Rho-kinase (ROCK) phosphorylates p190A RhoGAP at Ser1150 and attenuates its GAP activity. This phosphorylation impairs Rnd binding to p190A (Rnd binding normally enhances p190A activation). A phosphomimetic S1150 mutation of p190A weakened Rnd binding and GAP activity. ET-1-induced sustained RhoA activation in vascular smooth muscle cells involves this ROCK-p190A feedback loop. In vitro phosphorylation assays; co-immunoprecipitation of Rnd and p190A; phosphomimetic/phosphoresistant mutations; Rho-kinase inhibitor Y-27632; COS7 and vascular smooth muscle cell experiments The Journal of biological chemistry High 19103606
2008 GSK-3beta phosphorylates p190A RhoGAP in a priming-dependent manner at C-terminal tail residues, inhibiting p190A GAP activity in vitro and in vivo and contributing to cell polarity during directional migration. p190A-deficient fibroblasts exhibit a defect in directional migration that reflects a requirement for GSK-3beta-mediated phosphorylation. In vitro kinase assay; phosphorylation mapping; p190A-deficient fibroblasts; reconstitution with phosphomimetic/phosphoresistant mutants; wound healing assays; RhoA activity assays The Journal of biological chemistry High 18502760
2008 Breast tumor kinase (Brk) phosphorylates p190RhoGAP-A at Y1105 in vitro and in vivo, promoting p190 association with p120RasGAP. This stimulates p190 GAP activity (RhoA inactivation) and attenuates p120RasGAP activity (Ras activation). Disruption of the p190/p120 complex abolishes Brk-mediated regulation of RhoA and Ras and Brk-driven proliferation, migration, invasion, and tumorigenicity. In vitro kinase assay; site-directed mutagenesis (Y1105); co-immunoprecipitation; RhoA and Ras activity assays; proliferation, migration, invasion, and xenograft tumor assays Cancer research High 18829532
2009 PTP-PEST directly dephosphorylates and thereby regulates p190RhoGAP activity. PTP-PEST null fibroblasts show enhanced p190RhoGAP activity (decreased RhoA) and exaggerated leading-edge protrusions; PTP-PEST acts to couple protrusion and retraction by reciprocally modulating VAV2 (Rac1 GEF) and p190RhoGAP (RhoA GAP). PTP-PEST null fibroblasts; RhoA and Rac1 activity assays; direct substrate phosphatase assays; co-immunoprecipitation The Journal of biological chemistry Medium 16513648
2009 Angiotensin II activates RhoA in vascular smooth muscle cells by causing SHP2-dependent dephosphorylation and inactivation of p190A RhoGAP. SHP2 maintains basal p190A phosphorylation via c-Abl; AT1R activation induces SHP2-mediated p190A dephosphorylation and RhoA activation. Phosphomimetic p190A mutant inhibits, and phosphoresistant mutant increases, basal RhoA-Rho kinase activity. siRNA knockdown of p190A and SHP2; phosphomimetic/phosphoresistant p190A mutants; RhoA/Rho-kinase activity assays; co-immunoprecipitation American journal of physiology. Cell physiology High 19692654
2009 Protein kinase C phosphorylates p190A RhoGAP at Ser1221 and Thr1226 within a polybasic region, preventing binding of acidic phospholipids to this region. Phospholipid binding to this region inhibits RhoGAP activity and promotes RacGAP activity. PKC-mediated phosphorylation thus indirectly alters substrate specificity by blocking phospholipid binding. In vitro PKC phosphorylation; liposome binding assays; site-directed mutagenesis; in vitro GAP activity assays with RhoA and Rac substrates; COS-7 cell morphology assays Biochemistry High 19673492
2006 Tiam1/Rac1 signaling downregulates Rho activity through p190-RhoGAP. p190-RhoGAP is required for this pathway; Src-kinase-dependent tyrosine phosphorylation of p190-RhoGAP and its recruitment to the membrane through p120-RasGAP SH2 domains are both necessary for Tiam1-mediated Rho downregulation. Dominant negative/active constructs of Tiam1, Rac isoforms, and p190-RhoGAP; phosphorylation mutants; dominant-negative p120 fragment; RhoA activity assays in COS-7 cells Biological chemistry Medium 16542153
2009 p190RhoGAP negatively regulates RhoA activity at the cleavage furrow, modulating cytokinetic furrow site selection and ring contraction. FRET analysis showed that wild-type p190 overexpression reduces RhoA-GTP at the furrow in a dose-dependent manner, causing abnormal furrow positioning and failed cytokinesis, while dominant-negative p190 causes hyper-activated Rho. FRET-based RhoA activity biosensor; time-lapse microscopy; overexpression of wild-type and dominant-negative p190RhoGAP; cleavage furrow localization by confocal imaging Experimental cell research High 19254711
2008 p190RhoGAP and Ect2 RhoGEF physically associate and colocalize at the cleavage furrow with opposing roles on RhoA activity and cytokinesis outcome; Ect2 can dose-dependently reduce p190-induced multinucleation. Their functional and physical interactions regulate RhoA activity levels at the furrow. Co-immunoprecipitation; immunofluorescence colocalization at cleavage furrow; multinucleation assays; RhoA pulldown activity assays Cell cycle (Georgetown, Tex.) Medium 18642445
2010 Mitotic down-regulation of p190RhoGAP via ubiquitin-proteasome-mediated degradation is required for successful cytokinesis. The N-terminal GBDS1 region (and four specific N-terminal residues) is necessary and sufficient for p190A mitotic ubiquitination and degradation; a degradation-resistant p190A mutant causes cytokinesis failure in an RNAi reconstitution approach. RNAi reconstitution with degradation-resistant mutant; N-terminal deletion mapping; ubiquitin-proteasome inhibitors; cell cycle synchronization; multinucleation assay The Journal of biological chemistry High 20534586
2014 p190RhoGAP-A forms a complex with anillin at the cytokinetic furrow. p190RhoGAP-A depletion causes accumulation of high RhoA-GTP in the furrow and failure to progress to abscission. Mutants of p190RhoGAP-A unable to bind anillin or lacking GAP activity fail to rescue cytokinesis defects; low-dose blebbistatin (myosin II inhibitor) rescues the cytokinesis failure of p190RhoGAP-A-depleted cells. Co-immunoprecipitation; siRNA knockdown; anillin-binding mutant and GAP-dead mutants; RhoA-GTP quantification at furrow; blebbistatin rescue experiment Journal of cell science High 25359885
2010 ERK promotes Rho-dependent focal adhesion formation by suppressing p190A RhoGAP. ERK activity is required for RhoA-GTP loading and focal adhesion maturation during cell spreading on fibronectin. ERK phosphorylates the C-terminus of p190A, affecting its peripheral localization and activity. MEK/ERK inhibitors; ERK phosphorylation site mapping; p190A localization by immunofluorescence; RhoA-GTP pulldown; focal adhesion maturation assays Molecular and cellular biology Medium 20439493
2011 Caveolin-1-deficiency leads to eNOS activation, peroxynitrite generation, and selective nitration of p190RhoGAP-A at Tyr1105, impairing its GAP activity and causing RhoA activation and adherens junction disassembly. Thrombin also induces nitration of p120-catenin-associated p190RhoGAP-A. Cav-1-/- endothelial cells; nitration assays (tyrosine nitration); eNOS inhibition; S-nitrosylation/nitration profiling; RhoA activity assays; endothelial permeability measurements; adherens junction imaging The Journal of cell biology High 21624953
2009 p190RhoGAP has RacGAP activity in cells, not only RhoGAP activity. The cellular RacGAP activity requires an intact polybasic region adjacent to the GAP domain (which inhibits RhoGAP activity), revealing that this polybasic region inversely regulates substrate preference between Rac and Rho. Mutagenesis of polybasic region; in vitro GAP activity assays with RhoA and Rac substrates; cellular Rac/RhoA activity readouts Cellular signalling Medium 23499677
2013 p120-catenin interacts with p190RhoGAP via a 23-amino acid stretch (CRAD, amino acids 820–843) in its C-terminal domain. This interaction is required for membrane translocation of p190RhoGAP, suppression of RhoA and upregulation of Rac1/PAK1/cortactin signaling. Expression of p120-catenin lacking CRAD prevents p190RhoGAP recruitment to the cell periphery and impairs endothelial barrier recovery. Truncation mutants of p120-catenin; co-immunoprecipitation; immunofluorescence localization; RhoA and Rac1 activity assays; endothelial permeability measurements The Journal of biological chemistry High 23653363
2009 p190A RhoGAP is phosphorylated by PDGF receptor alpha on Y308 within the FF1 domain, but phosphorylation requires prior domain unfolding since Y308 is buried in the hydrophobic core. Phosphorylation irreversibly destabilizes the FF1 structure, likely accounting for its inhibitory effect on TFII-I interaction. NMR structure determination of FF1 domain; in vitro phosphorylation at different temperatures; thermal denaturation studies Journal of molecular biology High 19393245
2018 The N-terminal domain of p190RhoGAP proteins is a pseudoGTPase (N-GTPase) that constitutively binds GTP but does not hydrolyze it. Crystal structure at 2.8 Å shows an unusual GTP-Mg2+ binding pocket with six inserts perturbing catalytic activity. GTP/Mg2+ binding stabilizes the domain, suggesting it functions as a protein-protein interaction platform. X-ray crystal structure (2.8 Å); biochemical GTP hydrolysis assays; nucleotide exchange under Mg2+ chelation; mutational analysis of GTP/Mg2+ binding Structure (London, England : 1993) High 30174148
2019 The p120RasGAP N-terminal SH2 domain binds the p190RhoGAP phosphopeptide centered on pTyr-1105 with a dissociation constant of 0.3 μM via a canonical SH2-pTyr interaction requiring the conserved FLVR motif arginine R207. Crystal structure at 1.6 Å shows that peptide binding stabilizes specific conformations of the βE-βF loop and key arginine residues. X-ray co-crystal structure (1.6 Å); site-directed mutagenesis (R207); native gel shifts; isothermal titration calorimetry PloS one High 31891593
2016 p190A localizes to membrane protrusions via a novel domain termed the PLS (protrusion localization sequence). The PLS is required for targeting to the leading edge and also negatively regulates p190A GAP activity. Cortactin binds the PLS and is required for p190A targeting to protrusions. Cancer-associated mutations in PLS disrupt localization, GAP activity regulation, and tumor cell migration. Truncation mutants; subcellular localization (immunofluorescence); GAP activity assays; cortactin co-immunoprecipitation; cancer-mutation panel analysis; cell migration assays The Journal of cell biology High 27646271
2016 A point mutation (L1396Q) in the GAP domain of p190A RhoGAP (Arhgap35) decreases GAP activity for RhoA and Rac1 and impairs primary cilia formation in renal nephrons. p190A localizes to the base of cilia; its GAP activity is required for axoneme elongation. Pharmacological inhibition of ROCK or F-actin polymerization rescues ciliogenesis defects, placing p190A upstream of Rho-ROCK-actin in cilia formation. ENU mutagenesis; in vitro GAP activity assay with L1396Q mutant; mouse glomerulocystic kidney model; immunofluorescence localization to cilia base; ROCK inhibitor and actin polymerization inhibitor rescue experiments PLoS genetics High 26859289
2019 p190RhoGAP acts in a GAP-independent mode to transiently suppress attraction to Netrin-1 while motor axons exit the spinal cord, and also uses GAP-dependent RhoA inhibition to guide a subset of axons to specific muscles. Identified by a mouse mutagenesis screen; multifunctional activity emerges from modular design. Mouse mutagenesis screen; in vivo motor axon guidance assays; genetic analysis distinguishing GAP-dependent and GAP-independent activities Neuron High 30902550
2020 p190A (ARHGAP35) is an upstream regulator of the Hippo-YAP signaling pathway. p190A knockout promotes YAP nuclear localization and transcriptional activity; wild-type but not cancer-associated p190A mutants suppress YAP. p190A promotes MET and CDH1 (E-cadherin) expression; E-cadherin amplifies p190A-mediated LATS activation and is required for contact inhibition of proliferation. CRISPR/Cas9 knockout; lentiviral expression of cancer mutants; YAP localization/activity assays; LATS kinase activity; xenograft mouse model; CDH1 expression analysis Signal transduction and targeted therapy High 32457342
2020 Polycystin-1 (PC1) regulates ARHGAP35-dependent centrosomal RhoA activation and ROCK signaling. PKD1-null cells show decreased centrosomal ARHGAP35, increased total and centrosomal active RhoA, and ROCK signaling. ARHGAP35 knockdown reduces primary ciliation in normal renal tubular cells. ROCK inhibitor hydroxyfasudil reduces cyst expansion in PKD1 3D cyst assays and an inducible Pkd1 mouse model. Centrosome-targeted proximity ligation assay; dual immunofluorescence; siRNA knockdown; cilia length phenotypic assay; 3D cyst assay; inducible Pkd1 mouse model JCI insight Medium 32663194
2020 p190A RhoGAP promotes CDH1 (E-cadherin) expression and cooperates with E-cadherin to activate LATS kinases and suppress tumor cell growth. p190A and E-cadherin are mutually required for LATS activation and contact inhibition of proliferation (CIP); p190A cancer mutations lose this function. Xenograft mouse model; LATS kinase assays; YAP phosphorylation; CDH1 induction assays; reconstitution with cancer mutant panel; co-expression/knockdown experiments Oncogene High 32641858
2019 TRIM65 E3 ubiquitin ligase mediates ubiquitination and proteasomal degradation of ARHGAP35 (p190A), leading to elevated Rho GTPase activity, increased migration-related structures (focal adhesions, filopodia), and enhanced CRC metastasis. Co-immunoprecipitation; ubiquitination assays; TRIM65 overexpression and knockdown; in vivo mouse metastasis model (liver, lung); RhoA activity assays Oncogene High 31332286
2023 p120 RasGAP and ZO-2 are both necessary for p190A to activate LATS kinases, elicit MET, promote contact inhibition of proliferation, and suppress tumorigenesis. The interaction of p190A with ZO-2 is dependent on RasGAP; RasGAP and ZO-2 are required for transcriptional modulation by p190A. Co-immunoprecipitation; siRNA knockdown of RasGAP and ZO-2; LATS kinase activity assays; contact inhibition assays; xenograft tumor assays; transcriptional reporter assays Cell reports High 37995182
2016 Interaction of p190A RhoGAP with eIF3A (and other translation preinitiation factors) involves the first FF motif of p190A and the winged helix/PCI domain of eIF3A; interaction is enhanced by serum and reduced by phosphatase treatment. Disrupted by S296A mutation in the first FF domain but not by Y308 mutation. Tandem mass spectrometry of endogenous p190A interactors; co-immunoprecipitation; site-directed mutagenesis (S296A, Y308); phosphatase treatment The Journal of biological chemistry Medium 28007963
2014 HPV16 E7 protein binds p190RhoGAP via conserved region 3 (CR3) of E7 and the middle domain of p190RhoGAP. This interaction dysregulates p190RhoGAP and alters the actin cytoskeleton, and negatively regulates cell spreading on fibronectin. Mass spectrometry identification; co-immunoprecipitation; domain-mapping with E7 CR3 mutants and p190 deletion constructs; cell spreading assays on fibronectin; actin cytoskeleton immunofluorescence Journal of virology Medium 24403595
2018 A Rnd3/p190RhoGAP pathway operates in idiopathic pulmonary fibrosis (IPF) fibroblasts. Rnd3 expression and p190RhoGAP activity are suppressed in IPF; restoration of Rnd3 increases p190 activity and decreases RhoA activity and fibrotic phenotype. IPF drugs nintedanib and pirfenidone decrease RhoA activity through up-regulation of Rnd3 and p190 activity. Rnd3 overexpression in IPF fibroblasts; p190RhoGAP activity assays; RhoA activity assays; nintedanib/pirfenidone treatment; collagen gel contraction (fibrotic phenotype) assays Molecular biology of the cell Medium 29995590
2022 The PLS of p190A acts as an autoinhibitory domain that masks the GAP domain through intramolecular interaction. Co-immunoprecipitation demonstrates that the PLS interacts with a region near the GAP domain; p190A lacking PLS (p190AΔPLS) has stronger RhoA-inhibiting activity. This intramolecular autoinhibition is disrupted by cancer-associated mutations S866F and Δ865-870 in the PLS. Yeast two-hybrid screen; co-immunoprecipitation of PLS with p190A GAP-proximal region; RhoA inactivation assays comparing WT vs. ΔPLS; cancer-associated PLS mutants The Journal of biological chemistry High 36516886
2024 Fuzzy (CPLANE protein) recruits ARHGAP35 (p190A RhoGAP) to the basal body/base of primary cilia to restrict actin polymerization. Loss of Fuzzy in mice reduces cilia length with increased RhoA activity and excessive basal body actin; genetic interaction between Fuzzy and Arhgap35 alleles confirms their functional cooperation at the basal body. Co-immunoprecipitation of Fuzzy with ARHGAP35; immunofluorescence localization at basal body; Fuzzy knockout mice; Fuzzy/Arhgap35 compound mutant genetic epistasis; actin and RhoA activity measurements Development (Cambridge, England) High 38546045
2023 In cardiac myocytes, M2 muscarinic receptor (M2R) stimulation by carbachol induces eNOS activation in caveolae, producing NO/peroxynitrite that nitrates p190A at Tyr1105. This nitration promotes p190A binding to RGS3L and shifts p190A substrate preference from RhoA to Rac1, resulting in net RhoA activation. Complex of eNOS, p190A, RGS3L, and caveolin-3 detected by co-immunoprecipitation. Carbachol stimulation; eNOS inhibitors (L-NIO, L-NAME); nitration assays; co-immunoprecipitation (eNOS/p190A/RGS3L/caveolin-3); GAP activity assays for RhoA vs. Rac1; caveolae disruption by methyl-β-cyclodextrin Cells Medium 37887276
2018 p190RhoGAP is required to prevent mitotic spindle fragmentation and to activate Aurora A kinase at acentriolar poles. Depletion of p190RhoGAP causes prolonged mitotic arrest with multipolar spindles. Low-dose Eg5 inhibitor rescues the multipolar phenotype. Aurora A localizes to all poles in p190-depleted cells but is only activated at centriolar poles. siRNA knockdown of p190RhoGAP; live-cell imaging of spindle dynamics; Aurora A activation (immunofluorescence with activation-specific antibody); Eg5 inhibitor rescue experiment Chromosoma Medium 29656322

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
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 56 31487506
2006 PTP-PEST couples membrane protrusion and tail retraction via VAV2 and p190RhoGAP. The Journal of biological chemistry 56 16513648
2019 Ubiquitin ligase TRIM65 promotes colorectal cancer metastasis by targeting ARHGAP35 for protein degradation. Oncogene 55 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
2014 A complex of p190RhoGAP-A and anillin modulates RhoA-GTP and the cytokinetic furrow in human cells. Journal of cell science 32 25359885
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
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
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 26 32457342
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
2018 A Rnd3/p190RhoGAP pathway regulates RhoA activity in idiopathic pulmonary fibrosis fibroblasts. Molecular biology of the cell 23 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 15 38263362
2020 p190A RhoGAP induces CDH1 expression and cooperates with E-cadherin to activate LATS kinases and suppress tumor cell growth. Oncogene 15 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
2018 Growth inhibition of KRAS‑ and EGFR‑mutant lung adenocarcinoma by cosuppression of STAT3 and the SRC/ARHGAP35 axis. Oncology reports 12 30015929
2014 The human papillomavirus E7 proteins associate with p190RhoGAP and alter its function. Journal of virology 12 24403595
2023 Extracellular matrix stiffness mediates uterine repair via the Rap1a/ARHGAP35/RhoA/F-actin/YAP axis. Cell communication and signaling : CCS 11 36691027
2022 ARHGAP35 is a novel factor disrupted in human developmental eye phenotypes. European journal of human genetics : EJHG 11 36450800
2018 The N-Terminal GTPase Domain of p190RhoGAP Proteins Is a PseudoGTPase. Structure (London, England : 1993) 11 30174148
2017 Regulation of Rho GTPase activity at the leading edge of migrating cells by p190RhoGAP. Small GTPases 11 28287334
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
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 Diverse p120RasGAP interactions with doubly phosphorylated partners EphB4, p190RhoGAP, and Dok1. The Journal of biological chemistry 9 37507023
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
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
2023 p120 RasGAP and ZO-2 are essential for Hippo signaling and tumor-suppressor function mediated by p190A RhoGAP. Cell reports 4 37995182
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
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
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 2 35949786
2018 P190RhoGAP prevents mitotic spindle fragmentation and is required to activate Aurora A kinase at acentriolar poles. Chromosoma 2 29656322
2025 A genome-wide screen identified ARHGAP35 as a regulator of regorafenib resistance in liver cancer. Anti-cancer drugs 1 41176659
2023 The Muscarinic Acetylcholine M2 Receptor-Induced Nitration of p190A by eNOS Increases RhoA Activity in Cardiac Myocytes. Cells 1 37887276
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 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

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