Affinage

ARHGAP18

Rho GTPase-activating protein 18 · UniProt Q8N392

Length
663 aa
Mass
75.0 kDa
Annotated
2026-06-09
44 papers in source corpus 17 papers cited in narrative 17 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ARHGAP18 (also called MacGAP or SENEX) is a Rho GTPase-activating protein that locally restrains RhoA activity to govern actin cytoskeletal organization, cell polarity and migration (PMID:21865595). It stimulates GTP hydrolysis on RhoA, so that its overexpression suppresses stress fibers and its loss drives sustained RhoA activation, stress fiber accumulation and cell rounding, while the protein itself concentrates at the leading edge to enable polarized spreading and migration (PMID:21865595); in the vascular endothelium it acts selectively on RhoC to restrain tip-cell behavior and stabilize junctions during angiogenesis (PMID:25425145). Its activity is gated by recruitment to discrete subcellular sites and by post-translational input: binding to active (phosphorylated) ezrin/Moesin recruits ARHGAP18 to the cell cortex and microvilli and enhances its GAP activity, forming a negative-feedback module that defines the microvilli/terminal-web boundary and limits myosin-2 assembly (PMID:23468526, PMID:38193818), and phosphorylation by PKN3 likewise augments GAP-domain activity (PMID:33092266). Through this RhoA control ARHGAP18 maintains endothelial junctional integrity, NF-κB restraint and alignment under laminar flow, coordinating with the Hippo effector YAP and with Merlin, with which it forms a complex at the cytoskeleton (PMID:30630384, PMID:32013974, PMID:42126958). It also tunes cell-fate and proliferative decisions, providing tonic RhoA inhibition that biases mesenchymal stem cells toward adipogenesis over osteogenesis (PMID:29208526), and its abundance is set by transcriptional (GATA1), microRNA (miR-200b) and autophagic-degradation inputs (PMID:37171759, PMID:28619708, PMID:33973626). Loss-of-function in mice produces a proinflammatory smooth-muscle phenotype predisposing to thoracic aortic aneurysm and early atherosclerosis, underscoring its protective vascular role (PMID:28701309, PMID:30630384).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2010 Medium

    Established the first functional context for the gene (SENEX) by linking it to endothelial stress responses and survival before its enzymatic identity was clear.

    Evidence siRNA depletion with H2O2 stress, senescence and apoptosis assays, p16/Rb pathway analysis in endothelial cells

    PMID:20664062

    Open questions at the time
    • No GAP activity or RhoA link established at this stage
    • Mechanism connecting SENEX to p16/Rb not resolved
    • Single lab, no reconstitution
  2. 2011 High

    Defined ARHGAP18 as a bona fide RhoA-inactivating GAP that controls stress fibers, polarity and migration, answering what the protein does biochemically.

    Evidence Reciprocal siRNA/overexpression with RhoA activity assays, stress fiber imaging, leading-edge localization and migration assays

    PMID:21865595

    Open questions at the time
    • Mechanism of leading-edge recruitment unknown
    • Selectivity among Rho isoforms not yet tested
    • Upstream regulators undefined
  3. 2013 High

    Identified ERM-protein binding (Moesin) as the means by which the GAP is recruited to the cortex, connecting localization to function.

    Evidence Co-IP, cortical localization rescue, GAP-domain mutagenesis and proliferation assays in Drosophila Conundrum orthologue

    PMID:23468526

    Open questions at the time
    • Conservation of the ERM-recruitment mechanism in mammals not yet shown
    • Rac-dependence of growth effect mechanistically unclear
  4. 2014 High

    Showed isoform-selective substrate use, with endogenous ARHGAP18 acting on RhoC to restrain angiogenic sprouting in vivo.

    Evidence Zebrafish/mouse retinal vessel loss-of-function, RhoC-specific activity assays, ROCK-dependent junctional relocalization

    PMID:25425145

    Open questions at the time
    • Basis for RhoC vs RhoA selectivity unresolved
    • Direct mechanism linking GAP activity to Dll4/Flk-1/Flt-4 not established
  5. 2017 High

    Expanded localization and regulation: ARHGAP18 stabilizes microtubules via GAP activity, is controlled by miR-200b in cancer, and provides tonic RhoA inhibition that directs MSC lineage choice.

    Evidence Super-resolution imaging plus knockout-EC microtubule analysis; miR-200b stable expression with metastasis assays; MSC differentiation and RhoA assays

    PMID:28251925 PMID:28619708 PMID:29208526

    Open questions at the time
    • How GAP activity feeds into microtubule acetylation mechanistically unclear
    • Direct miR-200b targeting versus indirect effects partially resolved
    • Lineage phenotypes single-lab
  6. 2017 Medium

    Demonstrated an in vivo protective vascular role, linking ARHGAP18 loss to aneurysm-prone smooth muscle phenotypes and epigenetic dysregulation.

    Evidence Global Arhgap18 knockout mice with angiotensin II challenge, ChIP at MMP2/TNF-α promoters, pAkt analysis and rapamycin rescue

    PMID:28701309

    Open questions at the time
    • Connection between GAP activity and chromatin marks not mechanistically explained
    • Akt/mTORC1 link correlative
  7. 2018 Medium

    Placed ARHGAP18 within an IP3R3-driven cytoskeletal signaling cascade in breast cancer cells.

    Evidence IP3R3 siRNA knockdown with RhoA activity, FAK phosphorylation and morphology readouts

    PMID:29630900

    Open questions at the time
    • Directness of IP3R3-to-ARHGAP18 regulation untested
    • Single-lab pathway placement
  8. 2019 Medium

    Connected ARHGAP18 to mechanotransduction, showing it is required for endothelial alignment to laminar flow and protection from atherosclerosis.

    Evidence siRNA with in vitro laminar flow; ApoE/Arhgap18 double-knockout atherosclerosis model; NF-κB/ICAM-1/eNOS readouts

    PMID:30630384

    Open questions at the time
    • Mechanism coupling flow sensing to ARHGAP18 activity unresolved
    • Single-lab in vivo model
  9. 2020 Medium

    Linked Rho GTPase control to Hippo signaling (YAP) and identified PKN3 as an activating kinase, defining upstream and downstream nodes.

    Evidence ARHGAP18 gain/loss with YAP localization and Cyr61 measurements in ECs; phosphoproteomic/in vitro kinase and GAP assays with PKN3

    PMID:32013974 PMID:33092266

    Open questions at the time
    • Direction of YAP regulation (expression vs localization) partially paradoxical
    • PKN3 phosphosites and their in vivo relevance not mapped
  10. 2021 Medium

    Identified autophagic degradation as a route controlling ARHGAP18 abundance and downstream RhoA-dependent migration.

    Evidence ATG16L1/ATG5 and SQSTM1 knockdown, G-LISA RhoA activity, organoid and primary colonic tissue analysis

    PMID:33973626

    Open questions at the time
    • Whether ARHGAP18 is a direct autophagy substrate not established
    • Recognition/adaptor mechanism unknown
  11. 2023 Medium

    Established GATA1 as a direct transcriptional driver of ARHGAP18 in hepatocellular carcinoma.

    Evidence Luciferase reporter, ChIP-qPCR and GATA1 overexpression rescue of ARHGAP18-silencing phenotypes

    PMID:37171759

    Open questions at the time
    • Generality beyond HCC untested
    • Downstream RhoA link in this context not measured
  12. 2024 High

    Resolved the recruitment-and-activation logic at microvilli: active ezrin both localizes ARHGAP18 and boosts its GAP activity to define the microvilli/terminal-web boundary.

    Evidence Co-IP with active ezrin, in vitro GAP activity enhancement, loss-of-function with myosin-2 filament distribution readout in epithelial cells

    PMID:38193818

    Open questions at the time
    • Structural basis of ezrin-mediated GAP enhancement undefined
    • How feedback is set spatially within a microvillus unclear
  13. 2025 High

    Showed ARHGAP18 physically integrates Rho and Hippo signaling by complexing with YAP and Merlin to organize the actin cytoskeleton.

    Evidence Co-IP of ARHGAP18 with YAP and Merlin, CRISPR knockout, STORM imaging and YAP localization in epithelial cells

    PMID:42126958

    Open questions at the time
    • Stoichiometry and architecture of the complex unknown
    • Whether complex formation depends on GAP activity untested
  14. 2025 Medium

    Positioned ARHGAP18 as the effector terminus of an ERK-LOK-Ezrin axis linking MAPK signaling to RhoA-dependent contractility.

    Evidence Phosphorylation mapping, LOK kinase and ezrin activity assays, ARHGAP18 recruitment and stress fiber readouts (preprint)

    PMID:bio_10.1101_2025.11.15.688645

    Open questions at the time
    • Preprint, not yet peer-reviewed
    • In vivo relevance of the ERK-LOK-Ezrin-ARHGAP18 axis untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how ARHGAP18 achieves context-dependent selectivity between RhoA and RhoC and how its multiple recruitment cues (ezrin, microtubules, junctions, leading edge) are coordinated within a single cell.
  • No structural model of GAP-substrate selectivity
  • No unified scheme integrating the distinct localization signals
  • No structure of the ezrin- or PKN3-activated state

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0060089 molecular transducer activity 2
Localization
GO:0005886 plasma membrane 3 GO:0005829 cytosol 1 GO:0005856 cytoskeleton 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1266738 Developmental Biology 2
Partners
EZRLOKMSNNF2PKN3RHOARHOCYAP1

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2011 ARHGAP18 (MacGAP) functions as a GTPase-activating protein for RhoA: overexpression suppresses RhoA activity and disrupts stress fiber formation, while siRNA knockdown enhances stress fibers, induces cell rounding, and causes sustained RhoA activation upon cell attachment. ARHGAP18 localizes to the leading edge during cell spreading and migration and is required for cell polarization. siRNA knockdown, overexpression, immunofluorescence, RhoA activity assays, cell spreading/migration assays Molecular biology of the cell High 21865595
2013 The Drosophila ARHGAP18 orthologue Conundrum (Conu) interacts with Moesin (ERM protein), which recruits Conu to the cell cortex to negatively regulate RhoA activity. Cortically localized Conu promotes cell proliferation in a RhoGAP activity-dependent manner, and this growth-promoting function also appears dependent on increased Rac activity. Co-immunoprecipitation, genetic epistasis, cortical localization assays, RhoA activity assays, cell proliferation assays in Drosophila Molecular biology of the cell High 23468526
2014 ARHGAP18 acts as a negative regulator of angiogenesis: loss of ARHGAP18 promotes endothelial cell hypersprouting in zebrafish and murine retinal vessel development. Endogenous ARHGAP18 acts specifically on RhoC (not other Rho isoforms) and relocalizes to angiogenic/destabilized EC junctions in a ROCK-dependent manner, suppressing tip cell behavior and stabilizing junctions at least partially through regulation of Dll4, Flk-1, and Flt-4. Zebrafish knockdown, murine retinal vessel analysis, siRNA in endothelial cells, ROCK inhibitor treatment, immunofluorescence localization, RhoC-specific activity assays Small GTPases High 25425145
2010 SENEX (ARHGAP18) regulates stress-induced premature senescence (SIPS) in endothelial cells through the p16(INK4a)/retinoblastoma protein pathway; depletion by siRNA or high-dose H2O2 causes apoptosis, establishing SENEX as essential for EC survival. SENEX levels are regulated by H2O2-mediated stress but unchanged during replicative senescence. siRNA knockdown, H2O2-induced stress, SA-β-gal senescence assay, apoptosis assays, p16/Rb pathway analysis Blood Medium 20664062
2017 ARHGAP18 localizes to microtubules in endothelial cells (confirmed by structured illumination, GSD, and TIRF microscopy and biochemical fractionation). Depletion of ARHGAP18 (siRNA or knockout mouse ECs) destabilizes microtubules (reduced acetylated α-tubulin and glu-tubulin), impairs endothelin-1 secretion, and reduces neutrophil transmigration; this destabilization is rescued by ROCK or HDAC6 inhibition but not by a GAP-mutant ARHGAP18. Thrombin enhances the plasma membrane-bound fraction of ARHGAP18. SIM, GSD, TIRF microscopy, biochemical fractionation, siRNA, ARHGAP18-knockout mouse ECs, ROCK/HDAC6 inhibitors, GAP-mutant rescue experiments Molecular biology of the cell High 28251925
2017 miR-200b directly controls ARHGAP18 levels in triple-negative breast cancer cells; enforced miR-200b expression reduces ARHGAP18, activates RhoA, enhances focal adhesions/stress fibers, and reduces migration and metastasis. Enforced ARHGAP18 re-expression where miR-200b is stably expressed reduces RhoA activity and rescues migration. ROCK inhibition reverses miR-200b's anti-migratory effect. miR-200b stable expression, ARHGAP18 deletion/overexpression, RhoA activity assays, ROCK inhibitor, in vivo metastasis assays Cancer research High 28619708
2017 ARHGAP18 depletion in mesenchymal stem cells increases basal RhoA activity and actin stress fiber formation, suppresses adipogenesis, and enhances osteogenic commitment. ARHGAP18 provides tonic RhoA inhibition in static conditions but is not required for mechanical strain-mediated RhoA activation (which depends on LARG GEF). siRNA knockdown, RhoA activity assays, Oil-Red-O staining, alkaline phosphatase staining, qPCR of lineage markers Bone Medium 29208526
2017 ARHGAP18 protects against thoracic aortic aneurysm: Arhgap18-/- mice show a synthetic, proteolytic, and proinflammatory smooth muscle cell phenotype. ChIP studies revealed enrichment of H3K4me3 and depletion of H3K27me3 at MMP2 and TNF-α promoters in Arhgap18-deficient SMCs. TAA formation in Arhgap18-/- mice is associated with loss of Akt activation, and rapamycin (mTORC1 inhibitor) partially rescues the phenotype. Global Arhgap18 knockout mice, angiotensin II challenge, chromatin immunoprecipitation (ChIP), Western blotting for pAkt, rapamycin rescue Circulation research Medium 28701309
2019 ARHGAP18 is required for endothelial cell alignment in the direction of laminar flow. Depletion of ARHGAP18 inhibits flow-induced alignment, disrupts junctions, activates NF-κB, and increases ICAM-1 while decreasing eNOS. ApoE-/-/Arhgap18-/- double-knockout mice on high-fat diet develop early atherosclerosis in normally atheroprotective regions. siRNA depletion, in vitro laminar flow, double-knockout mouse atherosclerosis model, NF-κB/ICAM-1/eNOS protein analysis Journal of the American Heart Association Medium 30630384
2020 YAP is downstream of ARHGAP18 in endothelial cells: ARHGAP18 depletion decreases YAP expression yet causes its nuclear localization (activation), disrupts VE-Cadherin at junctions, and impairs flow-mediated alignment. ARHGAP18 overexpression upregulates YAP, promotes its phosphorylation, and decreases the YAP target Cyr61. YAP depletion itself also causes loss of alignment and NF-κB activation. siRNA knockdown, ARHGAP18 overexpression, confocal imaging of YAP nuclear localization, ARHGAP18-knockout mouse in vivo analysis, Cyr61/NF-κB target gene measurements Cell communication and signaling Medium 32013974
2020 PKN3 phosphorylates ARHGAP18 in vitro; PKN3-ARHGAP18 interaction is mediated via the N-terminal part of ARHGAP18 and is enhanced by ARHGAP18 phosphorylation. Phosphorylation by PKN3 enhances ARHGAP18's GAP domain activity, contributing to negative regulation of active RhoA. Phosphoproteomic screen with analog-sensitive PKN3, in vitro kinase assay, Co-immunoprecipitation, GAP domain activity assay International journal of molecular sciences Medium 33092266
2018 IP3R3 silencing decreases ARHGAP18 expression, reduces RhoA activity, decreases Cdc42 expression, and reduces FAK Y861 phosphorylation in breast cancer cells, placing ARHGAP18 in an IP3R3/ARHGAP18/RhoA/mDia1/FAK pathway that coordinates cytoskeletal remodeling and cell morphology. siRNA knockdown of IP3R3, Western blot, RhoA activity assay, immunofluorescence Biochimica et biophysica acta. Molecular cell research Medium 29630900
2024 ARHGAP18 is localized by binding active (phosphorylated) microvillar ezrin, and this interaction enhances ARHGAP18's RhoGAP activity. Loss of ARHGAP18 disrupts the boundary between microvilli and the terminal web, causing aberrant assembly of myosin-2 filaments inside microvilli, indicating that the ezrin-ARHGAP18 module acts as a negative autoregulatory feedback to locally reduce RhoA activity in microvilli. Localization studies in epithelial cells, Co-IP of ARHGAP18 with active ezrin, GAP activity assays, ARHGAP18 loss-of-function with myosin-2 filament distribution readout eLife High 38193818
2023 Transcription factor GATA1 binds the ARHGAP18 promoter and drives ARHGAP18 expression in hepatocellular carcinoma cells, as confirmed by luciferase reporter assay and ChIP-qPCR. GATA1 overexpression rescues the anti-proliferative effects of ARHGAP18 silencing. Luciferase reporter assay, ChIP-qPCR, GATA1 overexpression rescue, gain/loss-of-function assays Applied biochemistry and biotechnology Medium 37171759
2021 ATG16L1 knockdown (impaired autophagy) causes accumulation of SQSTM1/p62 and ARHGAP18 protein, leading to decreased RhoA activity and reduced epithelial cell migration. Thiopurines mitigate this effect. ARHGAP18 protein accumulation in autophagy-impaired cells places ARHGAP18 as a substrate of the autophagic degradation machinery upstream of RhoA. ATG16L1/ATG5 siRNA knockdown, pharmacological autophagy inhibition, SQSTM1 knockdown, G-LISA RhoA activity, immunofluorescence, primary colonic tissue staining Disease models & mechanisms Medium 33973626
2025 ARHGAP18 forms a complex with Hippo pathway components YAP and Merlin (NF2) in human epithelial cells. CRISPR/Cas9 knockout of ARHGAP18 causes cytoskeletal alterations (loss of basal actin bundles) driven by both dysregulated RhoA signaling and aberrant nuclear localization of YAP, indicating spatiotemporal coordination between Rho GTPase and Hippo signaling at the cytoskeleton. Co-immunoprecipitation (ARHGAP18 with YAP and Merlin), CRISPR/Cas9 knockout, super-resolution STORM microscopy, YAP nuclear localization assays Molecular biology of the cell High 42126958
2025 ERK inhibits Ezrin activity in the cell body by phosphorylating the C-terminal tail of the Ezrin-activating kinase LOK, thereby releasing Ezrin's ability to recruit and activate ARHGAP18. This ERK-LOK-Ezrin-ARHGAP18-RhoA signaling axis controls RhoA activity and contractile stress fiber assembly for cell migration. Phosphorylation mapping, LOK kinase assay, Ezrin activity measurements, ARHGAP18 recruitment assay, stress fiber and RhoA activity readouts bioRxivpreprint Medium bio_10.1101_2025.11.15.688645

Source papers

Stage 0 corpus · 44 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 ARHGAP18, a GTPase-activating protein for RhoA, controls cell shape, spreading, and motility. Molecular biology of the cell 89 21865595
2017 ARHGAP18 Downregulation by miR-200b Suppresses Metastasis of Triple-Negative Breast Cancer by Enhancing Activation of RhoA. Cancer research 73 28619708
2017 ARHGAP18 Protects Against Thoracic Aortic Aneurysm Formation by Mitigating the Synthetic and Proinflammatory Smooth Muscle Cell Phenotype. Circulation research 51 28701309
2010 Stress-induced premature senescence mediated by a novel gene, SENEX, results in an anti-inflammatory phenotype in endothelial cells. Blood 50 20664062
2024 Bioinspired Selenium-Nitrogen Exchange (SeNEx) Click Chemistry Suitable for Nanomole-Scale Medicinal Chemistry and Bioconjugation. Angewandte Chemie (International ed. in English) 35 38343199
2014 ARHGAP18: an endogenous inhibitor of angiogenesis, limiting tip formation and stabilizing junctions. Small GTPases 35 25425145
2013 Conundrum, an ARHGAP18 orthologue, regulates RhoA and proliferation through interactions with Moesin. Molecular biology of the cell 35 23468526
2017 LARG GEF and ARHGAP18 orchestrate RhoA activity to control mesenchymal stem cell lineage. Bone 27 29208526
2018 IP3R3 silencing induced actin cytoskeletal reorganization through ARHGAP18/RhoA/mDia1/FAK pathway in breast cancer cell lines. Biochimica et biophysica acta. Molecular cell research 26 29630900
2022 Liquiritigenin alleviates doxorubicin-induced chronic heart failure via promoting ARHGAP18 and suppressing RhoA/ROCK1 pathway. Experimental cell research 21 34990617
2019 ARHGAP18: A Flow-Responsive Gene That Regulates Endothelial Cell Alignment and Protects Against Atherosclerosis. Journal of the American Heart Association 20 30630384
2017 The RhoGAP protein ARHGAP18/SENEX localizes to microtubules and regulates their stability in endothelial cells. Molecular biology of the cell 20 28251925
2021 The long noncoding RNA HOTAIRM1 controlled by AML1 enhances glucocorticoid resistance by activating RHOA/ROCK1 pathway through suppressing ARHGAP18. Cell death & disease 18 34262023
2020 YAP and the RhoC regulator ARHGAP18, are required to mediate flow-dependent endothelial cell alignment. Cell communication and signaling : CCS 18 32013974
2015 Expression of RXR, EcR, E75 and VtG mRNA levels in the hepatopancreas and ovary of the freshwater edible crab, Oziothelphusa senex senex (Fabricius, 1798) during different vitellogenic stages. Die Naturwissenschaften 13 25839079
2020 Stress-induced premature senescence activated by the SENEX gene mediates apoptosis resistance of diffuse large B-cell lymphoma via promoting immunosuppressive cells and cytokines. Immunity, inflammation and disease 12 33015970
2025 Multicomponent Reaction Integrating Selenium(II)-Nitrogen Exchange (SeNEx) Chemistry and Copper-Catalyzed Azide-Alkyne Cycloaddition (CuAAC). Angewandte Chemie (International ed. in English) 11 40000436
2024 ARHGAP18-ezrin functions as an autoregulatory module for RhoA in the assembly of distinct actin-based structures. eLife 11 38193818
2024 Selenium(II)-Nitrogen Exchange (SeNEx) Chemistry: A Good Chemistry Suitable for Nanomole-Scale Parallel Synthesis, DNA-encoded Library Synthesis and Bioconjugation. Chembiochem : a European journal of chemical biology 10 39379308
2018 Over-expression of ARHGAP18 suppressed cell proliferation, migration, invasion, and tumor growth in gastric cancer by restraining over-activation of MAPK signaling pathways. OncoTargets and therapy 10 29386906
2014 A novel cellular senescence gene, SENEX, is involved in peripheral regulatory T cells accumulation in aged urinary bladder cancer. PloS one 10 24505313
2021 Thiopurines correct the effects of autophagy impairment on intestinal healing - a potential role for ARHGAP18/RhoA. Disease models & mechanisms 9 33973626
2020 Advanced glycosylation end products (AGEs) controls proliferation, invasion and permeability through orchestrating ARHGAP18/RhoA pathway in human umbilical vein endothelial cells. Glycoconjugate journal 9 32016689
2018 Evidence for retinoic acid involvement in the regulation of vitellogenesis in the fresh water edible crab, Oziotelphusa senex senex. Comparative biochemistry and physiology. Part A, Molecular & integrative physiology 9 29655815
2007 Effect of retinoic acid on hemolymph glucose regulation in the fresh water edible crab Oziotelphusa senex senex. General and comparative endocrinology 7 17964575
2023 ARHGAP18 is Upregulated by Transcription Factor GATA1 Promotes the Proliferation and Invasion in Hepatocellular Carcinoma. Applied biochemistry and biotechnology 6 37171759
2020 A Screen for PKN3 Substrates Reveals an Activating Phosphorylation of ARHGAP18. International journal of molecular sciences 6 33092266
2017 Activation of human gonadotropin-releasing hormone receptor promotes down regulation of ARHGAP18 and regulates the cell invasion of MDA-MB-231 cells. Molecular and cellular endocrinology 6 28709956
1991 SENEX: a computer-based representation of cellular signal transduction processes in the central nervous system. Computer applications in the biosciences : CABIOS 6 2059842
2025 Chemotherapy-induced cellular senescence promotes stemness of aggressive B-cell non-Hodgkin's lymphoma via CCR7/ARHGAP18/IKBα signaling activation. Journal for immunotherapy of cancer 5 39773566
2019 Stress-Induced Premature Senescence Promotes Proliferation by Activating the SENEX and p16INK4a/Retinoblastoma (Rb) Pathway in Diffuse Large B-Cell Lymphoma. Turkish journal of haematology : official journal of Turkish Society of Haematology 5 31327185
2017 Association of ARHGAP18 polymorphisms with schizophrenia in the Chinese-Han population. PloS one 5 28384650
1994 Modulation of protein metabolism in selected tissues of the crab, Oziotelphusa senex senex (Fabricius), under fenvalerate-induced stress. Ecotoxicology and environmental safety 5 7516287
2025 Upregulation of ARHGAP18 by miR-613 Inhibits Cigarette Smoke Extract-Induced Apoptosis and Epithelial-Mesenchymal Transition in Bronchial Epithelial Cells. International journal of chronic obstructive pulmonary disease 4 40698118
1995 Pesticidal impact on the protein metabolism of freshwater field crab, Oziotelphusa senex senex (Fabricius). Biomedical and environmental sciences : BES 4 7546342
1983 In vivo acute physiological stress induced by BHC on hemolymph biochemistry of Oziotelphusa senex senex, the Indian rice field crab. Toxicology letters 4 6194578
1983 Muscle nitrogen metabolism of freshwater crab, Oziotelphusa senex senex Fabricius, during acute and chronic sumithion intoxication. Toxicology letters 4 6353673
2017 ARHGAP18 is a novel gene under positive natural selection that influences HbF levels in β-thalassaemia. Molecular genetics and genomics : MGG 3 28983712
2025 The Rho effector ARHGAP18 coordinates a Hippo pathway feedback loop through YAP and Merlin to regulate the cytoskeleton and epithelial cell polarity. bioRxiv : the preprint server for biology 1 39651219
2022 Psectrascelis senex sp. nov. (Coleoptera: Tenebrionidae), a new species from the southern Atacama Desert, Chile. Zootaxa 1 36095396
2026 ARHGAP18 complexes with both YAP and Merlin and is required for basal actin bundles. Molecular biology of the cell 0 42126958
2026 Calcium(II)-Catalyzed Three-Component Alkoxyselenation of Allenes with Selenium-Nitrogen Exchange (SeNEx) Reagents. Organic letters 0 42253243
2025 The Imatinib-miR-335-5p-ARHGAP18 Axis Attenuates PDGF-Driven Pathological Responses in Pulmonary Artery Smooth Muscle Cells. International journal of molecular sciences 0 41096636
1992 The SENEX Project: knowledge representation in molecular pathology. Proceedings. Symposium on Computer Applications in Medical Care 0 1482900

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