Affinage

ARHGAP18

Rho GTPase-activating protein 18 · UniProt Q8N392

Length
663 aa
Mass
75.0 kDa
Annotated
2026-04-28
42 papers in source corpus 19 papers cited in narrative 19 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ARHGAP18 is a RhoGAP that spatially restricts Rho GTPase signaling to coordinate actin cytoskeleton organization, cell shape, migration, and vascular homeostasis. It catalyzes GTP hydrolysis on RhoA (and selectively RhoC in endothelial cells), and its GAP activity is enhanced by binding to active (phosphorylated) ERM proteins (ezrin, Moesin), which recruit it to specific cortical and microvillar domains to create local negative-feedback circuits that prevent aberrant myosin-II assembly and maintain epithelial and endothelial architecture (PMID:21865595, PMID:23468526, PMID:38193818). PKN3 phosphorylation further stimulates ARHGAP18 GAP activity, while upstream signals including shear stress, miR-200b, and the ERK–LOK–Ezrin axis regulate its expression and subcellular localization to control processes ranging from endothelial flow alignment and junction stability to mesenchymal stem cell lineage commitment (PMID:33092266, PMID:30630384, PMID:28619708, PMID:29208526). ARHGAP18 additionally stabilizes microtubules in a GAP-activity-dependent manner, modulates YAP nuclear localization downstream of Rho, and its loss in mice causes endothelial hypersprouting, accelerated atherosclerosis, and thoracic aortic aneurysm (PMID:28251925, PMID:32013974, PMID:25425145, PMID:28701309).

Mechanistic history

Synthesis pass · year-by-year structured walk · 8 steps
  1. 2010 Medium

    Before ARHGAP18's catalytic specificity was known, its depletion was shown to be required for endothelial cell survival under oxidative stress, establishing it as a regulator of stress-induced premature senescence via the p16/Rb pathway.

    Evidence siRNA knockdown with H2O2 stress, SA-β-gal staining and apoptosis assays in ECs

    PMID:20664062

    Open questions at the time
    • Single lab study
    • Mechanism linking ARHGAP18 to p16/Rb not defined at a molecular level
    • Whether RhoGAP activity is required for the senescence phenotype was not tested
  2. 2011 High

    Identification of ARHGAP18 as a RhoA-specific GAP resolved which Rho family member it inactivates and showed that it controls stress fiber dynamics, cell polarization, and migration by suppressing RhoA at the leading edge.

    Evidence Overexpression and siRNA knockdown with RhoA activity assays, immunofluorescence, cell spreading/migration assays

    PMID:21865595

    Open questions at the time
    • Mechanism of leading-edge recruitment was unknown
    • Substrate specificity toward other Rho GTPases in different cell types not tested
  3. 2013 High

    The Drosophila ortholog study revealed that ERM proteins (Moesin) recruit ARHGAP18 to the cell cortex, providing the first evidence that cortical localization and hence spatial control of RhoA inactivation depends on ERM interaction.

    Evidence Co-IP/pulldown, genetic epistasis, cortical localization assays in Drosophila

    PMID:23468526

    Open questions at the time
    • Whether mammalian ERM proteins use the same recruitment mechanism was not yet shown
    • Rac activation downstream of cortical ARHGAP18 lacked a defined molecular link
  4. 2014 High

    In endothelial cells, ARHGAP18 was found to preferentially target RhoC rather than RhoA, demonstrating cell-type-specific substrate selectivity; its loss caused vascular hypersprouting in zebrafish and mice, establishing a physiological role in angiogenesis.

    Evidence siRNA, ARHGAP18-KO mice, zebrafish morpholinos, tumor vascularization assays

    PMID:25425145

    Open questions at the time
    • Structural basis for RhoC vs. RhoA selectivity in ECs not determined
    • ROCK-dependent relocalization to junctions not fully mechanistically resolved
  5. 2017 High

    Multiple 2017 studies expanded ARHGAP18's functional scope: it stabilizes microtubules (via GAP-dependent ROCK/HDAC6 suppression), controls SMC phenotypic switching and aortic aneurysm through epigenetic mechanisms, determines MSC lineage fate by setting tonic RhoA levels, and is a target of miR-200b in breast cancer migration—collectively establishing ARHGAP18 as a broad integrator of Rho signaling across tissues.

    Evidence SIM/GSD/TIRF microscopy and biochemical fractionation for MT localization; Arhgap18-KO mice with ChIP and angiotensin-II challenge for aortic phenotype; G-LISA and lineage marker analysis in MSCs; miR-200b rescue and in vivo metastasis assays in breast cancer

    PMID:28251925 PMID:28619708 PMID:28701309 PMID:29208526

    Open questions at the time
    • How ARHGAP18 influences H3K4me3/H3K27me3 at target promoters mechanistically remains unknown
    • Whether microtubule stabilization is direct or entirely through Rho/ROCK/HDAC6 suppression is not resolved
  6. 2019 High

    ARHGAP18 was identified as a flow-responsive gene in endothelial cells required for atheroprotective alignment; its genetic ablation in ApoE-null mice accelerated atherosclerosis, linking it to cardiovascular disease pathogenesis.

    Evidence Laminar flow assays, ApoE/Arhgap18 double-KO mice on high-fat diet, NF-κB and ICAM-1 staining

    PMID:30630384

    Open questions at the time
    • Whether ARHGAP18 directly suppresses NF-κB or acts indirectly through RhoA is unknown
    • Flow-sensing mechanism upstream of ARHGAP18 expression not defined
  7. 2020 High

    The discovery that ARHGAP18 regulates YAP phosphorylation and nuclear localization connected Rho GTPase control to the Hippo pathway, showing that ARHGAP18 promotes YAP inactivation (cytoplasmic retention) in shear-stressed endothelial cells and that PKN3 phosphorylation enhances ARHGAP18 GAP activity.

    Evidence siRNA/overexpression with YAP localization and Cyr61 readouts; phosphoproteomic screen with analog-sensitive PKN3, in vitro kinase and GAP activity assays

    PMID:32013974 PMID:33092266

    Open questions at the time
    • Whether ARHGAP18 interaction with YAP is direct was not established until later
    • PKN3 phosphorylation sites on ARHGAP18 and their individual contributions remain unmapped
  8. 2024 High

    Reconstitution of the ezrin–ARHGAP18 interaction in vitro demonstrated that active (phosphorylated) ezrin directly binds ARHGAP18 and stimulates its GAP activity, establishing a local negative autoregulatory circuit in microvilli that prevents ectopic myosin-II assembly.

    Evidence Co-IP, in vitro GAP activity reconstitution with purified ezrin, CRISPR KO, structured illumination microscopy in epithelial cells

    PMID:38193818

    Open questions at the time
    • Binding interface between ezrin and ARHGAP18 not structurally resolved
    • Whether other ERM family members activate GAP activity to the same extent in mammalian cells needs quantification

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis for ERM-mediated GAP activation, the identity of PKN3 phosphorylation sites, how ARHGAP18 mechanistically couples to the Hippo/YAP pathway, and whether its direct interaction with YAP has functional consequences independent of RhoA regulation.
  • No crystal or cryo-EM structure of ARHGAP18 or its complex with ezrin/YAP
  • PKN3 phosphorylation sites on ARHGAP18 not mapped
  • RhoA-dependent versus RhoA-independent functions of ARHGAP18 on YAP not separated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 7
Localization
GO:0005856 cytoskeleton 3 GO:0005886 plasma membrane 3 GO:0005829 cytosol 2
Pathway
R-HSA-162582 Signal Transduction 7 R-HSA-1643685 Disease 2
Partners
EZRMSNPKN3RHOARHOCROCK1YAP1

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2011 ARHGAP18 functions as a GTPase-activating protein (GAP) for RhoA; overexpression suppresses RhoA activity and disrupts stress fiber formation, while siRNA knockdown enhances stress fiber formation and sustained RhoA activation upon cell attachment. ARHGAP18 localizes to the leading edge during cell spreading and migration and is required for cell polarization. Overexpression/siRNA knockdown, RhoA activity assays, immunofluorescence, cell spreading/migration assays Molecular biology of the cell High 21865595
2013 The Drosophila ARHGAP18 orthologue Conundrum (Conu) interacts with Moesin (an 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 function also requires increased Rac activity. Genetic interaction, Co-IP/pulldown, cell cortex localization assays, epistasis in Drosophila Molecular biology of the cell High 23468526
2014 ARHGAP18 acts specifically on RhoC (not RhoA) in endothelial cells to suppress tip cell behavior and stabilize junctions; loss of ARHGAP18 promotes endothelial hypersprouting in zebrafish and murine retinal vessels. ARHGAP18 relocalizes to angiogenic/destabilized EC junctions in a ROCK-dependent manner, suppressing tip cell genes Dll4, Flk-1, and Flt-4. siRNA knockdown, ARHGAP18-knockout mice, zebrafish genetics, immunofluorescence, tumor vascularization assays Small GTPases High 25425145
2017 ARHGAP18 localizes to microtubules in endothelial cells (confirmed by structured illumination, GSD, and TIRF microscopy, plus biochemical fractionation); ARHGAP18 depletion destabilizes microtubules (reduced acetylated α-tubulin and glu-tubulin), impairing endothelin-1 secretion and neutrophil transmigration. Microtubule stabilization by ARHGAP18 requires its GAP activity and is rescued by ROCK and HDAC6 inhibition. Thrombin enhances the plasma membrane-bound fraction of ARHGAP18. SIM/GSD/TIRF microscopy, biochemical fractionation, siRNA knockdown, ARHGAP18-KO mouse endothelial cells, GAP-mutant rescue experiments Molecular biology of the cell High 28251925
2017 miR-200b directly downregulates ARHGAP18 in triple-negative breast cancer cells; enforced miR-200b expression activates RhoA, increases focal adhesions and stress fibers, and reduces migration/metastasis. Overexpression of ARHGAP18 in miR-200b-expressing cells reduces RhoA activity and restores migration, and ROCK inhibition phenocopies miR-200b effects, placing ARHGAP18 upstream of ROCK in this axis. miR-200b overexpression/ARHGAP18 KO, RhoA activity assays, cell migration assays, ROCK inhibitor pharmacology, in vivo metastasis assays Cancer research High 28619708
2017 In smooth muscle cells, ARHGAP18 deficiency (global KO mice) leads to a synthetic/proinflammatory phenotype with H3K4me3 enrichment and H3K27me3 depletion at MMP2 and TNF-α promoters, and loss of Akt activation; mTORC1 inhibitor rapamycin partially rescues the abnormal SMC phenotype. ARHGAP18 KO mice develop thoracic aortic aneurysm with increased frequency upon angiotensin II challenge. Arhgap18-/- mice, ChIP for histone marks, rapamycin pharmacological rescue, angiotensin II challenge Circulation research High 28701309
2017 LARG GEF and ARHGAP18 coordinately control RhoA activity in mesenchymal stem cells to determine lineage fate: ARHGAP18 knockdown increases basal RhoA activity, actin stress fibers, suppresses adipogenesis, and enhances osteogenic commitment (alkaline phosphatase, Sp7/Alpl/Bglap). ARHGAP18 provides tonic RhoA inhibition in static conditions, whereas LARG mediates mechanical strain-induced RhoA activation. siRNA knockdown, RhoA activity assays (G-LISA), Oil-Red-O staining, alkaline phosphatase staining, qPCR of lineage markers, mechanical strain experiments Bone High 29208526
2018 IP3R3 silencing in breast cancer cells decreases ARHGAP18 expression and reduces RhoA activity (G-LISA), Cdc42, and Y861-FAK phosphorylation, placing ARHGAP18 downstream of IP3R3 in the IP3R3/ARHGAP18/RhoA/mDia1/FAK pathway that controls actin cytoskeletal organization and cell morphology. siRNA knockdown of IP3R3, RhoA G-LISA activity assay, Western blot for ARHGAP18/FAK phosphorylation, immunofluorescence Biochimica et biophysica acta. Molecular cell research Medium 29630900
2019 ARHGAP18 is a flow-responsive gene in endothelial cells; its depletion inhibits EC alignment in the direction of laminar flow, promotes NF-κB activation, disrupts junctions, increases ICAM-1, and decreases eNOS. ApoE-/- Arhgap18-/- double-KO mice on high-fat diet develop early-onset atherosclerosis in atheroprotected regions. siRNA depletion, laminar flow chamber assays, ApoE/Arhgap18 double-KO mouse atherosclerosis model, immunofluorescence for NF-κB/ICAM-1/eNOS Journal of the American Heart Association High 30630384
2020 YAP is downstream of ARHGAP18 in mature endothelial cells under laminar shear stress: ARHGAP18 depletion decreases YAP expression but causes its nuclear localization (activation) and disrupts VE-Cadherin at junctions; ARHGAP18 overexpression upregulates YAP, promotes its phosphorylation (inactivation), and decreases the YAP target gene Cyr61. This ARHGAP18-YAP axis is required for atheroprotective EC alignment. siRNA depletion, ARHGAP18 overexpression, confocal imaging of YAP nuclear localization, Cyr61 reporter, ARHGAP18-KO mouse in vivo imaging Cell communication and signaling : CCS Medium 32013974
2020 PKN3 (a serine/threonine kinase) phosphorylates ARHGAP18 in vitro; the interaction between PKN3 and ARHGAP18 is mediated via the N-terminal part of ARHGAP18, is enhanced upon ARHGAP18 phosphorylation, and PKN3-mediated phosphorylation of ARHGAP18 enhances its GAP domain activity to further reduce active RhoA levels. Phosphoproteomic screen with analog-sensitive PKN3, in vitro kinase assay, Co-IP, GAP domain activity assay, RhoA activity measurement International journal of molecular sciences High 33092266
2021 ATG16L1 knockdown (autophagy impairment) causes accumulation of SQSTM1/p62 and ARHGAP18 protein, leading to decreased RhoA activity and impaired epithelial cell migration; thiopurines reverse this effect. ARHGAP18 accumulation appears mediated by impaired autophagic degradation and observed in human Crohn's disease tissue. Lentiviral ATG16L1/ATG5 KD, G-LISA for RhoA activity, immunofluorescence for ARHGAP18/p62, scratch assay, pharmacological autophagy inhibition, human tissue staining Disease models & mechanisms Medium 33973626
2021 The lncRNA HOTAIRM1 (controlled by AML1) represses ARHGAP18 expression by binding to its transcriptional inhibitory region and by sequestering the transcription factor AML1 from binding the ARHGAP18 regulatory region; HOTAIRM1-mediated ARHGAP18 suppression increases RhoA/ROCK1 signaling to promote glucocorticoid resistance in leukemia cells. ChIRP-seq, RNA interference, luciferase reporter, co-immunoprecipitation of HOTAIRM1-AML1, ChIP for AML1 at HOTAIRM1 promoter, ROCK1 inhibitor rescue Cell death & disease Medium 34262023
2024 ARHGAP18 is localized by binding to active (phosphorylated) microvillar ezrin, and this interaction enhances ARHGAP18's RhoGAP activity; the ezrin-ARHGAP18 complex acts as a negative autoregulatory module to locally reduce RhoA activity in microvilli. Loss of ARHGAP18 causes aberrant assembly of myosin-2 filaments inside microvilli and disrupts the distinction between microvilli and the terminal web. Co-immunoprecipitation, in vitro RhoGAP activity assay with ezrin, CRISPR/Cas9 KO, immunofluorescence, structured illumination microscopy eLife High 38193818
2025 ERK inhibits Ezrin activity in the cell body by phosphorylating the C-terminal tail of the Ezrin-activating kinase LOK; reduced Ezrin activity releases Ezrin's recruitment/activation of ARHGAP18, thereby de-repressing RhoA and enabling stress fiber assembly for cell migration. Thus ARHGAP18 operates downstream of an ERK-LOK-Ezrin axis. Phosphoproteomics, kinase assays, Ezrin/ARHGAP18 interaction studies, cell migration assays, RhoA activity measurements bioRxivpreprint Medium bio_10.1101_2025.11.15.688645
2025 ARHGAP18 forms a complex with the Hippo pathway transcription factor YAP; CRISPR/Cas9 KO of ARHGAP18 causes cytoskeletal alterations driven by both dysregulated RhoA signaling and aberrant nuclear localization of YAP, demonstrating coordinate regulation of the Hippo and Rho GTPase pathways through ARHGAP18. Co-immunoprecipitation of ARHGAP18-YAP complex, CRISPR/Cas9 KO, STORM super-resolution microscopy of actin filaments, immunofluorescence for YAP localization bioRxivpreprint Medium 39651219
2010 ARHGAP18/SENEX regulates stress-induced premature senescence in endothelial cells through the p16(INK4a)/retinoblastoma protein pathway; SENEX depletion by siRNA causes endothelial apoptosis, indicating it is required for EC survival under H2O2-mediated stress. siRNA knockdown, H2O2 stress induction, senescence-associated β-galactosidase staining, apoptosis assays Blood Medium 20664062
2017 Activation of the GnRH receptor in MDA-MB-231 breast cancer cells decreases ARHGAP18 expression, which correlates with increased cell adhesion and reduced tumor invasion, placing ARHGAP18 downstream of GnRHR signaling in regulation of cell invasiveness. Microarray gene expression, GnRHR activation, siRNA knockdown of ARHGAP18, cell adhesion and invasion assays Molecular and cellular endocrinology Low 28709956
2023 Transcription factor GATA1 binds directly to the ARHGAP18 promoter and activates its transcription in hepatocellular carcinoma cells; GATA1 overexpression rescues the effects of ARHGAP18 silencing, defining GATA1 as an upstream transcriptional activator of ARHGAP18. Luciferase reporter assay, ChIP-qPCR, immunofluorescence, gain/loss-of-function rescue experiments Applied biochemistry and biotechnology Medium 37171759

Source papers

Stage 0 corpus · 42 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 87 21865595
2017 ARHGAP18 Downregulation by miR-200b Suppresses Metastasis of Triple-Negative Breast Cancer by Enhancing Activation of RhoA. Cancer research 71 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
2014 ARHGAP18: an endogenous inhibitor of angiogenesis, limiting tip formation and stabilizing junctions. Small GTPases 34 25425145
2013 Conundrum, an ARHGAP18 orthologue, regulates RhoA and proliferation through interactions with Moesin. Molecular biology of the cell 34 23468526
2024 Bioinspired Selenium-Nitrogen Exchange (SeNEx) Click Chemistry Suitable for Nanomole-Scale Medicinal Chemistry and Bioconjugation. Angewandte Chemie (International ed. in English) 31 38343199
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 20 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
2020 YAP and the RhoC regulator ARHGAP18, are required to mediate flow-dependent endothelial cell alignment. Cell communication and signaling : CCS 18 32013974
2021 The long noncoding RNA HOTAIRM1 controlled by AML1 enhances glucocorticoid resistance by activating RHOA/ROCK1 pathway through suppressing ARHGAP18. Cell death & disease 17 34262023
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
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
2025 Multicomponent Reaction Integrating Selenium(II)-Nitrogen Exchange (SeNEx) Chemistry and Copper-Catalyzed Azide-Alkyne Cycloaddition (CuAAC). Angewandte Chemie (International ed. in English) 9 40000436
2024 ARHGAP18-ezrin functions as an autoregulatory module for RhoA in the assembly of distinct actin-based structures. eLife 9 38193818
2021 Thiopurines correct the effects of autophagy impairment on intestinal healing - a potential role for ARHGAP18/RhoA. Disease models & mechanisms 9 33973626
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
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 8 39379308
2020 Advanced glycosylation end products (AGEs) controls proliferation, invasion and permeability through orchestrating ARHGAP18/RhoA pathway in human umbilical vein endothelial cells. Glycoconjugate journal 7 32016689
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
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
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
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 3 40698118
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 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 2 39773566
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
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