Affinage

ARHGAP5

Rho GTPase-activating protein 5 · UniProt Q13017

Length
1502 aa
Mass
172.5 kDa
Annotated
2026-06-09
30 papers in source corpus 24 papers cited in narrative 24 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

ARHGAP5 (p190-B RhoGAP) is a Rho-family GTPase-activating protein that inactivates RhoA, Rac1, and CDC42 to govern actin cytoskeleton organization, cell migration/invasion, and tissue morphogenesis (PMID:8537347, PMID:10939588). The protein comprises an N-terminal GTPase domain and a C-terminal Rho GAP domain, the latter conferring GAP activity toward RhoA, Rac1, and CDC42 in vitro; it is recruited to the plasma membrane beneath sites of integrin (α5β1) engagement with fibronectin, coupling adhesion signaling to local Rho regulation (PMID:8537347). Across multiple cell types ARHGAP5 acts as the effector that deactivates RhoA downstream of upstream receptors—including CD147 in hepatocellular carcinoma (PMID:27601938), ANGPTL4 in brain endothelium (PMID:31766605), and N-cadherin/ARVCF in hepatocytes [PMID:bio_10.1101_2025.10.06.680681]—to control cell spreading, motility, and epithelial-mesenchymal transition (PMID:18996642, PMID:32483433). In vivo, p190-B operates upstream of IGF-IRS signaling to drive mammary ductal and embryonic bud morphogenesis, where both loss and overexpression disrupt terminal end bud development (PMID:12637587, PMID:16469769, PMID:17662267), and it restrains hematopoietic stem cell self-renewal through a TGF-β–p38MAPK–p16(Ink4a) network and supports the bone marrow niche via mesenchymal Wnt signaling (PMID:19713466, PMID:23563238, PMID:28176763). In endothelium, p190-B is required for RhoB inactivation and barrier recovery; a patient point mutation impairing this function underlies fatal systemic capillary leak syndrome (PMID:29097442). ARHGAP5 expression is transcriptionally activated by CREB1 (PMID:32483433), c-JUN (repressed by SIRT1-mediated deacetylation) (PMID:30250020), and DEC1 (PMID:39191013), and is post-transcriptionally tuned by miR-486-5p targeting its 3'-UTR (PMID:23474761, PMID:35477045), by m6A modification via METTL3/YTHDF1 (PMID:36077054), and by DKC1-dependent pseudouridylation (PMID:39368791). p190-B is functionally redundant with the paralog p190-A (ARHGAP35), and their double knockout is synthetically lethal in endometrial cancer cells [PMID:bio_10.1101_2025.10.16.682927].

Mechanistic history

Synthesis pass · year-by-year structured walk · 23 steps
  1. 1995 High

    Established that ARHGAP5 is a bifunctional GTPase/Rho-GAP protein with intrinsic GAP activity and that adhesion couples it to membrane Rho regulation, defining its core biochemical identity.

    Evidence Recombinant GAP activity assay on RhoA/Rac1/CDC42, immunofluorescence, and fibronectin bead adhesion in fibroblasts

    PMID:8537347

    Open questions at the time
    • Function of the N-terminal GTPase domain and middle domain not resolved
    • Which GTPase is the physiological substrate in cells not established here
  2. 1998 Medium

    Defined the gene's exon structure, domain architecture, and cross-species conservation, enabling mouse genetic study of p190-B.

    Evidence cDNA/genomic sequencing and genetic cross mapping of mouse Arhgap5

    PMID:9838117

    Open questions at the time
    • No functional assay performed
    • Role of the uncharacterized middle domain unknown
  3. 2000 Medium

    Connected p190-B activity to actin cytoskeleton remodeling in mammary epithelial cells, linking its biochemistry to cell shape and migration.

    Evidence Transient overexpression with actin staining in MCF-10A cells

    PMID:10939588

    Open questions at the time
    • Overexpression-only readout
    • Specific GTPase mediating the actin phenotype not pinned down
  4. 2003 High

    Positioned p190-B upstream of IGF-IRS signaling in mammary ductal development through cell-autonomous loss-of-function genetics.

    Evidence p190-B knockout/heterozygous mice, mammary transplantation, IRS-1/2 Western blot

    PMID:12637587

    Open questions at the time
    • Molecular link between RhoGAP activity and IRS expression unresolved
    • Whether the effect requires GAP catalytic function not tested
  5. 2006 High

    Showed that precise dosage of p190-B is required for normal branching morphogenesis, complementing loss-of-function with gain-of-function in vivo.

    Evidence Inducible transgenic overexpression, histology, IGF pathway signaling analysis

    PMID:16469769

    Open questions at the time
    • Direct GTPase target driving morphogenesis defects not defined
    • Mechanism connecting p190-B to stromal/macrophage phenotypes unclear
  6. 2007 High

    Established genetic epistasis placing p190-B upstream of IGF-IRS in embryonic mammary bud epithelial-mesenchymal interactions.

    Evidence Multiple knockout models (p190-B, IRS-1/2, IGF-1R), embryonic bud and proliferation analysis

    PMID:17662267

    Open questions at the time
    • Biochemical mechanism linking p190-B to IGF-IRS not resolved
  7. 2009 High

    Identified p190-B as a restraint on HSC self-renewal acting through p16(Ink4a), extending its role into stem cell biology.

    Evidence p190-B knockout mice, serial bone marrow transplantation, p16Ink4a transcriptional analysis

    PMID:19713466

    Open questions at the time
    • Link from RhoGAP activity to p16Ink4a regulation not mechanistically defined
  8. 2013 High

    Revealed a non-cell-autonomous niche role: p190-B is required in mesenchymal stem cells for Wnt-dependent hematopoietic support and lineage fate.

    Evidence p190-B knockout mice, MSC/BM co-culture, Wnt assays, CFU lineage assays

    PMID:23563238

    Open questions at the time
    • How p190-B/Rho activity intersects Wnt signaling not detailed
  9. 2013 Medium

    Demonstrated that p190-B negatively regulates RhoA to drive HCC cell spreading and migration, and that the gene is amplified at 14q12 in cancer.

    Evidence Copy-number microarray, RhoA activity assay, migration/spreading assays with RNAi in Huh-7 cells

    PMID:18996642

    Open questions at the time
    • Single cell line
    • Upstream regulators of p190-B in HCC not addressed here
  10. 2017 High

    Showed p190-B controls HSPC fate choice and symmetric self-renewal via a non-canonical TGF-β–p38MAPK network, refining its stem cell mechanism.

    Evidence p190-B knockout mice, single-cell HSPC culture, TGF-β1 ELISA, p38MAPK activity, asymmetric division analysis

    PMID:28176763

    Open questions at the time
    • Direct biochemical chain from RhoGTPase to TGF-β not established
  11. 2017 High

    Provided human genetic evidence that p190-B-mediated RhoB inactivation is required for endothelial barrier recovery, linking the gene to systemic capillary leak syndrome.

    Evidence Patient-derived endothelial cells, siRNA phenocopy, TEER/permeability assays, RhoB activity measurement

    PMID:29097442

    Open questions at the time
    • How the point mutation alters GAP catalysis structurally not resolved
    • RhoB as substrate selectivity mechanism not defined
  12. 2016 Medium

    Placed p190-B downstream of CD147 in a RhoA-deactivating motility pathway in HCC.

    Evidence FRET RhoA biosensor, wound-healing, qRT-PCR/Western, siRNA epistasis

    PMID:27601938

    Open questions at the time
    • Single lab
    • How CD147 upregulates p190-B transcription/protein unresolved
  13. 2018 Medium

    Identified the SIRT1–c-JUN axis as a transcriptional repressor of ARHGAP5, adding a layer of expression control relevant to gastric cancer invasion.

    Evidence Co-IP, deacetylation assay, ChIP, migration/invasion assays, in vivo metastasis

    PMID:30250020

    Open questions at the time
    • Single lab
    • Direct c-JUN occupancy dynamics on ARHGAP5 promoter limited
  14. 2015 Medium

    Showed miR-744 non-canonically upregulates ARHGAP5 via promoter interaction to enhance migration/invasion, expanding post-transcriptional regulation.

    Evidence Promoter luciferase, qRT-PCR/Western, migration/invasion gain/loss in NPC cells

    PMID:25961434

    Open questions at the time
    • Non-canonical mechanism single lab
    • Direct promoter binding mode not structurally defined
  15. 2013 Medium

    Established miR-486-5p as a direct 3'-UTR repressor of ARHGAP5 that suppresses lung cancer metastasis, later independently confirmed in trophoblasts.

    Evidence Luciferase 3'-UTR reporter, migration/invasion, in vivo metastasis (2013); replicated in HTR8/SVneo trophoblasts (2022)

    PMID:23474761 PMID:35477045

    Open questions at the time
    • Broader miRNA regulatory network not mapped
  16. 2019 Medium

    Embedded ARHGAP5 in the ANGPTL4/RhoA/MYL5 cascade controlling blood-brain barrier disruption during bacterial meningitis.

    Evidence siRNA, recombinant ANGPTL4, permeability assays in vitro/in vivo, RhoA activity assay

    PMID:31766605

    Open questions at the time
    • Single lab
    • How ANGPTL4 signals to ARHGAP5 not defined
  17. 2020 Medium

    Showed CREB1 directly drives ARHGAP5 transcription and miR-137 loss stabilizes its mRNA to promote colorectal cancer EMT and metastasis.

    Evidence ChIP, RNAi, RhoA activity assay, EMT markers, RNA-Seq, xenografts

    PMID:32483433

    Open questions at the time
    • Single lab
    • Relative contribution of transcriptional vs mRNA-stability control unquantified
  18. 2022 Medium

    Defined an ADAR1–METTL3–m6A–YTHDF1 axis that increases ARHGAP5 expression to drive breast cancer progression, adding RNA-modification control.

    Evidence Co-IP, RNA editing-seq, m6A-RIP, miRNA luciferase, in vivo tumor growth

    PMID:36077054

    Open questions at the time
    • Single lab
    • Direct functional consequence of m6A on ARHGAP5 translation/stability not separately resolved
  19. 2022 Medium

    Showed lncRNA ZFHX2-AS1 limits DKC1-dependent pseudouridylation of ARHGAP5 mRNA to control its stability and ovarian cancer EMT.

    Evidence RNA pulldown, DKC1 enzymatic/pseudouridylation assays, rescue, Rho GTPase activity assays

    PMID:39368791

    Open questions at the time
    • Single lab
    • Specific pseudouridylated residues and their mechanistic effect not mapped
  20. 2022 Low

    Tested but did not support a developmental role for ARHGAP5 orthologs in GnRH neuronal development, despite RhoGAP-domain variants in IHH patients.

    Evidence Exome sequencing and zebrafish gnrh3:egfp mutant modeling (negative result)

    PMID:36178483

    Open questions at the time
    • Negative zebrafish result; GAP assay was for paralog ARHGAP35 not ARHGAP5
    • Causality of ARHGAP5 variants in IHH not established
  21. 2024 Medium

    Identified DEC1 as a direct transcriptional regulator of ARHGAP5 controlling extravillous trophoblast invasion and linked it to environmental exposure.

    Evidence RNA-seq, ChIP on ARHGAP5 promoter, siRNA/overexpression, mouse miscarriage model

    PMID:39191013

    Open questions at the time
    • Single lab
    • Downstream Rho effector in trophoblasts not fully defined
  22. 2025 Medium

    Demonstrated functional redundancy with the paralog p190-A and a synthetic lethal vulnerability of dual p190 loss, defined through actin/Rho-ROCK phenotypes.

    Evidence CRISPR/Cas9 knockout, actin (CLAN) imaging, ROCK inhibition, synthetic lethality assay in endometrial cancer cells (preprint)

    PMID:bio_10.1101_2025.10.16.682927

    Open questions at the time
    • Preprint, not peer-reviewed
    • Molecular basis of redundancy and lethality not detailed
  23. 2025 Medium

    Placed p190-B downstream of N-cadherin/ARVCF in RhoA inactivation controlling hepatic polarity and bile canaliculi formation, via a direct ARVCF interaction.

    Evidence Live imaging, FRAP, genetic rescue, RhoA activity assay, ARVCF-p190B Co-IP (preprint)

    PMID:bio_10.1101_2025.10.06.680681

    Open questions at the time
    • Preprint, not peer-reviewed
    • Reciprocal validation and binding interface of ARVCF-p190B not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • The structural basis for p190-B's GTPase substrate selectivity (RhoA vs RhoB vs Rac1/CDC42) in different tissues and the function of its N-terminal GTPase and middle domains remain unresolved.
  • No structural model of substrate engagement in the corpus
  • Roles of the N-terminal GTPase and middle domains uncharacterized
  • How diverse upstream receptors converge on p190-B recruitment not unified

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 3
Localization
GO:0005829 cytosol 1 GO:0005886 plasma membrane 1
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-1266738 Developmental Biology 3 R-HSA-1643685 Disease 2
Partners
ARVCFCDC42ITGA5RAC1RHOARHOB

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 p190-B (ARHGAP5) was cloned and shown to contain an N-terminal GTPase domain and a C-terminal Rho GAP domain. A recombinant Rho GAP domain polypeptide demonstrated GAP activity for RhoA, Rac1, and CDC42Hs in vitro. p190-B localizes diffusely in the cytoplasm and in fibrillar patterns co-localizing with the α5β1 integrin receptor for fibronectin. Adhesion of fibronectin-coated latex beads recruited significant amounts of p190-B and Rho to the plasma membrane beneath the bead binding site, establishing an integrin-dependent membrane recruitment mechanism. Recombinant protein GAP activity assay (in vitro), immunoprecipitation, immunofluorescence, fibronectin bead adhesion assay The Journal of biological chemistry High 8537347
1998 The mouse p190-B (Arhgap5/Gfi2) gene encodes a protein with ~97% amino acid identity to human p190-B, with a domain architecture comprising an N-terminal GTPase domain, a middle domain of unknown function, and a C-terminal Rho GAP domain distributed across multiple exons. The gene maps to mouse chromosome 12, syntenic with the human 14q locus. cDNA cloning, genomic sequencing, Northern blot, multilocus genetic cross mapping Biochimica et biophysica acta Medium 9838117
2000 Transient transfection of a p190-B expression construct into MCF-10A human mammary epithelial cells disrupted the actin cytoskeleton, indicating that p190-B modulates Rho-regulated signaling pathways that influence cell migration and invasion. Transient transfection, actin cytoskeleton staining (immunofluorescence) Cell growth & differentiation Medium 10939588
2003 p190-B haploinsufficiency in mice caused decreased ductal outgrowth due to reduced proliferation in cap cells of terminal end buds, phenocopying IGF-I receptor null mammary epithelium. p190-B-deficient epithelial transplants failed to produce outgrowths in cleared fat pads, confirming a cell-autonomous role. Decreased expression of IRS-1 and IRS-2 was observed in TEBs of p190-B heterozygous mice, placing p190-B upstream of IGF signaling. p190-B knockout/heterozygous mouse model, mammary transplantation, proliferation assays, Western blot for IRS-1/2 Molecular endocrinology High 12637587
2006 Tetracycline-inducible overexpression of p190-B in the developing mammary gland caused abnormal terminal end buds with aberrant budding, thickened stroma, increased branching, delayed ductal elongation, and hyperplastic lesions during pregnancy. Overexpression altered IGF pathway signaling and caused discontinuous myoepithelial cell layer and macrophage infiltration, demonstrating that precise control of p190-B activity is required for normal branching morphogenesis. Inducible transgenic mouse overexpression, histology, immunostaining, signaling analysis Molecular endocrinology High 16469769
2007 p190-B-deficient embryos displayed defects in embryonic mammary bud development (smaller buds, fewer cells, impaired mesenchymal proliferation). These phenotypes overlapped with IRS-1/2 double knockout embryos, placing p190-B upstream of IGF-IRS signaling in epithelial-mesenchymal interactions required for mammary bud morphogenesis. p190-B knockout mouse model, IRS-1/2 double knockout, IGF-1R knockout, embryonic mammary bud analysis, proliferation assays Developmental biology High 17662267
2008 ARHGAP5 (p190-B RhoGAP) is amplified at chromosomal region 14q12 in hepatocellular carcinoma cells. p190-B promotes cell spreading and migration by negatively regulating RhoA activity in Huh-7 hepatocellular carcinoma cells. High-density oligonucleotide microarray (copy number), RhoA activity assay, cell spreading and migration assays, RNAi knockdown Cancer letters Medium 18996642
2009 Loss of p190-B RhoGAP in hematopoietic stem cells (HSCs) enhanced long-term engraftment during serial transplantation and maintained functional HSC-enriched cells. p190-B deficiency repressed upregulation of p16(Ink4a) in HSCs during transplantation, providing a mechanism for p190-B-mediated control of HSC self-renewal. p190-B knockout mouse, serial bone marrow transplantation, ex vivo culture, transcriptional analysis (p16Ink4a) Blood High 19713466
2013 p190-B deletion in mice causes hematopoietic failure during ontogeny in a non-cell-autonomous manner. p190-B-/- mesenchymal stem cells (MSCs) are dysfunctional in supporting hematopoiesis due to impaired Wnt signaling, and p190-B loss alters MSC lineage fate specification to osteoblast and adipocyte lineages, disrupting the functional bone marrow niche. p190-B knockout mouse, MSC/bone marrow co-culture, Wnt signaling assay, colony-forming unit assays (CFU-F, CFU-adipocyte, CFU-osteoblast) Leukemia High 23563238
2013 miR-486-5p directly binds to the 3'-UTR of ARHGAP5 mRNA (validated by luciferase assay), reducing ARHGAP5 expression and thereby inhibiting lung cancer cell migration and invasion. Reduced ARHGAP5 expression phenocopied miR-486-5p overexpression. Luciferase reporter assay, qRT-PCR, Western blot, migration/invasion assays, in vivo metastasis model Oncogene Medium 23474761
2015 miR-744 directly interacts with the ARHGAP5 promoter and transcriptionally upregulates ARHGAP5 expression (rather than the typical miRNA mechanism of mRNA degradation). Reintroduction of ARHGAP5 mimicked miR-744-enhanced migration and invasion in NPC cells, while silencing ARHGAP5 abrogated miR-744-induced effects. Promoter luciferase assay, qRT-PCR, Western blot, migration/invasion assays, gain/loss-of-function Oncotarget Medium 25961434
2016 CD147 promotes hepatocellular carcinoma cell motility by upregulating p190-B RhoGAP at both mRNA and protein levels, leading to RhoA deactivation, reduced stress fiber and focal adhesion formation. Silencing p190-B blunted CD147's effect on cell movement, placing p190-B downstream of CD147 in a motility pathway. Wound-healing assay, RhoA biosensor (FRET-based), qRT-PCR, Western blot, immunofluorescence, siRNA knockdown Cancer cell international Medium 27601938
2017 A point mutation in p190B RhoGAP (ARHGAP5) in a patient with fatal systemic capillary leak syndrome impairs RhoB inactivation in dermal microvascular endothelial cells. TNF transiently activates RhoB in ECs coincident with barrier leak, and p190B is required for RhoB inactivation and barrier recovery. siRNA knockdown of p190B in normal ECs replicated the patient-derived EC phenotype of impaired barrier recovery. Patient-derived endothelial cell culture, siRNA knockdown, transendothelial electrical resistance (TEER), permeability assay, RhoB activity measurement The Journal of experimental medicine High 29097442
2017 Loss of p190-B RhoGAP in HSPCs normalizes TGF-β1 levels and p38MAPK activity. p190-B loss promotes symmetric retention of multi-lineage capacity in single HSPCs, linking p190-B-RhoGTPase activity to a non-canonical TGF-β–p38MAPK signaling network that controls HSPC fate choice and self-renewal. p190-B knockout mouse, HSPC transplantation, single-cell culture, TGF-β1 ELISA, p38MAPK activity assay, asymmetric division analysis Nature communications High 28176763
2018 SIRT1 suppresses ARHGAP5 expression by physically associating with transcription factor c-JUN and deacetylating and inhibiting c-JUN's transcriptional activity, reducing ARHGAP5 promoter-driven transcription. ARHGAP5 knockdown inhibited GC cell migration and invasion, and ARHGAP5 was found to be in the SIRT1-mediated inhibition pathway. mRNA microarray, Co-immunoprecipitation (SIRT1-c-JUN interaction), deacetylation assay, ChIP, migration/invasion assays, in vivo metastasis model Cell death & disease Medium 30250020
2019 ANGPTL4 promotes blood-brain barrier disruption via the ARHGAP5/RhoA/MYL5 signaling cascade in brain microvascular endothelial cells infected with meningitic E. coli. ARHGAP5 acts as an intermediate between ANGPTL4 and RhoA activation, with downstream MYL5 negatively regulating barrier function. siRNA knockdown, recombinant ANGPTL4 treatment, permeability assay in vitro and in vivo, Western blot, RhoA activity assay Pathogens Medium 31766605
2020 ARHGAP5 promotes colorectal cancer epithelial-mesenchymal transition by negatively regulating RhoA activity. CREB1 transcriptionally upregulates ARHGAP5 expression (established by ChIP), and decreased miR-137 contributes to ARHGAP5 mRNA stability. ARHGAP5 suppression reduces CRC cell metastasis in vitro and in xenograft models. ChIP assay, RNAi, RhoA activity assay, EMT markers, RNA-Seq, xenograft models, Western blot Theranostics Medium 32483433
2022 ADAR1 interacts with METTL3 and edits METTL3 mRNA to change its miR-532-5p binding site, leading to increased METTL3 protein, which then targets ARHGAP5 mRNA for m6A modification recognized by YTHDF1, promoting ARHGAP5 expression and breast cancer progression. Co-IP (ADAR1-METTL3), RNA editing sequencing, m6A-RIP, miRNA luciferase assay, in vivo tumor growth, knockdown/overexpression International journal of molecular sciences Medium 36077054
2022 ARHGAP5 promotes ovarian cancer epithelial-mesenchymal transition by regulating Rho GTPase activities. The lncRNA ZFHX2-AS1 interacts with and attenuates DKC1 pseudouridine synthase activity, thereby reducing pseudouridylation of ARHGAP5 mRNA and decreasing its stability. Re-expression of ARHGAP5 partially reversed the tumor-suppressive effects of ZFHX2-AS1. RNA pulldown, DKC1 enzymatic activity assay, pseudouridylation assay, in vitro and in vivo functional assays, ARHGAP5 rescue experiments, Rho GTPase activity assays Cellular signalling Medium 39368791
2022 miR-486-5p directly targets the 3'-UTR of ARHGAP5 mRNA (validated by luciferase reporter assay in HTR8/SVneo trophoblast cells), reducing ARHGAP5 expression and suppressing trophoblast cell migration and invasion. ARHGAP5 siRNA knockdown phenocopied miR-486-5p overexpression. Luciferase reporter assay (ARHGAP5 3'-UTR), RT-qPCR, Western blot, wound healing assay, invasion assay, siRNA Placenta Medium 35477045
2022 ARHGAP5 missense variants in the RhoGAP domain identified in IHH patients; arhgap5 zebrafish mutants did not display significant GnRH3-GFP+ neuronal area abnormalities, providing a negative result for a developmental role of ARHGAP5 orthologs in GnRH neuronal development in zebrafish. Exome sequencing, in vitro GAP activity assay (for ARHGAP35 variant), zebrafish gnrh3:egfp modeling Genetics in medicine Low 36178483
2024 DEC1 directly regulates ARHGAP5 transcription in extravillous trophoblasts (EVTs); DEC1 inhibits trophoblast invasion by directly regulating ARHGAP5 transcription. BaA suppresses DEC1 (by promoting abnormal methylation), leading to altered ARHGAP5 expression and impaired trophoblast invasion. RNA-seq, ChIP (DEC1 on ARHGAP5 promoter), siRNA knockdown, overexpression, mouse miscarriage model Journal of hazardous materials Medium 39191013
2025 CRISPR/Cas9 knockout of p190B (ARHGAP5) in endometrial cancer cells causes actin remodeling with formation of Cross-Linked Actin Networks (CLANs) dependent on the Rho/ROCK pathway, phenocopying p190A (ARHGAP35) knockout. Double knockout of both p190A and p190B is synthetically lethal in endometrial cancer cells, revealing functional redundancy and a synthetic lethal vulnerability. CRISPR/Cas9 knockout, actin cytoskeleton imaging, ROCK inhibitor treatment, proteomic analysis, synthetic lethality assay bioRxivpreprint Medium bio_10.1101_2025.10.16.682927
2025 N-cadherin maintains hepatic polarity by facilitating RhoA inactivation through the p120-catenin family member ARVCF and its partner p190B/ARHGAP5. This places p190B downstream of N-cadherin/ARVCF and upstream of RhoA in the control of bile canaliculi formation. Live imaging, FRAP, genetic rescue, RhoA activity assay, co-immunoprecipitation (ARVCF-p190B interaction) bioRxivpreprint Medium bio_10.1101_2025.10.06.680681

Source papers

Stage 0 corpus · 30 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 Downregulation of miR-486-5p contributes to tumor progression and metastasis by targeting protumorigenic ARHGAP5 in lung cancer. Oncogene 210 23474761
2019 Impaired autophagic degradation of lncRNA ARHGAP5-AS1 promotes chemoresistance in gastric cancer. Cell death & disease 159 31097692
1995 p190-B, a new member of the Rho GAP family, and Rho are induced to cluster after integrin cross-linking. The Journal of biological chemistry 113 8537347
2018 SIRT1 suppresses the migration and invasion of gastric cancer by regulating ARHGAP5 expression. Cell death & disease 52 30250020
2015 MiR-744 functions as a proto-oncogene in nasopharyngeal carcinoma progression and metastasis via transcriptional control of ARHGAP5. Oncotarget 44 25961434
2003 p190-B RhoGAP regulates mammary ductal morphogenesis. Molecular endocrinology (Baltimore, Md.) 42 12637587
2022 N6 -methyladenosine-modified lncRNA ARHGAP5-AS1 stabilises CSDE1 and coordinates oncogenic RNA regulons in hepatocellular carcinoma. Clinical and translational medicine 40 36354136
2008 A novel amplification target, ARHGAP5, promotes cell spreading and migration by negatively regulating RhoA in Huh-7 hepatocellular carcinoma cells. Cancer letters 40 18996642
2006 P190-B Rho GTPase-activating protein overexpression disrupts ductal morphogenesis and induces hyperplastic lesions in the developing mammary gland. Molecular endocrinology (Baltimore, Md.) 39 16469769
2022 RNA Editing Enzyme ADAR1 Regulates METTL3 in an Editing Dependent Manner to Promote Breast Cancer Progression via METTL3/ARHGAP5/YTHDF1 Axis. International journal of molecular sciences 38 36077054
2017 p190-B RhoGAP and intracellular cytokine signals balance hematopoietic stem and progenitor cell self-renewal and differentiation. Nature communications 36 28176763
2000 P190-B, a Rho-GTPase-activating protein, is differentially expressed in terminal end buds and breast cancer. Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 35 10939588
2007 Crosstalk between the p190-B RhoGAP and IGF signaling pathways is required for embryonic mammary bud development. Developmental biology 34 17662267
2018 Lactic acid induced microRNA-744 enhances motility of SiHa cervical cancer cells through targeting ARHGAP5. Chemico-biological interactions 31 30423314
2021 High-throughput sequencing identified circular RNA circUBE2K mediating RhoA associated bladder cancer phenotype via regulation of miR-516b-5p/ARHGAP5 axis. Cell death & disease 24 34285193
2020 Investigation of the role and mechanism of ARHGAP5-mediated colorectal cancer metastasis. Theranostics 23 32483433
2017 A p190BRhoGAP mutation and prolonged RhoB activation in fatal systemic capillary leak syndrome. The Journal of experimental medicine 21 29097442
2009 Loss of the Rho GTPase activating protein p190-B enhances hematopoietic stem cell engraftment potential. Blood 19 19713466
2021 Long non-coding RNA ARHGAP5-AS1 inhibits migration of breast cancer cell via stabilizing SMAD7 protein. Breast cancer research and treatment 16 34370213
1998 Cloning, genomic organization and chromosomal assignment of the mouse p190-B gene. Biochimica et biophysica acta 16 9838117
2022 miR-486-5p inhibits invasion and migration of HTR8/SVneo trophoblast cells by down-regulating ARHGAP5. Placenta 15 35477045
2019 Meningitic Escherichia coli Induction of ANGPTL4 in Brain Microvascular Endothelial Cells Contributes to Blood-Brain Barrier Disruption via ARHGAP5/RhoA/MYL5 Signaling Cascade. Pathogens (Basel, Switzerland) 15 31766605
2022 Exosomes derived from human umbilical cord mesenchymal stem cells reduce tendon injuries via the miR-27b-3p/ARHGAP5/RhoA signaling pathway. Acta biochimica et biophysica Sinica 12 35130628
2023 Circular RNA ARHGAP5 inhibits cisplatin resistance in cervical squamous cell carcinoma by interacting with AUF1. Cancer science 10 36632741
2016 CD147 promotes cell motility via upregulation of p190-B RhoGAP in hepatocellular carcinoma. Cancer cell international 7 27601938
2013 p190-B RhoGAP regulates the functional composition of the mesenchymal microenvironment. Leukemia 7 23563238
2023 Silencing of the circ-Arhgap5 RNA protects neuronal PC12 cells against injury and depends on the miR-29a-3p/Rock1 axis. Metabolic brain disease 4 36790698
2022 The p190 RhoGAPs, ARHGAP35, and ARHGAP5 are implicated in GnRH neuronal development: Evidence from patients with idiopathic hypogonadotropic hypogonadism, zebrafish, and in vitro GAP activity assay. Genetics in medicine : official journal of the American College of Medical Genetics 4 36178483
2024 ZFHX2-AS1 interacts with DKC1 to regulate ARHGAP5 pseudouridylation and suppress ovarian cancer progression. Cellular signalling 3 39368791
2024 Exposure to BaA inhibits trophoblast cell invasion and induces miscarriage by regulating the DEC1/ARHGAP5 axis and promoting ubiquitination-mediated degradation of MMP2. Journal of hazardous materials 2 39191013

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