Affinage

ARHGAP29

Rho GTPase-activating protein 29 · UniProt Q52LW3

Length
1261 aa
Mass
142.1 kDa
Annotated
2026-06-09
32 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 4/4 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ARHGAP29 (PARG1) is a RhoA-specific GTPase-activating protein that inactivates RhoA-GTP and thereby suppresses the downstream RhoA–ROCK–LIMK–cofilin contractility axis to drive actin cytoskeletal remodeling, cell spreading, and migration (PMID:15752761, PMID:28538170, PMID:29599137). It executes Rap1-dependent endothelial barrier and spreading programs as part of a membrane-localized Rasip1/Radil effector complex, where successive Rap1-induced translocations assemble Rasip1 and a Radil–ARHGAP29 module at the plasma membrane to inhibit Rho signaling and suppress stress fiber formation (PMID:23798437, PMID:25963656); at the leading edge of migrating endothelial cells, afadin binds ARHGAP29 and its RhoGAP domain to support lamellipodia formation and VEGF-induced migration (PMID:29599137). ARHGAP29 sits downstream of multiple transcriptional and epigenetic regulators—YAP/TAZ transcriptionally upregulate it to promote cancer cell migration and to control podocyte protrusion via the YAP/TAZ–ARHGAP29–RhoA axis (PMID:28538170, PMID:37443829), while EHMT2-mediated repression and TBX21-mediated activation tune its level in uveal melanoma and colorectal cancer respectively, with corresponding effects on RhoA activity and proliferation (PMID:37067748, PMID:38486999). Through suppression of RhoA–ROCK contractility, ARHGAP29 governs keratinocyte morphology, proliferation, and migration (PMID:36778214, PMID:39560169) and is required for oral epithelial periderm integrity and palatal shelf fusion during craniofacial development, where its loss elevates α-SMA and phospho-myosin light chain and produces cleft palate (PMID:28817352, PMID:40161602); a GAP-inactivating missense variant (p.Ser552Pro) found in a cleft palate family abolishes its pro-migratory function, linking ARHGAP29 to orofacial clefting downstream of the IRF6 gene regulatory network (PMID:28029220, PMID:23008150).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2005 Medium

    Established that PARG1/ARHGAP29 is an intrinsic RhoGAP whose cytoskeletal RhoA-inactivating action is regulated by a small GTPase, defining its core biochemical identity.

    Evidence Yeast two-hybrid, in vitro RhoGAP assay, ZPH-deletion mutagenesis and cytoskeletal rescue in fibroblasts

    PMID:15752761

    Open questions at the time
    • Rap2 regulatory relevance in physiological tissue contexts not established
    • no structural basis for RhoA selectivity
    • single lab
  2. 2012 Medium

    Placed Arhgap29 within the IRF6 gene regulatory network in craniofacial development, connecting an orofacial clefting pathway to Rho signaling.

    Evidence In situ hybridization in murine embryos comparing Irf6-deficient vs wild-type

    PMID:23008150

    Open questions at the time
    • expression epistasis does not prove direct transcriptional control
    • functional consequence in palatogenesis not yet tested
  3. 2015 High

    Defined the upstream activation logic: ARHGAP29 is the Rho-inhibitory effector arm of a Rap1–Rasip1/Radil membrane complex controlling endothelial barrier function and spreading.

    Evidence FRET, reciprocal Co-IP/pulldown, live-cell translocation imaging, siRNA with TEER barrier readouts (2013 and 2015 studies)

    PMID:23798437 PMID:25963656

    Open questions at the time
    • stoichiometry of the multimeric complex unresolved
    • direct GAP stimulation by the complex not reconstituted
  4. 2017 High

    Showed YAP transcriptionally drives ARHGAP29 to suppress RhoA–LIMK–cofilin, defining a transcription-to-cytoskeleton circuit that promotes cancer cell migration and metastasis.

    Evidence ChIP/luciferase reporter, siRNA, F-actin/G-actin assay, LIMK/cofilin western blot, transwell migration, mouse CTC model

    PMID:28538170

    Open questions at the time
    • direct YAP/TEAD binding site detail at the ARHGAP29 locus
    • generalizability across tumor types
  5. 2017 Medium

    Demonstrated context-dependent roles in proliferation and invasion downstream of RhoA–ROCK, including links to p53/p21 cell-cycle control and miR-1291 regulation in fibrosis.

    Evidence siRNA/overexpression with cell-cycle, invasion, and pathway westerns in RCC/HEK293T; miR-1291 antagomir in intrauterine adhesion mouse model

    PMID:28131798 PMID:28849001

    Open questions at the time
    • mechanism linking RhoA–ROCK to p53/p21 indirect
    • miR-1291 targeting not validated by reporter in these reports
  6. 2017 Medium

    Connected ARHGAP29 to human cleft palate through a GAP-inactivating variant and to oral epithelial/periderm integrity through mouse loss-of-function.

    Evidence Family variant (p.Ser552Pro) with keratinocyte migration and zebrafish assays; K326X knock-in mouse with periderm immunofluorescence

    PMID:28029220 PMID:28817352

    Open questions at the time
    • Ser552 mechanistic role in catalysis not structurally defined
    • homozygous lethality limits adult tissue analysis
  7. 2018 High

    Identified afadin as a direct leading-edge partner that recruits ARHGAP29 to restrain ROCK activity and enable lamellipodia formation and VEGF-driven endothelial migration.

    Evidence Reciprocal Co-IP, co-localization, siRNA, domain-mutant rescue, ROCK activity assay and inhibitor rescue, migration/network assays

    PMID:29599137

    Open questions at the time
    • afadin binding interface on ARHGAP29 not mapped at residue level
    • spatial relationship to Rap1/Rasip1 recruitment unclear
  8. 2023 Medium

    Extended transcriptional/epigenetic control of ARHGAP29 to additional regulators—YAP/TAZ in podocytes, TBX21 in colorectal cancer, EHMT2 repression in uveal melanoma—each converging on RhoA activity.

    Evidence EPB41L5 KO podocytes with ChIP-seq and RhoA assays; TBX21 ChIP/phospho-kinase array with xenograft; EHMT2 ChIP-seq with constitutively active RhoA rescue and xenograft

    PMID:37067748 PMID:37443829 PMID:38486999

    Open questions at the time
    • whether these regulators act in shared or distinct tissue contexts
    • TBX21-linked RSK/GSK3β inhibition mechanism downstream of RhoA unclear
  9. 2024 Medium

    Consolidated the RhoA–ROCK-dependent control of keratinocyte morphology, proliferation, and migration, while revealing that in vivo wound healing is unexpectedly robust to Arhgap29 loss.

    Evidence CRISPR/shRNA knockdown with F-actin, pMLC, migration assays, ROCK-inhibitor and add-back rescue, keratinocyte-specific conditional KO mouse wound healing (preprint and peer-reviewed)

    PMID:36778214 PMID:39560169

    Open questions at the time
    • redundancy compensating for loss in vivo not identified
    • single lab
  10. 2025 Medium

    Used tissue-specific and global mouse knockouts to causally tie Arhgap29 loss to cleft palate via increased epithelial contractility, and to broader craniofacial/skeletal defects via osteogenesis and calcium/MAPK signaling.

    Evidence Ectodermal/K14-Cre and global Arhgap29 KO mice with histology, micro-CT, immunofluorescence (α-SMA, pMRLC), transcriptomics, calvarial osteogenesis assays (one preprint, one peer-reviewed)

    PMID:40161602 PMID:40429791

    Open questions at the time
    • how RhoA–ROCK contractility drives fusion failure mechanistically
    • direct role in osteoblast/osteoclast Rho signaling not dissected
  11. 2025 Low

    Proposed a structural basis for RhoA substrate recognition by the GAP domain and the impact of disease mutations, though by computation only.

    Evidence HDOCK docking and molecular dynamics simulation of WT and mutant PARG1–RhoA complexes

    PMID:40632829

    Open questions at the time
    • computational prediction lacking experimental structural or biochemical validation
    • predicted interface residues not mutationally tested for GAP activity

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ARHGAP29's distinct upstream recruiters (Rap1/Rasip1, afadin, YAP/TAZ, TBX21, EHMT2) are integrated within a given cell to set RhoA tone, and the experimental structure of the ARHGAP29–RhoA complex, remain unresolved.
  • no experimental 3D structure of the GAP domain–RhoA complex
  • no unified model of competing upstream inputs
  • tissue-specific functional redundancy unmapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0140096 catalytic activity, acting on a protein 3 GO:0016787 hydrolase activity 1
Localization
GO:0005886 plasma membrane 2
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-162582 Signal Transduction 4 R-HSA-1643685 Disease 3
Partners
MLLT4RADILRAP2ARASIP1RHOA
Complex memberships
Radil–ARHGAP29 complexRap1–Rasip1–ARHGAP29 complex

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 PARG1 (ARHGAP29) was identified as a putative effector of Rap2: the ZPH (ZK669.1a and PARG1 homology) region of PARG1 mediates GTP-dependent interaction with Rap2 (but not Ras or Rap1), and Rap2 suppresses the in vivo RhoA-inactivating cytoskeletal action of PARG1 but not of a PARG1 mutant lacking the ZPH region. PARG1 also exhibits RhoGAP activity in vitro. Yeast two-hybrid screening, in vitro RhoGAP activity assay, co-immunoprecipitation, mutagenesis (ZPH deletion), morphological cytoskeletal assay in fibroblasts Biochemical and biophysical research communications Medium 15752761
2013 Rasip1 acts as a Rap1 effector and binds ARHGAP29 (ArhGAP29); the Rap1–Rasip1–ArhGAP29 complex mediates Rap1-induced cell spreading and endothelial barrier function by inhibiting Rho signaling and suppressing stress fiber formation. Rasip1 cooperates with Radil to promote junctional tightening through this pathway. FRET (Rasip1–Rap1 interaction in cells), Co-IP/pulldown (Rasip1–ArhGAP29), siRNA knockdown with cell spreading and barrier function readouts (TEER), dominant-negative Rho constructs Proceedings of the National Academy of Sciences of the United States of America High 23798437
2015 Rap1 induces independent translocation of Rasip1 and a Radil–ArhGAP29 complex to the plasma membrane, where they assemble into a multimeric complex required for Rap1-induced inhibition of Rho signaling and increased endothelial barrier function, revealing spatiotemporal control via successive membrane translocations. Live-cell imaging of protein translocation, Co-IP to detect Radil–ArhGAP29 complex, siRNA knockdown with TEER/barrier assay, Rap1 activation assays Molecular and cellular biology High 25963656
2017 YAP transcriptionally upregulates ARHGAP29, which then suppresses the RhoA–LIMK–cofilin pathway, destabilizing F-actin and promoting F-actin/G-actin turnover; this cytoskeletal rearrangement increases cancer cell migration and metastatic potential. ChIP/luciferase reporter (YAP→ARHGAP29 transcription), siRNA knockdown, ARHGAP29 overexpression, F-actin/G-actin ratio assay, LIMK/cofilin phosphorylation western blot, transwell migration assay, mouse CTC model Cell reports High 28538170
2017 A missense variant in ARHGAP29 (p.Ser552Pro) identified in a family with cleft palate lacks the GAP activity of wild-type ARHGAP29; keratinocytes transfected with wild-type ARHGAP29 migrate faster than those transfected with p.Ser552Pro or empty vector, demonstrating that Ser552 is required for ARHGAP29's pro-migratory function. Zebrafish functional assay (in vivo), keratinocyte migration assay (transfection with WT vs. variant ARHGAP29), Sanger sequencing validation Birth defects research Medium 28029220
2017 Depletion of PARG1 (ARHGAP29) by siRNA in human RCC cell lines inhibited proliferation via G1 arrest through upregulation of p53 and p21Cip1/Waf1, and inhibited invasion; both effects were mediated by increased RhoA–ROCK activity. Conversely, PARG1 overexpression in HEK293T cells promoted proliferation and invasion via inhibition of RhoA–ROCK. siRNA knockdown, cell cycle analysis, western blot (p53, p21, RhoA-GTP, ROCK activity), invasion assay, overexpression in HEK293T Translational oncology Medium 28131798
2017 ARHGAP29 heterozygosity for a nonsense allele (K326X) in mice causes embryonic lethality in homozygotes and abnormal oral epithelial adhesions in heterozygotes; Arhgap29 protein is present in periderm cells at sites of adhesion, demonstrating a role for ARHGAP29 in periderm integrity and oral epithelial organization during craniofacial development. CRISPR/knock-in mouse model (K326X allele), coronal sectioning, immunofluorescence (keratin 6, keratin 17, p63, Arhgap29), embryo harvest and genotyping Journal of dental research Medium 28817352
2017 miR-1291 negatively regulates ArhGAP29 expression; in an intrauterine adhesion mouse model, miR-1291 inhibition increased ArhGAP29 and decreased RhoA/ROCK1 activity, ameliorating endometrial fibrosis and reducing EMT markers, placing ArhGAP29 downstream of miR-1291 in the RhoA/ROCK1–EMT pathway. miR-1291 antagomir injection, western blot and RT-qPCR (ArhGAP29, RhoA, ROCK1, EMT markers), immunofluorescence, histological staining (H&E, Masson's trichrome) Molecular medicine reports Medium 28849001
2018 Afadin binds ArhGAP29 and co-localizes with it at the leading edge of migrating endothelial cells. Both the afadin–ArhGAP29 interaction and the RhoGAP domain of ArhGAP29 are required for proper lamellipodia/ruffle formation and VEGF-induced migration; afadin knockdown increases Rho-associated kinase activity through loss of ArhGAP29 function. Co-IP (afadin–ArhGAP29), immunofluorescence co-localization, siRNA knockdown (afadin, ArhGAP29), ROCK activity assay, rescue with ArhGAP29 deletion/point mutants, network formation and migration assay, ROCK inhibitor (Y-27632, fasudil) rescue Arteriosclerosis, thrombosis, and vascular biology High 29599137
2020 ARHGAP29 knockdown in breast cancer cells with mesenchymal transformation reduces invasion by decreasing RhoA inhibition and increasing stress fiber formation; reduced ARHGAP29 expression is accompanied by reduced AKT1 protein levels but unchanged ratio of active pAKT1 to total AKT1. siRNA knockdown, invasion assay, F-actin staining, western blot (RhoA, AKT1, pAKT1), interaction analysis Cells Medium 33291460
2023 In podocytes, YAP/TAZ transcriptionally regulates ARHGAP29 expression (downstream of EPB41L5/Yurt-dependent mechanotransduction); ARHGAP29 knockdown causes increased RhoA activation, defective lamellipodia formation, and increased maturation of integrin adhesion complexes, establishing a YAP/TAZ–ARHGAP29–RhoA signaling axis in podocyte protrusion regulation. EPB41L5 KO podocytes, TEADi pharmacological inhibition, transcriptomic/proteomic analysis, siRNA knockdown of ARHGAP29, RhoA activation assay, immunofluorescence (lamellipodia, integrin adhesions), ChIP-seq analysis Cells Medium 37443829
2023 TBX21 directly binds the ARHGAP29 promoter to transcriptionally upregulate ARHGAP29; ARHGAP29 in turn inhibits RSK and GSK3β phosphorylation, suppressing colorectal cancer cell proliferation and promoting apoptosis. Knockdown of ARHGAP29 abolishes TBX21-mediated proliferation suppression and kinase inhibition. RNA-seq (TBX21 target identification), ChIP (TBX21 binding to ARHGAP29 promoter), phospho-kinase array, siRNA knockdown (ARHGAP29), cell proliferation/apoptosis assays, xenograft mouse model Cellular oncology Medium 37067748
2023 ARHGAP29 knockdown in keratinocytes increases filamentous actin (stress fibers), phospho-myosin regulatory light chain (contractility), cell area, and population doubling time, and delays scratch wound closure in single-cell and collective migration; these delays are rescued by ARHGAP29 add-back or by ROCK inhibition, demonstrating that ARHGAP29 controls keratinocyte morphology, proliferation, and migration via the RhoA–ROCK pathway. CRISPR/Cas9 and shRNA knockdown, phalloidin staining (F-actin), western blot (phospho-myosin light chain), scratch wound/live-cell migration assay, ROCK inhibitor rescue, ARHGAP29 re-expression rescue bioRxivpreprint Medium 36778214
2024 ARHGAP29 knockdown in keratinocytes increases filamentous actin, phospho-myosin regulatory light chain, cell area, and population doubling time, and delays scratch wound closure; these defects are rescued by ARHGAP29 re-expression or ROCK inhibition. In vivo, Arhgap29 heterozygotes or keratinocyte-specific knockouts show on-time wound healing, demonstrating that ARHGAP29 is required for keratinocyte biology in vitro but dispensable for in vivo wound healing. ARHGAP29 knockdown cell lines, F-actin staining, phospho-myosin light chain western blot, scratch wound assay, ROCK inhibitor rescue, ARHGAP29 rescue, Arhgap29 conditional KO mouse (keratinocyte-specific), in vivo wound healing assay Developmental dynamics Medium 39560169
2023 EHMT2 epigenetically suppresses ARHGAP29 transcription in a methyltransferase-dependent manner in GNAQ/11-mutant uveal melanoma cells, leading to elevated RhoA activity; rescue of constitutively active RhoA in EHMT2-depleted cells restores oncogenic phenotypes, placing EHMT2 upstream of ARHGAP29 in a RhoA-dependent oncogenic pathway. ChIP-seq (EHMT2 binding at ARHGAP29 locus), siRNA/pharmacological EHMT2 inhibition, RhoA activity assay, constitutively active RhoA rescue, xenograft in vivo model Acta pharmaceutica Sinica. B Medium 38486999
2025 Computational structural modeling of the PARG1 (ARHGAP29) RhoGAP domain shows that the C1-linker region N-terminal to the GAP domain is required for RhoA substrate recognition: docking and molecular dynamics simulations identify specific interface residues (catalytic loop, α4 and α9–10 helices of the GAP domain) mediating stable RhoA binding, and disease-associated missense mutations (T622M, I845V) disorganize or reduce this interface. Computational docking (HDOCK), molecular dynamics simulation, structural modeling of WT and mutant PARG1–RhoA complexes PloS one Low 40632829
2025 Tissue-specific (ectodermal) deletion of Arhgap29 in mice causes a delay in palatal shelf fusion at E14.5 and significantly penetrant cleft palate at E18.5; loss of Arhgap29 in palatal epithelium increases cell area and upregulates α-smooth muscle actin and phospho-myosin regulatory light chain, implicating increased cell contractility as a driver of the cleft palate phenotype. Conditional KO mouse (ectodermal and K14-Cre), histological analysis, immunofluorescence (α-SMA, phospho-MRLC), embryo staging and phenotyping bioRxivpreprint Medium 40161602
2025 In glioma cells, ARHGAP29 regulates transitional morphological states via Src kinase signaling, and GSK-3 inhibition coupled with β-catenin translocation alters ARHGAP29 transcription; silencing ARHGAP29 causes morphological changes consistent with phenotype switching. siRNA knockdown, western blot (N-cadherin, GSK-3, β-catenin), morphological analysis, Src kinase signaling assays Cell reports Low 40053455
2012 Arhgap29 expression in murine embryos is enriched in craniofacial structures and is reduced in mice deficient for Irf6, placing ARHGAP29 downstream of the IRF6 gene regulatory network and linking the IRF6 pathway to Rho signaling via ARHGAP29. In situ hybridization (murine embryos), comparison of Arhgap29 expression in Irf6-deficient vs. wild-type mice Birth defects research. Part A, Clinical and molecular teratology Medium 23008150
2025 Global knockout of Arhgap29 in mice causes cleft palate with additional craniofacial and systemic skeletal abnormalities including delayed Meckel's cartilage fusion, widened cranial sutures, reduced bone quality, and digit defects; Arhgap29 is expressed in both osteoblasts and osteoclasts, and its loss impairs osteogenesis in vitro (calvarial cells) and disrupts calcium and MAPK signaling pathways. Arhgap29 global KO mouse, micro-CT, histological analysis, transcriptomics, spatial transcriptomics, immunohistochemistry (osteoblast/osteoclast markers), in vitro osteogenesis assay (calvarial cells) International journal of molecular sciences Medium 40429791

Source papers

Stage 0 corpus · 32 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 YAP Regulates Actin Dynamics through ARHGAP29 and Promotes Metastasis. Cell reports 205 28538170
2013 Rasip1 mediates Rap1 regulation of Rho in endothelial barrier function through ArhGAP29. Proceedings of the National Academy of Sciences of the United States of America 118 23798437
2012 Expression and mutation analyses implicate ARHGAP29 as the etiologic gene for the cleft lip with or without cleft palate locus identified by genome-wide association on chromosome 1p22. Birth defects research. Part A, Clinical and molecular teratology 83 23008150
2015 Rap1 Spatially Controls ArhGAP29 To Inhibit Rho Signaling during Endothelial Barrier Regulation. Molecular and cellular biology 71 25963656
2017 Exome sequencing provides additional evidence for the involvement of ARHGAP29 in Mendelian orofacial clefting and extends the phenotypic spectrum to isolated cleft palate. Birth defects research 49 28029220
2017 MicroRNA-1291 promotes endometrial fibrosis by regulating the ArhGAP29-RhoA/ROCK1 signaling pathway in a murine model. Molecular medicine reports 40 28849001
2007 Promoter methylation of PARG1, a novel candidate tumor suppressor gene in mantle-cell lymphomas. Haematologica 31 17488656
2017 ARHGAP29 Mutation Is Associated with Abnormal Oral Epithelial Adhesions. Journal of dental research 30 28817352
2005 PARG1, a protein-tyrosine phosphatase-associated RhoGAP, as a putative Rap2 effector. Biochemical and biophysical research communications 30 15752761
2016 Impact of rare variants in ARHGAP29 to the etiology of oral clefts: role of loss-of-function vs missense variants. Clinical genetics 29 27350171
2014 Further evidence suggesting a role for variation in ARHGAP29 variants in nonsyndromic cleft lip/palate. Birth defects research. Part A, Clinical and molecular teratology 25 25163644
2023 A YAP/TAZ-ARHGAP29-RhoA Signaling Axis Regulates Podocyte Protrusions and Integrin Adhesions. Cells 20 37443829
2018 Afadin Facilitates Vascular Endothelial Growth Factor-Induced Network Formation and Migration of Vascular Endothelial Cells by Inactivating Rho-Associated Kinase Through ArhGAP29. Arteriosclerosis, thrombosis, and vascular biology 18 29599137
2017 Progression of Human Renal Cell Carcinoma via Inhibition of RhoA-ROCK Axis by PARG1. Translational oncology 15 28131798
2014 Identification of a novel heterozygous truncation mutation in exon 1 of ARHGAP29 in an Indian subject with nonsyndromic cleft lip with cleft palate. European journal of dentistry 14 25512736
2020 Influence of ARHGAP29 on the Invasion of Mesenchymal-Transformed Breast Cancer Cells. Cells 12 33291460
2023 TBX21 attenuates colorectal cancer progression via an ARHGAP29/RSK/GSK3β dependent manner. Cellular oncology (Dordrecht, Netherlands) 11 37067748
2020 A novel splicing mutation of ARHGAP29 is associated with nonsyndromic cleft lip with or without cleft palate. The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians 10 32698641
2022 circTMEM181 upregulates ARHGAP29 to inhibit hepatocellular carcinoma migration and invasion by sponging miR-519a-5p. Hepatology research : the official journal of the Japan Society of Hepatology 8 36519254
2023 EHMT2 promotes tumorigenesis in GNAQ/11-mutant uveal melanoma via ARHGAP29-mediated RhoA pathway. Acta pharmaceutica Sinica. B 7 38486999
2024 ARHGAP29 promotes keratinocyte proliferation and migration in vitro and is dispensable for in vivo wound healing. Developmental dynamics : an official publication of the American Association of Anatomists 6 39560169
2025 TBX21 inhibits colorectal cancer metastasis through ARHGAP29/GSK3β inhibitory signaling- and MYCT1/ZO-1 signaling-dependent manner. International journal of biological sciences 5 39744435
2024 Four putative pathogenic ARHGAP29 variants in patients with non-syndromic orofacial clefts (NsOFC). European journal of human genetics : EJHG 4 39506048
2020 Gene-gene interactions between BMP4 and ARHGAP29 among non-syndromic cleft lip only (NSCLO) trios from western Han Chinese population. International journal of clinical and experimental pathology 4 32211112
2025 Arhgap29 Deficiency Directly Leads to Systemic and Craniofacial Skeletal Abnormalities. International journal of molecular sciences 3 40429791
2020 The SNP rs560426 Within ABCA4-ARHGAP29 Locus and the Risk of Nonsyndromic Oral Clefts. The Cleft palate-craniofacial journal : official publication of the American Cleft Palate-Craniofacial Association 3 31950859
2023 ARHGAP29 is required for keratinocyte proliferation and migration. bioRxiv : the preprint server for biology 2 36778214
2025 The ectodermal loss of ARHGAP29 alters epithelial morphology and organization and disrupts murine palatal development. bioRxiv : the preprint server for biology 1 40161602
2025 ARHGAP12 and ARHGAP29 exert distinct regulatory effects on switching between two cell morphological states through GSK-3 activity. Cell reports 0 40053455
2025 C1-linker region of PARG1 RhoGAP promotes the catalytic recognition fold of RhoA substrate. PloS one 0 40632829
2025 Emerging role of ARHGAP29 in melanoma cell phenotype switching. Molecular oncology 0 40906537
2023 PARG1 and EXA1 genes as possible components of the facultative epigenetic control of plant development. Physiologia plantarum 0 37350155

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