ARHGAP29 Is Involved in Increased Invasiveness of Tamoxifen-resistant Breast Cancer Cells and its Expression Levels Correlate With Clinical Tumor Parameters of Breast Cancer Patients. | ARHGAP29 Is Involved in Increased Invasiveness of Tamoxifen-resistant Breast Cancer Cells and its Expression Levels Correlate With Clinical Tumor Parameters of Breast Cancer Patients. Kansy M, Wert K, Kolb K, Gallwas J, Gründker C., Free PMC Article | 07/22/2024 |
TBX21 attenuates colorectal cancer progression via an ARHGAP29/RSK/GSK3beta dependent manner. | TBX21 attenuates colorectal cancer progression via an ARHGAP29/RSK/GSK3β dependent manner. Jiang X, Du W, Yang C, Wang S, Li Y, Shen X, Yang X, Yao J, Du R, Zhang X, Huang Y, Shen W. | 12/1/2023 |
ARHGAP29 expression may be a novel prognostic factor of cell proliferation and invasion in prostate cancer. | ARHGAP29 expression may be a novel prognostic factor of cell proliferation and invasion in prostate cancer. Shimizu K, Matsumoto H, Hirata H, Ueno K, Samoto M, Mori J, Fujii N, Kawai Y, Inoue R, Yamamoto Y, Yano S, Shimabukuro T, Furutani-Seiki M, Matsuyama H. | 08/7/2021 |
Influence of ARHGAP29 on the Invasion of Mesenchymal-Transformed Breast Cancer Cells. | Influence of ARHGAP29 on the Invasion of Mesenchymal-Transformed Breast Cancer Cells. Kolb K, Hellinger J, Kansy M, Wegwitz F, Bauerschmitz G, Emons G, Gründker C., Free PMC Article | 07/10/2021 |
Identification of a Novel Variant of ARHGAP29 in a Chinese Family with Nonsyndromic Cleft Lip and Palate. | Identification of a Novel Variant of ARHGAP29 in a Chinese Family with Nonsyndromic Cleft Lip and Palate. Tang JX, Xiao XS, Wang K, Jin JY, Fan LL, Xiang R., Free PMC Article | 05/15/2021 |
The SNP rs560426 Within ABCA4-ARHGAP29 Locus and the Risk of Nonsyndromic Oral Clefts. | The SNP rs560426 Within ABCA4-ARHGAP29 Locus and the Risk of Nonsyndromic Oral Clefts. Wu-Chou YH, Chen KP, Lu YC, Lin YT, Chang HF, Lo LJ. | 12/12/2020 |
Risk haplotypes affect ARHGAP29 expression causing non-syndromic orofacial clefting. | Identification of common non-coding variants at 1p22 that are functional for non-syndromic orofacial clefting. Liu H, Leslie EJ, Carlson JC, Beaty TH, Marazita ML, Lidral AC, Cornell RA., Free PMC Article | 11/17/2018 |
The variant in question segregates as an autosomal dominant trait caused by an heterozygous missense variant in ARHGAP29 (p.Ser552Pro) that had not previously been identified in a population genomic databases. The p.Ser552Pro ARHGAP29 variant was not present in genomic databases and was predicted to be pathogenic by multiple in silico programs. | Exome sequencing provides additional evidence for the involvement of ARHGAP29 in Mendelian orofacial clefting and extends the phenotypic spectrum to isolated cleft palate. Liu H, Busch T, Eliason S, Anand D, Bullard S, Gowans LJJ, Nidey N, Petrin A, Augustine-Akpan EA, Saadi I, Dunnwald M, Lachke SA, Zhu Y, Adeyemo A, Amendt B, Roscioli T, Cornell R, Murray J, Butali A., Free PMC Article | 03/17/2018 |
YAP promotes the expression of ARHGAP29 to suppress the RhoA-LIMK-cofilin pathway, destabilizing F-actin. | YAP Regulates Actin Dynamics through ARHGAP29 and Promotes Metastasis. Qiao Y, Chen J, Lim YB, Finch-Edmondson ML, Seshachalam VP, Qin L, Jiang T, Low BC, Singh H, Lim CT, Sudol M. | 03/3/2018 |
The of loss-of-function and ARHGAP29 missense variants in the etiology of oral clefts | Impact of rare variants in ARHGAP29 to the etiology of oral clefts: role of loss-of-function vs missense variants. Savastano CP, Brito LA, Faria ÁC, Setó-Salvia N, Peskett E, Musso CM, Alvizi L, Ezquina SA, James C, GOSgene, Beales P, Lees M, Moore GE, Stanier P, Passos-Bueno MR. | 06/3/2017 |
Data indicate that through GTPase-activating proteins ArhGAP29 complex formation Rap1 GTP-binding protein spatially restricts Rho-mediated signaling, which is necessary for endothelial barrier potentiation. | Rap1 Spatially Controls ArhGAP29 To Inhibit Rho Signaling during Endothelial Barrier Regulation. Post A, Pannekoek WJ, Ponsioen B, Vliem MJ, Bos JL., Free PMC Article | 09/26/2015 |
Genetic variants in ARHGAP29 contribute to the development of nonsyndromic cleft lip with cleft palate. | Further evidence suggesting a role for variation in ARHGAP29 variants in nonsyndromic cleft lip/palate. Letra A, Maili L, Mulliken JB, Buchanan E, Blanton SH, Hecht JT., Free PMC Article | 05/23/2015 |
We identified genetic variants in TGFB3 and ARHGAP29 associated with suboptimal healing outcome. | Digital imaging analysis to assess scar phenotype. Smith BJ, Nidey N, Miller SF, Moreno Uribe LM, Baum CL, Hamilton GS 3rd, Wehby GL, Dunnwald M., Free PMC Article | 12/20/2014 |
Rasip1-ArhGAP29 pathway also functions in Rap1-mediated regulation of endothelial junctions, which controls endothelial barrier function | Rasip1 mediates Rap1 regulation of Rho in endothelial barrier function through ArhGAP29. Post A, Pannekoek WJ, Ross SH, Verlaan I, Brouwer PM, Bos JL., Free PMC Article | 10/19/2013 |
ARHGAP29 is the etiologic gene for the cleft lip with or without cleft palate locus identified by genome-wide association on chromosome 1p22. | 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. Leslie EJ, Mansilla MA, Biggs LC, Schuette K, Bullard S, Cooper M, Dunnwald M, Lidral AC, Marazita ML, Beaty TH, Murray JC., Free PMC Article | 06/22/2013 |
Observational study of gene-disease association. (HuGE Navigator) | Mutation of ARHGAP9 in patients with coronary spastic angina. Takefuji M, Asano H, Mori K, Amano M, Kato K, Watanabe T, Morita Y, Katsumi A, Itoh T, Takenawa T, Hirashiki A, Izawa H, Nagata K, Hirayama H, Takatsu F, Naoe T, Yokota M, Kaibuchi K. | 01/20/2010 |
PARG1 expression was substantially reduced & it displayed at least partial promoter methylation in all investigated mantle-cell lines & in 31 primary cases. PARG1 is a strong candidate tumor suppressor gene in MCL. | Promoter methylation of PARG1, a novel candidate tumor suppressor gene in mantle-cell lymphomas. Ripperger T, von Neuhoff N, Kamphues K, Emura M, Lehmann U, Tauscher M, Schraders M, Groenen P, Skawran B, Rudolph C, Callet-Bauchu E, van Krieken JH, Schlegelberger B, Steinemann D. | 01/21/2010 |