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Rho GTPase activating protein 29

mutant has Long free-running circadian period; Poly (ADP-ribose) Glycohydrolase (from NCBI)
Top mentioned proteins: Rhodopsin, LIP, RhoGAP, NSCL, RhoA
Papers on PARG1
PARP2 Is the Predominant Poly(ADP-Ribose) Polymerase in Arabidopsis DNA Damage and Immune Responses.
Bent et al., Oshkosh, United States. In Plos Genet, May 2015
For poly(ADP-ribose) glycohydrolase (PARG) enzymes, we find that Arabidopsis PARG1 and not PARG2 is the major contributor to poly(ADP-ribose) removal from acceptor proteins.
Identification of functional variants for cleft lip with or without cleft palate in or near PAX7, FGFR2, and NOG by targeted sequencing of GWAS loci.
Murray et al., Pittsburgh, United States. In Am J Hum Genet, Apr 2015
We furthermore identified significant clusters of non-coding rare variants near NTN1 and NOG and found several rare coding variants likely to affect protein function, including four nonsense variants in ARHGAP29.
Arabidopsis PARG1 is the key factor promoting cell survival among the enzymes regulating post-translational poly(ADP-ribosyl)ation.
Ge et al., Shanghai, China. In Sci Rep, 2014
Poly(ADP-ribosyl)ation is a reversible post-translational modification of proteins, characterized by the addition of poly(ADP-ribose) (PAR) to proteins by poly(ADP-ribose) polymerase (PARP), and removal of PAR by poly(ADP-ribose) glycohydrolase (PARG).
Identification of Pathways Mediating Growth Differentiation Factor5-Induced Tenogenic Differentiation in Human Bone Marrow Stromal Cells.
Kamarul et al., Kuala Lumpur, Malaysia. In Plos One, 2014
The genes identified as potentially associated with tenogenic differentiation were ARHGAP29, CCL2, integrin alpha 8 and neurofilament medium polypeptides.
Rare functional variants in genome-wide association identified candidate genes for nonsyndromic clefts in the African population.
Murray et al., Iowa City, United States. In Am J Med Genet A, 2014
Genome-wide association studies (GWAS) for nonsyndromic cleft lip with or without cleft palate (NSCL[P]) revealed significant association for common single nucleotide polymorphisms near genes involved in craniofacial development i.e., MAFB, PAX7, VAX1, ARHGAP29 (ABCA4 locus), and IRF6.
Identification of a novel heterozygous truncation mutation in exon 1 of ARHGAP29 in an Indian subject with nonsyndromic cleft lip with cleft palate.
Ramanathan et al., Chennai, India. In Eur J Dent, 2014
OBJECTIVE: Mutations in exon 1 of ARHGAP29, a RhoA specific GTPase have been identified in North American and Filipino subjects with nonsyndromic cleft palate and cleft lip with or without cleft palate.
Further evidence suggesting a role for variation in ARHGAP29 variants in nonsyndromic cleft lip/palate.
Hecht et al., Houston, United States. In Birth Defects Res A Clin Mol Teratol, 2014
METHODS: ARHGAP29 was suggested as a candidate gene for NSCL/P as it is located in close proximity to ABCA4 (1p22), a gene previously identified in a genome-wide association study of NSCL/P.
Impaired proliferative potential of bone marrow mesenchymal stromal cells in patients with myelodysplastic syndromes is associated with abnormal WNT signaling pathway.
Papadaki et al., Irákleion, Greece. In Stem Cells Dev, 2014
Patient MSCs displayed decreased gene expression of the senescence-associated cyclin-dependent kinase inhibitors CDKN1A, CDKN2A, and CDKN2B, along with PARG1, whereas the mean telomere length was upregulated in patient MSCs.
Interferon regulatory factor 6 regulates keratinocyte migration.
Dunnwald et al., Iowa City, United States. In J Cell Sci, 2014
The expression of Arhgap29, a Rho GTPase-activating protein, was reduced in Irf6-deficient keratinocytes.
Exploratory genotype-phenotype correlations of facial form and asymmetry in unaffected relatives of children with non-syndromic cleft lip and/or palate.
Moreno Uribe et al., Iowa City, United States. In J Anat, 2014
Cases and controls were genotyped for 20 SNPs across 13 candidate genes for NSCL/P (PAX7, ABCA4-ARHGAP29, IRF6, MSX1, PITX2, 8q24, FOXE1, TGFB3 and MAFB) and left-right body patterning (LEFTY1, LEFTY2, ISL1 and SNAI1).
Digital imaging analysis to assess scar phenotype.
Dunnwald et al., Iowa City, United States. In Wound Repair Regen, 2014
Finally, we identified genetic variants in TGFB3 and ARHGAP29 associated with suboptimal healing outcome.
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.
Murray et al., Iowa City, United States. In Birth Defects Res A Clin Mol Teratol, 2012
Because neither expression analysis nor mutation screening support a role for ABCA4 in NSCL/P, we investigated the adjacent gene ARHGAP29.
Pair-wise regulation of convergence and extension cell movements by four phosphatases via RhoA.
den Hertog et al., Utrecht, Netherlands. In Plos One, 2011
Downstream of the PTPs, we identified NGEF and Arhgap29, regulating RhoA activation and inactivation, respectively, in convergence and extension cell movements.
Blood vessel tubulogenesis requires Rasip1 regulation of GTPase signaling.
Cleaver et al., Dallas, United States. In Dev Cell, 2011
We show that endothelial tubulogenesis requires the Ras interacting protein 1, Rasip1, and its binding partner, the RhoGAP Arhgap29.
Arabidopsis poly(ADP-ribose) glycohydrolase 1 is required for drought, osmotic and oxidative stress responses.
Song et al., Hangzhou, China. In Plant Sci, 2011
In the present study, we used genetic mutant parg1-3 and transgenic PARG1-overexpressing Arabidopsis plants to examine the role of poly(ADP-ribose) glycohydrolase1 (PARG1) in abiotic stress resistance.
Promoter methylation of PARG1, a novel candidate tumor suppressor gene in mantle-cell lymphomas.
Steinemann et al., Hannover, Germany. In Haematologica, 2007
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.
PARG1, a protein-tyrosine phosphatase-associated RhoGAP, as a putative Rap2 effector.
Kariya et al., Okinawa, Japan. In Biochem Biophys Res Commun, 2005
These results suggest that PARG1 is a putative specific effector of Rap2 to regulate Rho.
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