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GTPase activator for the Rho-type GTPases by converting them to an inactive GDP-bound state. Additionally we are shipping PARG1 Proteins (4) and many more products for this protein.
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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.
Genetic variants in ARHGAP29 contribute to the development of nonsyndromic cleft lip with cleft palate.
We identified genetic variants in TGFB3 (show TGFB3 Antibodies) and ARHGAP29 associated with suboptimal healing outcome.
Rasip1-ArhGAP29 pathway also functions in Rap1-mediated regulation of endothelial junctions, which controls endothelial barrier function
ARHGAP29 is the etiologic gene for the cleft lip with or without cleft palate locus identified by genome-wide association on chromosome 1p22.
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 (show FH Antibodies).
These results suggest that PARG1 is a putative specific effector of Rap2 (show RAP2A Antibodies) to regulate Rho.
GTPase activator for the Rho-type GTPases by converting them to an inactive GDP-bound state. Has strong activity toward RHOA, and weaker activity toward RAC1 and CDC42. May act as a specific effector of RAP2A to regulate Rho (By similarity). In concert with RASIP1, suppresses RhoA signaling and dampens ROCK and MYH9 activities in endothelial cells and plays an essential role in blood vessel tubulogenesis (By similarity).
Rho GTPase activating protein 29
, rho GTPase-activating protein 29
, rho-type GTPase-activating protein 29
, PTPL1-associated RhoGAP 1
, rho GTPase-activating protein 29-like
, PTPL1-associated RhoGAP 1 (PARG1)
, PTPL1-associated RhoGAP protein 1