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人 ARHGAP29 抗体对
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人 ARHGAP29 抗体对

01AB01632

Rho GTPase activating protein 29 (ARHGAP29) is a cytoplasmic GTPase-activating protein that negatively regulates Rho-family GTPases, exhibiting high specificity for RHOA. By stimulating GTP hydrolysis, it inactivates RHOA and modulates actin cytoskeleton dynamics, cell-matrix adhesion, and cell polarity. ARHGAP29 also participates in signaling complexes with RASIP1 and Afadin to facilitate endothelial cell migration and blood vessel tubulogenesis. Its expression is transcriptionally regulated by the YAP/Hippo signaling pathway. Clinically, ARHGAP29 is strongly associated with orofacial clefts; genetic variants and reduced expression levels are linked to nonsyndromic cleft lip with or without cleft palate, where it functions downstream of IRF6 during craniofacial development. In oncology, dysregulation of the ARHGAP29–RHOA–ROCK axis is implicated in the invasion and metastasis of various cancers, including breast and gastric tumors.

Human
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技术参数

靶点基因名
ARHGAP29
基因别名
PARG1
蛋白别名
Rho GTPase activating protein 29; ARHGAP29
UniProt
Q52LW3
物种
Human

产品详情

靶点名称
ARHGAP29
蛋白名称
Rho GTPase activating protein 29
蛋白别名
Rho GTPase-activating protein 29; PTPL1-associated RhoGAP protein 1; Rho-type GTPase-activating protein 29
靶点基因名
ARHGAP29
基因别名
PARG1
UniProt
Q52LW3
来源物种
Homo sapiens (Human)
物种反应性
Human

背景介绍

Rho GTPase activating protein 29 (ARHGAP29) is a cytoplasmic GTPase-activating protein that negatively regulates Rho-family GTPases, exhibiting high specificity for RHOA. By stimulating GTP hydrolysis, it inactivates RHOA and modulates actin cytoskeleton dynamics, cell-matrix adhesion, and cell polarity. ARHGAP29 also participates in signaling complexes with RASIP1 and Afadin to facilitate endothelial cell migration and blood vessel tubulogenesis. Its expression is transcriptionally regulated by the YAP/Hippo signaling pathway. Clinically, ARHGAP29 is strongly associated with orofacial clefts; genetic variants and reduced expression levels are linked to nonsyndromic cleft lip with or without cleft palate, where it functions downstream of IRF6 during craniofacial development. In oncology, dysregulation of the ARHGAP29–RHOA–ROCK axis is implicated in the invasion and metastasis of various cancers, including breast and gastric tumors.