ARHGAP32

Last update 08 May 2025

Basic Info

Synonyms

ARHGAP32, Brain-specific Rho GTPase-activating protein, GAB-associated Cdc42/Rac GTPase-activating protein

+ [13]

Introduction

GTPase-activating protein (GAP) promoting GTP hydrolysis on RHOA, CDC42 and RAC1 small GTPases. May be involved in the differentiation of neuronal cells during the formation of neurite extensions. Involved in NMDA receptor activity-dependent actin reorganization in dendritic spines. May mediate cross-talks between Ras- and Rho-regulated signaling pathways in cell growth regulation. Isoform 2 has higher GAP activity (By similarity).

100 Clinical Results associated with ARHGAP32

100 Translational Medicine associated with ARHGAP32

0 Patents (Medical) associated with ARHGAP32

Literatures (Medical) associated with ARHGAP32

30 Apr 2025·The FASEB Journal

Pathogenesis of Focal Segmental Glomerulosclerosis Caused by a Leu754Val Mutation in ARHGAP32

Article

Author: Li, Guisen ; Zou, Yang ; Li, Yi ; Wang, Li ; Chen, Sipei ; Zhong, Xiang

ABSTRACTFocal segmental glomerulosclerosis (FSGS) shows a poor response to hormones and other treatment schemes and rapidly progresses to end‐stage renal disease. Genetic factors are important causes of FSGS. We recently identified a new candidate pathogenic ARHGAP32 mutation in a family affected by FSGS and further investigated its functional impact through in vivo and in vitro studies. We established in vitro models of ARHGAP32 overexpression in podocytes and COS‐7 kidney cells by plasmid transfection. Mice with the point mutation were established using CRISPR/Cas9 technology, followed by the establishment of a kidney injury model by adriamycin administration via the tail vein. The ARHGAP32 protein was found to be expressed in human kidney tissues. Podocytes transfected with mutant ARHGAP32 showed a significant decrease in the expression of the podocyte markers nephrin. Similarly, COS‐7 cells transfected with mutant ARHGAP32 showed decreased expression of the cytoskeletal protein F‐actin. The ARHGAP32 mutant protein had 20‐fold higher affinity for Cdc42 than the wild‐type protein. Adriamycin‐induced L405V mutant mice showed slow growth, proteinuria, increased serum creatinine and blood urea nitrogen levels, and pathological kidney damage. RhoA, Rac1, and Cdc42 all showed decreased expression in podocytes overexpressing mutant ARHGAP32 and in the kidneys of mutant mice. These findings suggest that the ARHGAP32 L754V mutation induces podocyte damage, leading to kidney damage and the potential development of FSGS. This study provides a new basis for elucidating the pathogenesis of FSGS and the exploration of new therapeutic measures.

01 Nov 2024·Taiwanese Journal of Obstetrics and Gynecology

Prenatal diagnosis of Jacobsen syndrome associated with a distal 11q deletion and a distal 8q duplication by chromosome microarray analysis in a fetus with a de novo unbalanced translocation of 46,XX,der(11)t(8;11)(q24.13;q23.3) and multiple congenital anomalies on fetal ultrasound

Article

Author: Chen, Wen-Lin ; Lee, Chen-Chi ; Wu, Fang-Tzu ; Wu, Peih-Shan ; Huang, Jian-Pei ; Wang, Wayseen ; Chen, Chih-Ping ; Pan, Yen-Ting

OBJECTIVEWe present prenatal diagnosis of Jacobsen syndrome associated with a distal 11q deletion and a distal 8q duplication by chromosome microarray analysis (CMA) in a fetus with multiple congenital anomalies on fetal ultrasound.CASE REPORTA 41-year-old, gravida 2, para 1, woman underwent amniocentesis at 25 weeks of gestation because of intrauterine growth restriction, endocardial cushion defect, clenched hands, arthrogryposis, rocker bottom feet and craniosynostosis on fetal ultrasound. Amniocentesis revealed a karyotype of 46,XX,add(11)(q23.3). Array comparative genomic hybridization (aCGH) analysis of the DNA extracted from the uncultured amniocytes revealed the result of arr 8q24.13q24.3 × 3, 11q23.3q25 × 1. Analysis of FGFR2 revealed no mutation. The karyotype was 46,XX,der(11)t(8;11)(q24.13;q23.3). The parental karyotypes were normal. The pregnancy was subsequently terminated, and a dead malformed fetus was delivered with craniofacial dysmorphism of low-set malformed ears, depressed nasal bridge, hypertelorism, small mouth, clenched hands and rocker bottom feet. Cytogenetic analysis of the placenta revealed a karyotype of 46,XX,der(11)t(8;11)(q24.13;q23.3). aCGH analysis of the DNA extracted from the umbilical cord showed the result of arr 8q24.13q24.3 (126,302,369-146,280,020) × 3.0, arr 11q23.3q25 (120,469,928-134,868,407) × 1.0 [GRCh37] with a 19.978-Mb duplication of 8q24.13-q24.3 and a 14.398-Mb deletion of 11q23.3-q25 encompassing the genes of BSX, ETS1, FLI1 and ARHGAP32.CONCLUSIONCMA is useful for detection of de novo chromosomal rearrangement in the fetus with multiple congenital anomalies on fetal ultrasound.

15 Sep 2024·Journal of Cell Science

The RhoGAP ARHGAP32 interacts with desmoplakin, and is required for desmosomal organization and assembly

Article

Author: Wang, Yan ; Ning, Wenxiu ; Zhou, Kaiyao ; Xie, Lin ; Duan, Xiufen ; Li, Hua ; Wu, Gangyun ; He, Yinzhen ; Liu, Xiayu

ABSTRACTDesmosomes play a crucial role in maintaining tissue barrier integrity, particularly in mechanically stressed tissues. The assembly of desmosomes is regulated by the cytoskeleton and its regulators, and desmosomes also function as a central hub for regulating F-actin. However, the specific mechanisms underlying the crosstalk between desmosomes and F-actin remain unclear. Here, we identified that ARHGAP32, a Rho GTPase-activating protein, is located in desmosomes through its interaction with desmoplakin (DSP) via its GAB2-interacting domain (GAB2-ID). We confirmed that ARHGAP32 is required for desmosomal organization, maturation and length regulation. Notably, loss of ARHGAP32 increased formation of F-actin stress fibers and phosphorylation of the regulatory myosin light chain Myl9 at T18/S19. Inhibition of ROCK activity in ARHGAP32-knockout (KO) cells effectively restored desmosomal organization and the integrity of epithelial cell sheets. Moreover, loss of DSP impaired desmosomal ARHGAP32 location and led to decreased actomyosin contractility. ARHGAP32 with a deletion of the GAB2-ID domain showed enhanced association with RhoA in the cytosol and failed to rescue the desmosomal organization in ARHGAP32-KO cells. Collectively, our study unveils that ARHGAP32 associates with and regulates desmosomes by interacting with DSP. This interaction potentially facilitates the crosstalk between desmosomes and F-actin.

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ARHGAP32

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