ARHGAP5
- Known as:
- ARHGAP5
- Catalog number:
- 001862A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ARHGAP5
Related genes to: ARHGAP5
- Gene:
- ARHGAP5 NIH gene
- Name:
- Rho GTPase activating protein 5
- Previous symbol:
- GFI2
- Synonyms:
- RhoGAP5, p190-B, p190BRhoGAP
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-28
- Date modifiied:
- 2015-09-11
Related products to: ARHGAP5
Related articles to: ARHGAP5
- Endometrial cancer is one of the main gynecological malignancies worldwide. Several studies highlight ARHGAP35 as a significantly mutated gene in these tumors. It encodes for p190RhoGAP-A (p190A), which is a major regulator of the small GTPase family of proteins. ARHGAP5 is a paralog of ARHGAP35 that encodes p190RhoGAP-B (p190B). By analyzing human endometrial cancer samples, we found a co-occurrence of mutations in ARHGAP35 and ARHGAP5 genes and reported that both are less expressed at the mRNA level in tumoral samples compared to healthy tissues. We then studied the impact of p190A/B under-expression in endometrial cancer and the relationship between the two paralogs. We generated CRISPR/Cas9-mediated HEC-1-A knockout cells for p190A and p190B. We showed that removal of each paralog led to a similar actin remodeling phenotype with the formation of Cross-Linked Actin Networks (CLANs), dependent on the Rho/ROCK pathway. Moreover, proteomic analysis of p190A and p190B knockout cells highlighted similar affected cell functions. Finally, our study demonstrates a functional interaction between p190A and p190B where removal of both paralogs is deleterious in endometrial cancer cells, unveiling a potential actionable vulnerability. - Source: PubMed
Publication date: 2026/09/10
Pinault MathildeHeraud CapucineOliveira Mélissa Correia deNeaud VéroniqueValesco ValérieProuzet-Mauleon ValérieTurcq BéatriceDupuy Jean-WilliamRaymond Anne-AurélieCroce SabrinaSaltel FrédéricLagrée ValérieMoreau Violaine - Hepatocytes display a unique polarity, forming narrow apical tubes-bile canaliculi (BCs)-between adjacent cells that are essential for liver function. Unlike most epithelial cells, hepatocytes express both E- and N-cadherin, yet their specific roles during BC tubulogenesis remain incompletely understood. Here, we show that these cadherins are collectively required for hepatic polarity and BC formation yet act through distinct mechanisms. E-cadherin localizes to adherens junctions, lateral membranes, and the cleavage furrow, where it promotes division-linked BC elongation and cell-cell contact formation by controlling spindle orientation and RhoA activation via NuMA and ARHGEF17. In contrast, N-cadherin is restricted to adherens junctions and maintains hepatic polarity by attenuating RhoA activity through the p120-catenin family member ARVCF and its partner p190B/ARHGAP5. Together, these findings reveal that dual cadherin expression drives hepatic polarity and BC formation by controlling RhoA activity in a coordinated yet opposing manner. - Source: PubMed
Publication date: 2026/05/27
Hayase JunyaYang LiZhou Yu-HengWang KangjiXu Cheng-RanBi Erfei - Hepatocytes exhibit distinct polarity, forming narrow apical tubes (bile canaliculi, BCs) between adjacent cells. These structures essential to liver architecture and function. Unlike most epithelial cells, hepatocytes express both E- and N-cadherin but their functions and mechanisms remain unknown. We show that E- and N-cadherin are collectively required for hepatic polarity and BC formation but act through distinct, spatially segregated pathways. Both localize to adherens junctions; E-cadherin additionally localizes to lateral membranes and the cleavage furrow during cell division, where it promotes BC elongation and new cell-cell contact formation by controlling spindle orientation and RhoA activation via NuMA and ARHGEF17. N-cadherin maintains hepatic polarity by facilitating RhoA inactivation through the p120-catenin family member ARVCF and its partner p190B/ARHGAP5. Thus, dual cadherin expression drives hepatic polarity and BC formation by controlling RhoA activity in a coordinated but opposing manner. - Source: PubMed
Publication date: 2025/10/06
Hayase JunyaYang LiZhou Yu-HengWang KangjiXu Cheng-RanBi Erfei - Due to a high rate of recurrence coupled with resistance towards modern therapies, colorectal cancer (CRC) is considered as the third cause of cancer-related death worldwide. Gemini curcumin (Gemini-Cur) is one of the last nanoformulation of curcumin with significant toxicity on colorectal cancer. Herein, we aimed to unravel the modulated lncRNAs, related mRNAs and downstream cellular pathways in Gemini-Cur treated HT-29 colorectal cancer cells. 9805 lncRNAs were found to be differentially expressed in nanocurcumin-treated cancer cells versus non treated group. The top 20 lncRNAs were selected for further studies and, 14,472 co-expression relationships between these RNAs and 70,711 mRNAs were identified. Among top 20 lncRNAs, tumor-suppressive C8orf31 and ARHGAP5-AS1, as well as oncogenic XIST, FTX, and NEAT1 were the most notable due to their involvements in cancer-related cellular pathways. Functional enrichment analyses demonstrated that the modulated lncRNAs and their targets are involved in cell cycle, p53 signaling, translation, and helicase activity pathways. In conclusion, our study elucidated new molecular mechanisms of nano-curcumin in the regulation of lncRNA expression and the discovery of potential targets in therapeutic interventions for CRC. More studies are needed to confirm the therapeutic implications of these findings. - Source: PubMed
Publication date: 2025/11/03
Zibaei ZohreAzeez Hewa JalalBabaei Esmaeil - Single-cell RNA sequencing (scRNA-seq) is a widely used method for classifying cell types and states and revealing disease mechanisms. However, most contemporary scRNA-seq platforms fail to explore the multilandscape of RNA. Here, a microfluidic chip is designed that combines oligo-dT primers and Random Bridging Co-labeling (RBCL) RNA sequencing to develop an innovative Chigene scRNA-seq technology that can identify gene expression, mutations, and RNA splicing landscapes at the single-cell level. The Chigene scRNA-seq platform demonstrated exceptional performance, with minimal doublet rates of 0.94% (Chigene V1) and 1.93% (Chigene V2). Both versions exhibit high sensitivity, with Chigene V2 achieving nearly 100% RNA coverage and detecting over 1800 genes per cell on average. Targeted capture of single-cell gene mutations enhances mutation detection sensitivity. Moreover, this Chigene V2 platform is validated in clinical samples for its ability to detect mutations, gene fusions, and alternative splicing. The reliability of the platform is further corroborated via known functional gene mutation (CDKN1A) and fusion (FGFR3-TACC). To validate this method's potential for discovering novel gene mutations in clinical samples, the investigation revealed an intriguing cell subpopulation carrying an ARHGAP5 mutation in urothelial carcinoma. These cells exhibited high-frequency mRNA splicing and exhibited specific crosstalk with T cells, distinguishing them from the subpopulation with the ARHGAP5 wild-type phenotype. Overall, this method provides a robust scRNA-seq platform suitable for comprehensive analyses of clinical specimens at different genetic information levels, thereby offering significant potential in the discovery of novel genes and interactions at the single-cell level. - Source: PubMed
Publication date: 2025/05/05
Zhong WenlongWang LigangZhang ChengjunyuGuo TongleiZhao LihuaWu DaqinXie FeiWang XiaoLi XiuxinWang FangxiaoLi MinghuiGu WeiyueLin TianxinChen Xu