ARFGAP2
- Known as:
- ARFGAP2
- Catalog number:
- 001847A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ARFGAP2
Related genes to: ARFGAP2
- Gene:
- ARFGAP2 NIH gene
- Name:
- ADP ribosylation factor GTPase activating protein 2
- Previous symbol:
- ZNF289
- Synonyms:
- IRZ, Zfp289, FLJ14576
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-23
- Date modifiied:
- 2016-10-05
Related products to: ARFGAP2
Related articles to: ARFGAP2
- Podocytes are specialized glomerular epithelial cells characterized by actin-rich projections known as foot processes, which are essential for maintaining the filtration barrier. The Rho-family small GTPases Rac1 and Cdc42 are key regulators of actin cytoskeletal dynamics in podocytes, influencing cell adhesion, polarity and survival. However, the regulatory mechanisms of Rho GTPase activities in foot processes remain poorly understood. We previously identified GIT ArfGAP2 (GIT2) as a protective protein in podocytes that suppresses Rac1 activity at focal adhesions. However, the role of its paralog, GIT ArfGAP1 (GIT1), is unknown. - Source: PubMed
Publication date: 2026/09/28
Matsuda JunTokuchi MahoShimada NaoyukiAsano-Matsuda KanaMiyakawa HiromitsuAoudjit LamineMartin Claire ETakano TomokoIsaka Yoshitaka - - Source: PubMed
Zhang MinWang YufeiZhao ZhenwangHu Xiaobo - - Source: PubMed
Publication date: 2025/04/18
Ishibe ShutaTian Xuefei - Kashin-Beck disease (KBD) is a chronic and deformable osteoarthropathy linked to low selenium. Limited cartilage regeneration poses challenges for its treatment. Previous studies have found that chondroitin sulfate A-selenium nanoparticle (CSA-SeNP) protects chondrocytes. This study used label-free LC-MS/MS quantitative proteomics to identify differentially expressed proteins and pathways in KBD chondrocytes post-CSA-SeNP treatment. Western blot (WB) was used to verify the key differential proteins, and transmission electron microscopy (TEM) was used to observe the ultrastructure of chondrocytes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed proteins mainly involved in RNA processing, translation, peptide biosynthesis, gene expression, rRNA metabolism, and ribonucleoprotein complex biogenesis. Notably, 121 proteins were up-regulated, 27 down-regulated, and 117 specifically expressed in the CSA-SeNP group. Enriched KEGG pathways included ribosome biogenesis, mRNA surveillance, endoplasmic reticulum protein processing, and endocytosis. Proteins related to autophagy, ER stress, cell homeostasis, protein processing and transport, including PELO, WES1, PLAA, RRBP1, ARC1B, ARFGAP2, and SH3KBP1, were significantly up-regulated in the CSA-SeNP group. In conclusion, our results demonstrated that CSA-SeNP may exert protective effects on chondrocytes in adult patients with KBD mainly through the regulation of target proteins and pathways related to ribosome biogenesis, mRNA surveillance, endoplasmic reticulum protein processing, endocytosis, autophagy, ER stress, and cell homeostasis. Further studies with larger sample size and in vivo to identify, screen and verify the regulatory effects of target proteins and pathways may provide more information for elucidating the mechanism of CSA-SeNP in the treatment of KBD. - Source: PubMed
Publication date: 2025/03/26
Deng HuanDeng FeidanWen XinyueJiang YudeAmhare Abebe FeyissaQiao LichunLi MiaoqianWan PingWang JunHan Jing - Focal adhesion protein GIT2 protected podocytes from injury in rodent proteinuric disease models. GIT2 facilitated translocation of tyrosine phosphatase PTP1B to focal adhesions where it dephosphorylates p130Cas, thereby suppressing Rac1 activity. Stabilizing GIT2 or facilitating GIT2 localization to focal adhesions in podocytes could be a therapeutic strategy in proteinuric kidney diseases. - Source: PubMed
Publication date: 2025/02/28
Shimada NaoyukiMatsuda JunAsano-Matsuda KanaTokuchi MahoAoudjit LamineMasztalerz AgnieszkaLemay SergeTakano TomokoIsaka Yoshitaka