ARFGAP2

Last update 08 May 2025

Basic Info

Synonyms

ADP ribosylation factor GTPase activating protein 2, ADP-ribosylation factor GTPase-activating protein 2, ARF GAP 2

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Introduction

GTPase-activating protein (GAP) for ADP ribosylation factor 1 (ARF1). Implicated in coatomer-mediated protein transport between the Golgi complex and the endoplasmic reticulum. Hydrolysis of ARF1-bound GTP may lead to dissociation of coatomer from Golgi-derived membranes to allow fusion with target membranes.

100 Clinical Results associated with ARFGAP2

100 Translational Medicine associated with ARFGAP2

0 Patents (Medical) associated with ARFGAP2

Literatures (Medical) associated with ARFGAP2

01 Mar 2025·Cell

ArfGAP2 promotes STING proton channel activity, cytokine transit, and autoinflammation

Article

Author: Fu, Jiayuan ; Qian, Wei ; Shiba, Yoko ; Stinson, W Alexander ; Ning, Yue ; Surve, Nehalee ; Balka, Katherine R ; Shin, Sunny ; Disbennett, W Miguel ; De Nardo, Dominic ; Miner, Jonathan J ; Rome, Kelly ; Miner, Cathrine A ; Castillo-Badillo, Jean A ; Naismith, Teresa V ; Yoh, Sunnie ; Venkatraman, Rajan ; Chauvin, Samuel D ; Poddar, Subhajit ; Roberson, Elisha D O ; Semenkovich, Clay F ; Yin, Xin ; Bailis, Will ; Kast, David J ; Cherry, Sara ; Liu, Canyu ; Holley, Joe A ; Chanda, Sumit K ; Wodzanowski, Kimberly A ; Archer, Christopher H ; Zaver, Shivam A ; Wei, Xiaochao ; Ochoa, Trini A

Stimulator of interferon genes (STING) transmits signals downstream of the cytosolic DNA sensor cyclic guanosine monophosphate-AMP synthase (cGAS), leading to transcriptional upregulation of cytokines. However, components of the STING signaling pathway, such as IRF3 and IFNAR1, are not essential for autoinflammatory disease in STING gain-of-function (STING-associated vasculopathy with onset in infancy [SAVI]) mice. Recent discoveries revealed that STING also functions as a proton channel that deacidifies the Golgi apparatus. Because pH impacts Golgi enzyme activity, protein maturation, and trafficking, we hypothesized that STING proton channel activity influences multiple Golgi functions. Here, we show that STING-mediated proton efflux non-transcriptionally regulates Golgi trafficking of protein cargos. This process requires the Golgi-associated protein ArfGAP2, a cell-type-specific dual regulator of STING-mediated proton efflux and signaling. Deletion of ArfGAP2 in hematopoietic and endothelial cells markedly reduces STING-mediated cytokine and chemokine secretion, immune cell activation, and autoinflammatory pathology in SAVI mice. Thus, ArfGAP2 facilitates STING-mediated signaling and cytokine release in hematopoietic cells, significantly contributing to autoinflammatory disease pathogenesis.

01 Jan 2024·SAGE Open Medicine

Label-free quantitative proteomics reveals the mechanisms of Aurora kinase B in renal cell carcinoma

Article

Author: Yang, Yang ; Li, Yulong

Background: Renal cell carcinoma is the most common form of kidney cancer which is a global threat to human health, needing to explore effective therapeutic targets and treatment methods. Aurora kinase B acts as an important carcinogenic role in various kinds of tumors, while its mechanism in renal cell carcinoma is indistinct. Herein we explore the underlying mechanism of Aurora kinase B in renal cell carcinoma. Methods and results: Label-free quantitative proteomics analysis was employed to analyze the differentially expressed proteins in 786-O cells which were treated with si-Aurora kinase B or si-ctrl. In the current study, 169 differentially expressed proteins were identified. The top 10 upregulated proteins were MX2, IFI44L, ISG20, DDX58, F3, IFI44, ECE1, PRIC285, NIT1, and IFIT2. The top 10 downregulated proteins were FKBP9, FSTL1, DDAH1, TGFB2, HMGN3, COIL, FAM65A, PTPN14, ARFGAP2, and EIF2C2. GO enrichment analysis showed that these differentially expressed proteins participated in biological processes, including defense response to virus, response to virus, and type I interferon signaling pathway. These differentially expressed proteins participated in cellular components, including focal adhesion, cell-substrate adherens junction, cell-substrate junction, and endoplasmic reticulum lumen. These differentially expressed proteins participated in molecule functions, including guanyl nucleotide binding, nucleotidase activity, double-stranded RNA binding, 2′-5′-oligoadenylate synthetase activity, and virus receptor activity. Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that the significantly changed proteins including OAS3, OAS2, JAK1, TAP1, and RAC1 were involved in Epstein-Barr virus infection. Conclusions: Taken together, our results demonstrate the possible mechanisms that Aurora kinase B may participate in renal cell carcinoma. These findings may provide insights into tumorigenesis and a theoretical basis for developing potential therapies of renal cell carcinoma.

27 Jun 2023·Journal of Experimental Botany

High temperature defense pathways mediate lodicule expansion and spikelet opening in maize tassels

Article

Author: Sheng, Dechang ; Gu, Mingqi ; Huang, Shoubing ; Wang, Xin ; Wang, Pu ; Liu, Xiaoli ; Lv, Xuanlong

AbstractHigh temperature (HT) at flowering hinders pollen shedding, but the mechanisms underlying stress-induced spikelet closure are poorly understood in maize. In this study, yield components, spikelet opening, and lodicule morphology/protein profiling upon HT stress during flowering were examined in two contrasting maize inbred lines, Chang 7-2 and Qi 319. HT induced spikelet closure and reduced pollen shed weight (PSW) and seed set in both lines, but Qi 319 had a 7-fold lower PSW than Chang 7-2, and was thus more susceptible to HT. In Qi 319, a smaller lodicule size reduced the spikelet opening rate and angle, and relatively more vascular bundles hastened lodicule shrinking compared with Chang 7-2. Lodicules were collected for proteomics analysis. In lodicules of HT-stressed plants, proteins involved in stress signals, cell wall, cell constructure, carbohydrate metabolism, and phytohormone signaling were associated with stress tolerance. HT down-regulated the expression of ADP-ribosylation factor GTPase-activating protein domain2, SNAP receptor complex member11, and sterol methyltransferase2 in Qi 319 but not in Chang 7-2, which was in good agreement with the observed changes in protein abundance. Exogenous epibrassinolide increased the spikelet opening angle and extended the duration of spikelet opening. These results suggest that dysfunction of the actin cytoskeleton and membrane remodeling induced by HT probably limits lodicule expansion. In addition, a reduction in the vascular bundles in the lodicules and application of epibrassinolide might confer spikelet tolerance to HT stress.

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ARFGAP2

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