Ask about this productRelated genes to: ARFGAP3 Blocking Peptide
- Gene:
- ARFGAP3 NIH gene
- Name:
- ADP ribosylation factor GTPase activating protein 3
- Previous symbol:
- ARFGAP1
- Synonyms:
- -
- Chromosome:
- 22q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-19
- Date modifiied:
- 2015-11-19
Related products to: ARFGAP3 Blocking Peptide
Related articles to: ARFGAP3 Blocking Peptide
- MicroRNAs (miRNAs) are key post-transcriptional regulators involved in crustacean immune responses, yet their roles during pattern recognition receptor activation remain poorly understood. In this study, we investigated the miRNA response of Macrobrachium rosenbergii to lipopolysaccharide (LPS), a conserved bacterial pathogen-associated molecular pattern (PAMP). High-throughput small RNA sequencing identified 155 differentially expressed miRNAs (DEMs) in the hepatopancreas following LPS injection. Pathway enrichment analysis revealed that target genes of these DEMs were significantly associated with immune pathways, including the ubiquitin-proteasome pathway (UPP) and endocytosis. Network analysis highlighted mro-miR-365-1-5p as a central regulator targeting key genes such as Rpn10, Rab11, Vps2, and ArfGAP3. Temporal expression profiling revealed rapid downregulation of mro-miR-365-1-5p after LPS exposure. The regulatory role of mro-miR-365-1-5p was validated by dual-luciferase reporter assays and an in vivo challenge experiment. In vivo overexpression of mro-miR-365-1-5p significantly increased mortality in prawns challenged with Vibrio harveyi, indicating impaired immune defense. These findings provide novel insights into the regulatory roles of LPS-responsive miRNAs in crustaceans and suggest that modulation of specific miRNAs may be crucial for effective immune activation during bacterial infection. - Source: PubMed
Publication date: 2025/12/09
Pangeson TanapatThammason RattikonOngvarrasopone ChalermpornWiengnak NalinnipaPhetrungnapha Amnat - Few researches have investigated the molecular mechanism responsible for the age-related loss of the pelvic floor muscle (PFM) mass and functionality-a pivotal contributor to pelvic organ prolapse and diminished physical well-being. ADP ribosylation factor GTPase activating protein 3 (ArfGAP3) is a member of ArfGAPs, which regulates the vesicular trafficking pathway and intracellular proteins transporting. However, its effects on skeletal muscle ageing remain largely unknown. - Source: PubMed
Chen MaoHuang XiaoyuLi BingshuXiao YaChen LiyingZhu FangyiHong ShashaTang JianmingLi SutingMin JieJin WenyiZhang YubiaoYang LianLi YangZhang ShufeiHong Li - A sudden rise in intra-abdominal pressure that causes the pressure in the bladder to rise during physical movement and/or activity, such as coughing, sneezing, laughing, running, or weightlifting, is known as stress urinary incontinence. This condition causes an uncontrollable overflow of urine. The study's goal was to determine whether effector molecules, specifically ADP ribosylation factor GTPase activated protein 3, might play a part in the female pelvic floor muscle's ability to heal after suffering damage during vaginal delivery. Pelvic floor muscle samples were taken from women who had at least one vaginal delivery and were enrolled in either the IU group (n = 45; issue of stress urinary incontinence) or the NL group (n = 85; no issue of stress urinary incontinence) depending on whether they had a problem with stress urinary incontinence. Vesicle transport-related genes in female pelvic floor muscle injury repair were discovered using Gene Expression Omnibus. For gene analysis and screening, RT-qPCR was employed. On the first day following injury, the expression level of ARFGAP3 mRNA increased by 2.8 times (p 0.05) and by 5 times (p 0.01) on the third day. On the first day following damage, STMN1 mRNA expression rose by 0.3 times (p 0.05). On the first day following injury, the expression level of THBS2 mRNA increased by 1.6 times (p 0.01). On the third day following the injury, the expression level of PLXNB2 mRNA increased by 1.2 times (p 0. 01), and on the fifth day following the injury, it increased by 2.5 times (p 0. 01). After pelvic floor muscle damage, the mRNA expression levels of the CSF1R, ANXA4, and EMR1 genes dropped. Between those with and without pelvic floor muscle damage, there was no statistically significant difference in the expression levels of LGARLS3, KDELR3, and KIF20A mRNA (p > 0. 05 for all). The differential expression of genes after pelvic floor muscle injury can identify the target in the process of pelvic floor muscle injury repair and regeneration. - Source: PubMed
Publication date: 2023/05/12
Liu XinWang XiaohuiXu TingnaLiu XiaLi Lingge - Skeletal muscle injuries are common, and damaged myofibers are repaired through proliferation and differentiation of muscle satellite cells. GLUT4 is enriched in GLUT4 storage vesicles (GSVs) and plays a crucial role in the maintenance of muscle function. ArfGAP3 regulates the vesicle transport especially for COPI coat assembly, but its effects on GSVs and the repair process after skeletal muscle injury remains unclear. In this study, datasets related to skeletal muscle injury and myoblast differentiation GSE469, GSE5413, GSE45577 and GSE108040 were retrieved through the GEO database and the expression of heptameric coat protein complex I (COPI) and Golgi vesicle transport-related genes in various datasets, as well as the expression correlation between ArfGAP2, ArfGAP3 and COPI-related genes COPA, COPB1, COPB2, COPE, COPZ1, COPZ2 were analyzed. The results suggested that ArfGAP3 was expressed in the process of repair after skeletal muscle injury and myoblast differentiation and that ArfGAP3 was positively correlated with COPI-related genes. In vitro experimental results showed that ArfGAP3 was colocalized with COPA, COPB, COPG protein, and GLUT4 in C2C12 myoblasts. After the downregulation of ArfGAP3 expression, intracellular vesicle transport, and glucose uptake were blocked, the proliferation of myoblasts under low glucose culture conditions was impaired, the proportion of apoptosis increased, and myotube differentiation was impaired. In summary, ArfGAP3 regulates COPI-associated vesicle and GSVs transport and affects the proliferation and differentiation ability of myoblasts by influencing glucose uptake, thereby modulating the repair process after skeletal muscle injury. - Source: PubMed
Publication date: 2022/12/05
Li SutingWang ZhiChen MaoXiao YaMin JieHu MingTang JianmingHong Li - The integrin αvβ6 is expressed at low levels in most normal healthy tissue but is very often upregulated in a disease context including cancer and fibrosis. Integrins use endocytosis and trafficking as a means of regulating their surface expression and thus their functions, however little is known of how this process is regulated in the context of αvβ6. As αvβ6 is a major target for the development of therapeutics in cancer and fibrosis, understanding these dynamics is critical in the development of αvβ6-targeted therapies. Following development of a flow cytometry-based assay to measure ligand (A20FMDV2 or LAP)-bound αvβ6 endocytosis, an siRNA screen was performed to identify which genes were responsible for internalising αvβ6. These data identified 15 genes (DNM2, CBLB, DNM3, CBL, EEA1, CLTC, ARFGAP3, CAV1, CYTH2, CAV3, CAV2, IQSEC1, AP2M1, TSG101) which significantly decreased endocytosis, predominantly within dynamin-dependent pathways. Inhibition of these dynamin-dependent pathways significantly reduced αvβ6-dependent migration (αvβ6-specific migration was 547 ± 128 under control conditions, reduced to 225 ± 73 with clathrin inhibition, and 280 ± 51 with caveolin inhibition). Colocalization studies of αvβ6 with endosome markers revealed that up to 6 h post-internalisation of ligand, αvβ6 remains in Rab11-positive endosomes in a perinuclear location, with no evidence of αvβ6 degradation up to 48 h post exposure to A20FMDV2. Additionally, 60% of ligand-bound αvβ6 was recycled back to the surface by 6 h. With studies ongoing using conjugated A20FMDV2 to therapeutically target αvβ6 in cancer and fibrosis, these data have important implications. Binding of A20FMDV2 seemingly removes much of the αvβ6 from the cell membrane, and upon its recycling, a large fraction appears to still be in the ligand-bound state. While these results are observed with A20FMDV2, these data will be of value in the design of αvβ6-specific therapeutics and potentially the types of therapeutic load. - Source: PubMed
Publication date: 2022/08/24
Meecham AmeliaCutmore Lauren CProtopapa PantelitsaRigby Lauren GMarshall John F