Ask about this productRelated genes to: ARF6 antibody
- Gene:
- ARF6 NIH gene
- Name:
- ADP ribosylation factor 6
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 14q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-01
- Date modifiied:
- 2015-11-19
Related products to: ARF6 antibody
Related articles to: ARF6 antibody
- Although the heterogeneity and plasticity of fibroblasts are recognized hallmarks of tissue fibrosis, their specific contributions to renal fibrosis progression and the therapeutic validity of targeting key effector subsets remain key unanswered questions. Here, we revealed that diverse, functionally exclusive fibroblast subpopulations actively shape their local microenvironment. Pro-inflammatory fibroblasts (i-Fibs) construct immune-active areas, while pro-fibrotic fibroblasts (ECM-Fibs) generate fibrogenic zones. These two distinct microenvironments form a spatial mosaic, occupying mutually exclusive territories within the kidney tissue. We identified mechanotransduction as a signal governing the switch from i-Fibs to the pathogenic ECM-Fib phenotype. Through unbiased bioinformatics and genetic tools, we pinpointed CD248 as a specific cell-surface protein on this matrix-producing subset. Mechanistically, CD248, via its C-type lectin-like domain, senses the disordered matrix, promoting focal adhesion assembly and YAP nuclear translocation through an IQGAP1/ARF6-GTP-dependent axis, leading to a sustained feedback loop between aberrant matrix and myofibroblasts activation. A monoclonal antibody targeting CD248, IgG78, effectively interrupted this feedback loop, mitigating fibrogenesis both in vitro and in vivo in male mice. Collectively, this study established that fibroblast heterogeneity drives pathological niche specification in the fibrotic kidney and validated CD248 as a promising therapeutic target to counteract tissue fibrosis by disrupting aberrant mechanosignaling. - Source: PubMed
Publication date: 2026/05/06
Xu ChaoLiu ShaojieZhou YikeYang FaLi ZhengxuanGan KaiLi YuZhang KeyingLu TongSong HongtaoJiang JunQin JiayangHu ZhihaoQi RuochenMa ShuaijunShi ChanghongZhang RuiSi DailingWen WeihongHan DonghuiQin Weijun - The present study investigated the effects of different intensities of blue light on papillae number growth and associated molecular mechanisms in the sea cucumber Apostichopus japonicus. The sea cucumber were exposed for 60 days under three blue light intensities (1500 lx, 3000 lx, and 4500 lx). Papillae numbers and body weight were measured regularly. Transcriptomic sequencing was performed to analyze gene expression differences in spine tissues. The results showed that the number of papillae was significantly highest in the sea cucumbers exposed to 1500 lx. Body weight growth was not significantly affected by any light intensity treatment. Compared with the control group, the 1500 lx group showed differentially expressed genes (DEGs) significantly enriched in pathways including the ras signaling pathway, ascorbate and aldarate metabolism, and fatty acid elongation. Seven key genes potentially related to the growth of papillae number were identified: Survivin, PHB2, SoxB, traf6, TRPML3, TGF-β1, and Rps13. In contrast, compared with the 1500 lx group, both the 3000 lx group and the 4500 lx group showed differentially expressed genes (DEGs) mainly enriched in pathways including axon regeneration, regulation of actin cytoskeleton, fc gamma R-mediated phagocytosis, and chemokine signaling. Six genes potentially inhibiting the growth of papillae number were identified: CRK, Smad4, Rac1, Arf6, ASAP2, and Wnt7. In conclusion, the light intensity of 1500 lx effectively increased the papillae number in A. japonicus. This study provides molecular evidence for enhancing papillae number in cultured sea cucumbers through light intensity regulation. - Source: PubMed
Publication date: 2026/04/22
Li WeiyanLiu ZiyuDeng YajieLiu JiaqiYu JingeXiao HaoranTian FenglinHan LingshuZhao ChongDing Jun - Novel Kinase 1 encodes a serine-threonine protein kinase, mutations in which are associated with autism spectrum disorder. Direct phosphorylation targets of NUAK1 have been elusive hindering mechanistic understanding of its role in brain development. Here, we characterize autism-associated NUAK1 variants and show their differential impact on catalytic activity and subcellular distribution. We engineered ATP-analog sensitive NUAK1 and utilized its specificity towards bulky analogs to identify over 30 hitherto unknown direct phosphorylation targets of NUAK1. We demonstrate that Pleckstrin Homology and Sec7-domain containing protein 3 (PSD3) is a phosphorylation target of NUAK1. A guanine exchange factor (GEF) for ARF6 GTPase, PSD3 is phosphorylated by NUAK1 at S476. Expression of phosphodeficient PSD3 leads to aberrant activation of ARF6 and generation of PI(4,5)P that accumulates in intracellular vesicles. In neurons, phosphomutant PSD3 leads to enhanced spine maturation in an ARF6 dependent fashion. This study reveals direct neuronal substrates of an autism risk gene NUAK1, and delineates a mechanism by which PSD3 phosphorylation regulates ARF6 activation and spine maturation. - Source: PubMed
Publication date: 2026/04/20
Sejd Josilyn RMarciniak Daphnée MCornell Moira ASondhi AngelOng Shao-EnYadav Smita - The intrinsic ability of cancer cells to evade death underpins tumorigenesis, progression, metastasis, and the survival of drug-tolerant persister (DTP) cells. Herein, we discovered that the small GTPase ARF6 plays a central role in tumor survival by fortifying RAF oncoprotein levels. ARF6 activation was sufficient to increase BRAF, ARAF, and CRAF proteins through a post-transcriptional mechanism, while sustained inhibition of ARF6 eventually led to decay. In a genetically engineered model of aggressive melanoma, tumor-specific Arf6 deletion attenuated BRAF protein expression and MAPK signaling and prevented rapid tumor progression. In human melanoma cells, pharmacologic inhibitors of BRAF uniformly induced swift activation of ARF6, driving a positive feedback loop that restored MAPK-driven anti-apoptotic signaling and supported drug-tolerant survival and growth. Furthermore, in patient-derived melanoma xenografts with innate or clinically acquired resistance to MAPK inhibitors, ARF6 silencing alone significantly suppressed tumor growth in vivo. When combined with BRAF and MEK targeted therapy in vitro, inhibition of ARF6 markedly reduced survival and drug-tolerant growth. Collectively, these findings reveal a previously unknown mechanism of maintaining BRAF protein expression that preserves the MAPK pathway during targeted therapy. This ARF6-dependent mechanism may be exploited in BRAF driven cancers as a therapeutic vulnerability. - Source: PubMed
Publication date: 2026/04/28
Wang JunhuaWee YinshenJacob ThomasRogers AaronSorensen Lise KBrooks Deja MGupta PrachiTay Joshua K HWilson Emily CLiu TongSmith Eric AGopal Y N VashishtDavies Michael AMcMahon MartinHolmen Sheri LJudson-Torres Robert LWolff Roger KGrossmann Allie H - Stone cells originate from secondary cell wall thickening and contain abundant lignin. Their excessive accumulation compromises pear fruit quality, yet the endogenous hormonal mechanisms governing stone cell formation remain unclear. Here, co-expression network analysis using transcriptome data - the flesh of 206 sand pear accessions sampled at the critical stage of stone cell formation and multitissues of 'Dangshansuli' - showed that auxin biosynthetic gene YUCCA6 and auxin signaling activator ARF6 were strongly co-expressed with lignin-related genes. A positive correlation was observed between endogenous indole-3-butyric acid (IBA) levels and the rate of stone cell accumulation. Moreover, both YUCCA6 overexpression and exogenous IBA treatment enhanced lignin deposition in pear, demonstrating that auxin promoted stone cell lignification. Additionally, ARF6 promoted stone cell lignification. Mechanistic analyses revealed that ARF6 activated HB49, which subsequently upregulated MYB169, a key transcriptional activator of lignin biosynthesis, thereby promoting stone cell lignification. Notably, ARF6 interacted with repressors IAA27 or RGL3, which suppressed HB49 activation; this repression was alleviated by auxin or gibberellin treatment, which restored ARF6-mediated activation of HB49. These results establish ARF6 as an integrator of auxin and gibberellin signaling pathways and provide new mechanistic insights into auxin-gibberellin crosstalk in regulating stone cell lignification. - Source: PubMed
Publication date: 2026/04/27
Shan YanfeiChen ShulinCai JianfaZhou ZhengPan ChongLiu JiahaoZheng PengfeiLi ChengLiu YueyuanXue ChengWu Jun