ARFRP1
- Known as:
- ARFRP1
- Catalog number:
- 001853A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ARFRP1
Related genes to: ARFRP1
- Gene:
- ARFRP1 NIH gene
- Name:
- ADP ribosylation factor related protein 1
- Previous symbol:
- -
- Synonyms:
- ARP, Arp1, ARL18
- Chromosome:
- 20q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-02
- Date modifiied:
- 2016-10-05
Related products to: ARFRP1
Related articles to: ARFRP1
- Colorectal cancer with peritoneal metastases (CRCPM) exhibits high recurrence post-cytoreductive surgery (CRS). This study evaluated tumor tissue biomarkers and combined circulating tumor DNA (ctDNA) and methylation analysis via ultra-deep next-generation sequencing (NGS) for recurrence prediction. - Source: PubMed
Publication date: 2025/04/29
Chen ChaoGong ZhiyuanZhang ZhiweiGu HaochenZhu AkaoPeng DiLi BingWang JianHu YetingWang DaSun Lifeng - ARL5 is a member of the ARF family of small GTPases that is recruited to the trans-Golgi network (TGN) by another ARF-family member, ARFRP1, in complex with the transmembrane protein SYS1. ARL5 recruits its effector, the multisubunit tethering complex GARP, to promote SNARE-dependent fusion of endosome-derived retrograde transport carriers with the TGN. To further investigate the function of ARL5, we sought to identify additional effectors. Using proximity biotinylation and protein interaction assays, we found that the armadillo-repeat protein ARMH3 (C10orf76) binds to active, but not inactive, ARL5, and that it is recruited to the TGN in a SYS1-ARFRP1-ARL5-dependent manner. Unlike GARP, ARMH3 is not required for the retrograde transport of various cargo proteins. Instead, ARMH3 functions to activate phosphatidylinositol 4-kinase IIIβ (PI4KB), accounting for the main pool of phosphatidylinositol 4-phosphate (PI4P) at the TGN. This function contributes to recruitment of the oncoprotein GOLPH3 and glycan modifications at the TGN. These studies thus identify the SYS1-ARFRP1-ARL5-ARMH3 axis as a regulator of PI4KB-dependent generation of PI4P at the TGN. - Source: PubMed
Publication date: 2024/11/23
Ishida MoriéGolding Adriana EKeren-Kaplan TalLi YanBalla TamasBonifacino Juan S - Genome-wide association studies (GWASs) have identified numerous lung cancer risk-associated loci. However, decoding molecular mechanisms of these associations is challenging since most of these genetic variants are non-protein-coding with unknown function. Here, we implemented massively parallel reporter assays (MPRAs) to simultaneously measure the allelic transcriptional activity of risk-associated variants. We tested 2,245 variants at 42 loci from 3 recent GWASs in East Asian and European populations in the context of two major lung cancer histological types and exposure to benzo(a)pyrene. This MPRA approach identified one or more variants (median 11 variants) with significant effects on transcriptional activity at 88% of GWAS loci. Multimodal integration of lung-specific epigenomic data demonstrated that 63% of the loci harbored multiple potentially functional variants in linkage disequilibrium. While 22% of the significant variants showed allelic effects in both A549 (adenocarcinoma) and H520 (squamous cell carcinoma) cell lines, a subset of the functional variants displayed a significant cell-type interaction. Transcription factor analyses nominated potential regulators of the functional variants, including those with cell-type-specific expression and those predicted to bind multiple potentially functional variants across the GWAS loci. Linking functional variants to target genes based on four complementary approaches identified candidate susceptibility genes, including those affecting lung cancer cell growth. CRISPR interference of the top functional variant at 20q13.33 validated variant-to-gene connections, including RTEL1, SOX18, and ARFRP1. Our data provide a comprehensive functional analysis of lung cancer GWAS loci and help elucidate the molecular basis of heterogeneity and polygenicity underlying lung cancer susceptibility. - Source: PubMed
Publication date: 2024/06/20
Long ErpingPatel HarshGolden AlyxandraAntony MichelleYin JinhuFunderburk KarenFeng JamesSong LeiHoskins Jason WAmundadottir Laufey THung Rayjean JAmos Christopher IShi JianxinRothman NathanielLan Qing Choi Jiyeon - Inflammatory bowel disease (IBD) poses a complex challenge due to its intricate underlying mechanisms, and curative treatments remain elusive. Consequently, there is an urgent need to identify genes causally associated with IBD. - Source: PubMed
Publication date: 2024/04/06
Luo QinghuaWang JiawenGe WeiLi ZihaoMao YuantingWang ChenZhang Leichang - The β-coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the global COVID-19 pandemic. Coronaviral Envelope (E) proteins are pentameric viroporins that play essential roles in assembly, release, and pathogenesis. We developed a nondisruptive tagging strategy for SARS-CoV-2 E and find that, at steady state, it localizes to the Golgi and to lysosomes. We identify sequences in E, conserved across , responsible for endoplasmic reticulum-to-Golgi export, and relate this activity to interaction with COP-II via SEC24. Using proximity biotinylation, we identify an ADP ribosylation factor 1/adaptor protein-1 (ARFRP1/AP-1)-dependent pathway allowing Golgi-to-lysosome trafficking of E. We identify sequences in E that bind AP-1, are conserved across β-coronaviruses, and allow E to be trafficked from Golgi to lysosomes. We show that E acts to deacidify lysosomes and, by developing a trans-complementation assay for SARS-CoV-2 structural proteins, that lysosomal delivery of E and its viroporin activity is necessary for efficient viral replication and release. - Source: PubMed
Publication date: 2024/04/03
Pearson Guy JMears Harriet VBroncel MalgorzataSnijders Ambrosius PBauer David L VCarlton Jeremy G