ARFIP1

Last update 08 May 2025

Basic Info

Synonyms

ADP ribosylation factor interacting protein 1, ADP-ribosylation factor-interacting protein 1, Arfaptin-1

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Introduction

Plays a role in controlling biogenesis of secretory granules at the trans-Golgi network (PubMed:22981988). Mechanistically, binds ARF-GTP at the neck of a growing secretory granule precursor and forms a protective scaffold (PubMed:22981988, PubMed:9038142). Once the granule precursor has been completely loaded, active PRKD1 phosphorylates ARFIP1 and releases it from ARFs (PubMed:22981988). In turn, ARFs induce fission (PubMed:22981988). Through this mechanism, ensures proper secretory granule formation at the Golgi of pancreatic beta cells (PubMed:22981988).

100 Clinical Results associated with ARFIP1

100 Translational Medicine associated with ARFIP1

0 Patents (Medical) associated with ARFIP1

Literatures (Medical) associated with ARFIP1

01 Jan 2025·DNA and Cell Biology

Inherited Spinocerebellar Ataxia Segregates with Intra-Familial Genetic Heterogeneity in a Consanguineous Pakistani Family: A Report of a Potential Novel Candidate Gene

Article

Author: Ji, lingchao ; Zhou, Yaqi ; Asif, Muhammad ; Shazly, Gamal A. ; Ye, Weiping ; Lu, Xiaochan ; Ejaz, Arusa ; Yang, Yuanyuan ; Yin, Na ; Qadir, Mahboob ; Liu, Su ; Zhong, Jiatao ; Hu, Hongyi ; Yang, Tao ; Liu, Lei ; Iqbal, Furhan ; Mei, Xueshuang ; Xu, Jun

Hereditary spinocerebellar ataxia (SCA) is a group of genetic neurodegenerative disorders caused by a variety of gene variants. At least 44 types of SCAs have been identified to date, and more than 35 genes and hundreds of variants have been reported that are associated with SCAs. We have investigated a Pakistani consanguineous six-generation family with SCA by using whole-exome sequencing analysis. We identified a reported SCA-associated variant, c.C2687G (p.P896R) in CACNA1A, in only a subgroup of the family, while a c.C262T (p.P88S) variant in ARFIP1 serves as a candidate pathogenic variant in the other subgroup as a possible novel cause of SCA. Our study showed that intra-familial heterogeneity may exist in SCA families and presented a candidate new causative gene for SCA.

01 Aug 2023·Fish & shellfish immunology

Transcriptome analysis reveals modulation of differentially expressed genes in LPS-treated mouse macrophages (RAW264.7 cells) by grouper (Epinephelus coioides) Epinecidin-1.

Article

Author: Chen, Jyh-Yih ; Hsieh, Chu-Yi ; Pan, Chieh-Yu ; Rajanbabu, Venugopal

The marine antimicrobial peptide Epinecidin (Epi)-1 has been shown to exert direct antimicrobial and immunomodulatory actions in teleost, mammalian and avian organisms. For instance, Epi-1 can suppress bacterial endotoxin lipolysachcharide (LPS)-induced proinflammatory cytokines in RAW264.7 murine macrophages. However, it remains unknown how Epi-1 might broadly affect non-activated and LPS-activated macrophages. To address this question, we performed a comparative transcriptomic analysis of non-treated and LPS-treated RAW264.7 cells in the presence and absence of Epi-1. Gene enrichment analysis was conducted on filtered reads, followed by GO and KEGG analyses. The results showed that Epi-1 treatment modulated pathways and genes associated with nucleoside binding, intramolecular oxidoreductase activity, GTPase activity, peptide antigen binding, GTP binding, ribonucleoside/nucleotide binding, phosphatidylinositol binding and phosphatidylinositol-4-phosphate binding. Based on the GO analysis results, we performed real-time PCR at different treatment times to compare expression levels of selected proinflammatory cytokines, anti-inflammatory cytokines, MHC, proliferation and differentiation genes. Epi-1 decreased expression of the proinflammatory cytokines, TNF-α, IL-6 and IL-1β, and it increased the anti-inflammatory cytokine TGFβ and Sytx1. MHC-associated genes, GM7030, Arfip1, Gpb11 and Gem, were induced by Epi-1, which is expected to enhance the immune response against LPS. Immunoglobulin-associated Nuggc was also upregulated by Epi-1. Finally, we found that Epi-1 downregulated the expression of host defense peptides CRAMP, Leap2 and BD3. Taken together, these findings suggest that Epi-1 treatment induces orchestrated changes in the transcriptome of LPS-stimulated RAW264.7 cells.

01 Jun 2013·Naunyn-Schmiedeberg's Archives of PharmacologyQ4 · MEDICINE

Inhibition of formyl peptide-stimulated phospholipase D activation by Fal-002-2 via blockade of the Arf6, RhoA and protein kinase C signaling pathways in rat neutrophils

Q4 · MEDICINE

Article

Author: Yun-Jie Hung ; Jih-Pyang Wang ; Sheng-Chu Kuo ; Mei-Feng Hsu ; Miau-Rong Lee ; Ya-Ru Tsai ; Hui-Yi Lin ; Li-Jiau Huang

Three recently developed selective phospholipase D (PLD) inhibitors N-(2-(4-(2-oxo-2,3-dihydro-1H-benzo[d]imidazol-1-yl)piperidin-1-yl)ethyl)-2-naphthamide (VU0155056), (S)-N-(1-(4-(5-chloro-2-oxo-2,3-dihydro-1H-benzo[d]imidazol-1-yl)piperidin-1-yl)propan-2-yl)-2-naphthamide (VU0155069), and N-(2-(4-oxo-1-phenyl-1,3,8-triazaspiro[4,5]decan-8-yl)ethyl)quinoline-3-carboxamide (VU0285655-1) inhibited O2 (•-) generation in formyl-Met-Leu-Phe (fMLP)-stimulated rat neutrophils. A novel 2-phenyl-4-quinolone compound 6-chloro-2-(2-chlorophenyl)-4-oxo-1,4-dihydroquinoline-3-carboxylate (Fal-002-2), which inhibited O2 (•-) generation, also reduced the fMLP- but not phorbol ester-stimulated PLD activity (IC50 16.0 ± 5.0 μM). Fal-002-2 attenuated the interaction of PLD1 with ADP-ribosylation factor (Arf) 6, Ras homology (Rho) A and protein kinase C (PKC) isoforms (α, βI, and βII), and also inhibited the membrane recruitment of Arf6 and RhoA in fMLP-stimulated neutrophils, but not in GTPγS-stimulated cell-free system. The cellular levels of GTP-bound Arf6 and GTP-bound RhoA were reduced by Fal-002-2. Fal-002-2 also attenuated the membrane recruitment of Rho-associated protein kinase 1, phosphorylation of myosin light chain 2 at Thr18/Ser19 and PLD1 at Thr147, and the interaction of Arf6 with both arfaptin 1 and phosphatidylinositol 4-phosphate 5-kinase 1A. The association between RhoA and Vav, the interaction of Vav with both Lyn and Lck, the membrane recruitment of Vav, and the phosphorylation of Vav at Tyr174, but not Src family at Tyr416, were all attenuated by Fal-002-2 in fMLP-stimulated neutrophils. These results indicate that Fal-002-2 is not a direct PLD inhibitor, but the inhibition of fMLP-stimulated PLD activity by Fal-002-2, which partly accounts for its suppression of O2 (•-) generation, is attributable to the blockade of both Arf6 and RhoA activation and attenuation of the interaction of Arf6, RhoA and PKC isoforms with PLD1 in rat neutrophils.

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ARFIP1

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