Les protéines ARF

Boulay, Pierre-Luc; Claing, Audrey

doi:10.1051/medsci/20092510783

Cited by 4 publications

(1 citation statement)

References 11 publications

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“…Osteoblast differentiation is a key biological process for the occurrence and development of HO. Other research showed that ARF proteins control tumor proliferation and metastasis (43). Whether ARF4 protein plays a role in the proliferation of heterotopic ossification cells remains to be verified.…”

Section: Discussionmentioning

confidence: 94%

Identification of the Biomarkers and Pathological Process of Heterotopic Ossification: Weighted Gene Co-Expression Network Analysis

et al. 2020

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Heterotopic ossification (HO) is the formation of abnormal mature lamellar bone in extra-skeletal sites, including soft tissues and joints, which result in high rates of disability. The understanding of the mechanism of HO is insufficient. The aim of this study was to explore biomarkers and pathological processes in HO+ samples. The gene expression profile GSE94683 was downloaded from the Gene Expression Omnibus database. Sixteen samples from nine HO- and seven HO+ subjects were analyzed. After data preprocessing, 3,529 genes were obtained for weighted gene co-expression network analysis. Highly correlated genes were divided into 13 modules. Finally, the cyan and purple modules were selected for further study. Gene ontology functional annotation and Kyoto Encyclopedia of Genes and Genomes pathway enrichment indicated that the cyan module was enriched in a variety of components, including protein binding, membrane, nucleoplasm, cytosol, poly(A) RNA binding, biosynthesis of antibiotics, carbon metabolism, endocytosis, citrate cycle, and metabolic pathways. In addition, the purple module was enriched in cytosol, mitochondrion, protein binding, structural constituent of ribosome, rRNA processing, oxidative phosphorylation, ribosome, and non-alcoholic fatty liver disease. Finally, 10 hub genes in the cyan module [actin related protein 3 (ACTR3), ADP ribosylation factor 4 (ARF4), progesterone receptor membrane component 1 (PGRMC1), ribosomal protein S23 (RPS23), mannose-6-phosphate receptor (M6PR), WD repeat domain 12 (WDR12), synaptosome associated protein 23 (SNAP23), actin related protein 2 (ACTR2), siah E3 ubiquitin protein ligase 1 (SIAH1), and glomulin (GLMN)] and 2 hub genes in the purple module [proteasome 20S subunit alpha 3 (PSMA3) and ribosomal protein S27 like (RPS27L)] were identified. Hub genes were validated through quantitative real-time polymerase chain reaction. In summary, 12 hub genes were identified in two modules that were associated with HO. These hub genes could provide new biomarkers, therapeutic ideas, and targets in HO.

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Section: Discussionmentioning

confidence: 94%

Identification of the Biomarkers and Pathological Process of Heterotopic Ossification: Weighted Gene Co-Expression Network Analysis

et al. 2020

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Creutzfeldt-Jakob Disease Subtype-Specific Regional and Temporal Regulation of ADP Ribosylation Factor-1-Dependent Rho/MLC Pathway at Pre-Clinical Stage

et al. 2015

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Small GTPases of the Arf family mainly activate the formation of coated carrier vesicles. We showed that class-I Arf1 interacts specifically with full length GPI-anchored cellular prion protein (PrP(C)). Several recent reports have also demonstrated a missing link between the endoplasmic reticulum and the Golgi-complex role for proper folding, but the exact molecular mechanism is not yet fully understood. In the present study, we identified and characterized the interactive role of Arf1 during PrP(C) intracellular distribution under pathophysiological conditions. PrP(C) interaction with Arf1 was investigated in cortical primary neuronal cultures of PrP(C) wild type and knockout mice (PrP(-/-)). Arf1 and PrP(C) co-binding affinity was confirmed using reverse co-immunoprecipitation, co-localization affinity using confocal laser-scanning microscopy. Treatment with brefeldin-A modulated Arf1 expression and resulted in down-regulation and redistribution of PrP(C) into cytosolic region. In the pre-symptomatic stage of the disease, Arf1 expression was significantly downregulated in the frontal cortex in tg340 mice expressing about fourfold of human PrP-M129 with PrP null background that had been inoculated with human sCJD MM1 brain tissue homogenates (sCJD MM1 mice). In addition, the frontal cortex of CJD human brain demonstrated significant binding capacity of Arf1 protein using co-immunoprecipitation analysis. We also examined Arf1 expression in the brain of CJD patients with the subtypes MM1 and VV2 and found that it was regulated in a region-specific manner. In the frontal cortex, Arf1 expression was not significantly changed in either MM1 or VV2 subtype. Interestingly, Arf1 expression was significantly reduced in the cerebellum in both subtypes as compared to controls. Furthermore, we observed altered RhoA activity, which in turn affects myosin light-chain (MLC) phosphorylation and Arf1-dependent PI3K pathway. Together, our findings underscore a key early symptomatic role of Arf1 in neurodegeneration. Targeting the Arf/Rho/MLC signaling axis might be a promising strategy to uncover the missing link which probably influences disease progression and internal homeostasis of misfolded proteins.

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Association between epidermal growth factor receptor amplification and ADP-ribosylation factor 1 methylation in human glioblastoma

et al. 2017

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Les protéines ARF

Cited by 4 publications

References 11 publications

Identification of the Biomarkers and Pathological Process of Heterotopic Ossification: Weighted Gene Co-Expression Network Analysis

Identification of the Biomarkers and Pathological Process of Heterotopic Ossification: Weighted Gene Co-Expression Network Analysis

Creutzfeldt-Jakob Disease Subtype-Specific Regional and Temporal Regulation of ADP Ribosylation Factor-1-Dependent Rho/MLC Pathway at Pre-Clinical Stage

Association between epidermal growth factor receptor amplification and ADP-ribosylation factor 1 methylation in human glioblastoma

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