Les IFITM, un obstacle commun à de nombreux virus

Tartour, Kévin; Cimarelli, Andrea

doi:10.1051/medsci/20153104011

Cited by 5 publications

(4 citation statements)

References 42 publications

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“…The genetic and molecular mechanisms of the IFITM that interfere with viral and bacterial cycles are not yet fully understood (Tartour and Cimarelli 2015;Ranjbar et al 2015). Interestingly, Shen et al (2013) identified a SNP in the IFITM3 promoter (rs3888188) that responded to IFN-γ stimulation, although not in the vicinity of the IFN-gamma activation site (GAS) element, and was associated with the risk for pediatric tuberculosis in Han Chinese population.…”

Section: Discussionmentioning

confidence: 99%

Population genetics of IFITM3 in Portugal and Central Africa reveals a potential modifier of influenza severity

et al. 2017

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Influenza epidemics are a serious global public health and economic problem. The IFITM3 allele (rs12252-C) was suggested as a population-based genetic risk factor for severe influenza virus infection by A(H1N1)pdm09. We analyzed the population genetics of IFITM3 variants in the Portuguese general population (n = 200) and Central Africans (largely Angolan) (n = 148) as well as its association to influenza severity in Portuguese patients (n = 41). Seven SNPs, within the 352 bp IFITM3 amplicon around rs12252, were identified. SNP distributions in the Portuguese appeared at an intermediate level between the Africans and other Europeans. According to HapMap, rs34481144 belongs to the same linkage disequilibrium (LD) block as rs12252 and is in strong LD with rs6421983. A negative association with severe relative to mild disease was observed for allele rs34481144-A, indicating a protective effect under the dominant model. Moreover, haplotype Hap4 with rs34481144-A, not including rs12252-C, was significantly associated to mild influenza. Conversely, although with borderline significance, haplotype Hap1 with rs34481144-G, not including rs12252-C, was associated to severe disease. Moreover, in comparison to the general Portuguese population, statistical significant differences in the frequencies of the protective allele rs34481144-A in the severe disease group, the deleterious Hap1 in the mild disease group, and the protective Hap4 in the severe disease group were observed. The population attributable risk (PAR) for the targeted rs34481144 allele or genotype was of 55.91 and 64.44% in the general population and the mildly infected individuals, respectively. Implication of these variants in disease phenotype needs further validation, namely through functional analysis as is discussed.

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Section: Discussionmentioning

confidence: 99%

Population genetics of IFITM3 in Portugal and Central Africa reveals a potential modifier of influenza severity

et al. 2017

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“…Osteoblastogenesis is tightly regulated by complex cytokine networks under physiological and pathophysiological conditions (2). The IFITM family is well known for their functions in viral infection and innate immunity (17,(23)(24)(25). IFITM5 is an osteoblastspecific membrane protein and functions as a positive regulatory factor for bone mineralization (26,27).…”

Section: Discussionmentioning

confidence: 99%

Role of IFITM2 in osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

Zhang,

Li,

Zhang

et al. 2024

IRDR

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Interferon-inducible transmembrane (IFITM) are a family of small proteins localized to plasma and endolysosomal membranes. Their functions beyond restricting viral entry and replication have been revealed in recent years. IFITM5 is involved in bone mineralization and is an osteogenic cell surface marker. IFITM1 and 3 interact with desmin and myosin, and are involved in myogenic differentiation. This study found upregulation of Ifitm2 during osteogenic differentiation of C3H10T1/2 cells. This positively correlated to the expression of osteogenic differentiation markers Col1a1, Alp, Runx2, and Ocn. Knockdown of Ifitm2 by siRNAs inhibited osteogenic differentiation, calcium deposition, and osteogenic marker expression of C3H10T1/2 cells. The osteoblast transcriptome revealed that knocking down Ifitm2 affected the expression Wnt signaling pathway-related genes, including Wnt family members, their receptors Lrp, Frizzled, and Lgr, and transmembrane molecule Rnf43 that suppresses the Wnt signaling pathway. Luciferase assays indicated enhancement of canonical Wnt signaling pathways by Ifitm2 overexpression. Furthermore, IFITM2 was colocalized in the metaphyseal bone and growth plate of the mouse tibial bone with SP7, a transcription factor essential for osteoblast differentiation and bone formation. These findings reveal a possible novel function and potential mechanisms of Ifitm2 in osteogenic differentiation.

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“…Interferon-induced transmembrane proteins (IFITMs) are interferon-induced transmembrane proteins with molecular weights between 10 and 15kD. There are four functional members in the IFITM family: IFITM1, IFITM2, IFITM3, and IFITM5 [ 7 , 8 ]. IFITMs were originally found to play a role in eukaryotic antiviral responses, and recent studies have confirmed that they play a role in tumor development.…”

Section: Introductionmentioning

confidence: 99%

Interferon-induced transmembrane protein 2 is a prognostic marker in colorectal cancer and promotes its progression by activating the PI3K/AKT pathway

Liu,

Liang,

et al. 2024

Discov Onc

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Background Interferon-induced transmembrane protein 2 (IFITM2) is involved in repressing viral infection. This study aim to investigate the expression of IFITM2 in colorectal cancer (CRC) and explore its effect on cell proliferation, migration, and invasion. Methods We analyzed The Cancer Genome Atlas (TCGA) database for IFITM2 expression in colorectal cancer and used western blots to detect IFITM2 protein in specimens and cell lines of colorectal cancers. To assess the association between IFITM2 and clinical features, both univariate and multivariate cox regression analysis were conducted. Kaplan–Meier plots were used in the TCGA database to assess IFITM2 gene expression's prognostic significance. Silencing IFITM2 in SW480 and HCT116 cells was achieved by transient transfection with siRNA. Proliferation of CRCs was examined using Cell Counting Kit-8. The effect of IFITM2 on the migration and invasion of CRC cells was studied using wound healing and transwell assays. Gene set enrichment analysis (GSEA) was used to examine IFITM2-associated pathways and Western blotting was used to confirm it. Results IFITM2 was over-expressed in the CRC tissues and cells, with high IFITM2 expression related to the tumor N, M, and pathologic stages. The presence of IFITM2 significantly impacted patient survival in CRC. The proliferation of SW480 and HCT116 cells was suppressed when IFITM2 was silenced, resulting in weakened migration and invasion of CRC cells. GSEA analysis showed that IFITM2 was positively related to the phosphoinositide 3-kinase (PI3K)/AKT pathway, and western blot results confirmed that IFITM2 activated it. Conclusions IFITM2 was over-expressed in CRC and modulated the PI3K/AKT pathway to promote CRC cells proliferation and metastasis.

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Les IFITM, un obstacle commun à de nombreux virus

Cited by 5 publications

References 42 publications

Population genetics of IFITM3 in Portugal and Central Africa reveals a potential modifier of influenza severity

Population genetics of IFITM3 in Portugal and Central Africa reveals a potential modifier of influenza severity

Role of IFITM2 in osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

Interferon-induced transmembrane protein 2 is a prognostic marker in colorectal cancer and promotes its progression by activating the PI3K/AKT pathway

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