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IFN-induced antiviral protein that mediate cellular innate immunity to at least three major human pathogens, namely influenza A H1N1 virus, West Nile virus, and dengue virus by inhibiting the early step(s) of replication.
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Identification of three distinct mutations that converted IFITM1 or IFITM3 (zeige IFITM3 Proteine) from inhibitors to enhancers of MERS-CoV or SARS (zeige SARS Proteine)-CoV spike protein-mediated entry revealed key structural motifs or residues determining the biological activities of IFITM proteins.
Epithelial-mesenchymal transition (EMT (zeige ITK Proteine)) signature was dysregulated by both loss and gain of function of IFITM1, which was partially reverted by Caveolin-1 (CAV1 (zeige CAV1 Proteine)).
These results indicate that IFITM1 protein can restrict alphavirus infection by inhibiting viral fusion with cellular membranes.
The transcriptional regulation of IFITM1, 2 and 3 expression.
IFITM1 and IFITM3 (zeige IFITM3 Proteine) inhibit Zika virus infection early in the viral life cycle.
IFITM1 suppression blocks proliferation and invasion of aromatase (zeige CYP19A1 Proteine) inhibitor-resistant breast cancer in vivo by JAK (zeige JAK3 Proteine)/STAT1 (zeige STAT1 Proteine)-mediated induction of p21 (zeige CDKN1A Proteine).
Compared with CD10 (zeige MME Proteine), IFITM1 has superior performance distinguishing endometrial stroma of adenomyosis from mesenchyma surrounding invasive endometrial adenocarcinoma.
Overexpression of IFITM1 is associated with Oral Squamous Cell Carcinomas.
High expression of IFITM1 is associated with poor prognosis of colorectal cancer.
These findings indicate that overexpression of IFITM1 enhances the aggressive phenotype of triple-negative SUM149 IBC cells and that this effect is dependent on STAT2 (zeige STAT2 Proteine)/BRG1 (zeige SMARCA4 Proteine) interaction.
the importance of the C-terminal region of IFITM1 in modulating the antiviral function through controlling protein subcellular localization.
Palmitoylation of IFITM1 regulates protein stability by preventing proteasomal degradation, and modification of the nonconserved cysteine at the IFITM1 C terminus supports an intramembrane topology with implications for anti-influenza A virus activity.
the fact that IFITM1 can function as a negative regulator of cell proliferation, and because the gene maps to chromosome band 11p15.5, previously associated with NSCLC, it is likely that IFITM1 in man has a key role in tumor formation
Fragilis2 regulates epithelialization of the somites and paraxial mesoderm formation.
The antiproliferative action of IFN-gamma (zeige IFNG Proteine) requires the induction of IFITM1.
IFN-induced antiviral protein that mediate cellular innate immunity to at least three major human pathogens, namely influenza A H1N1 virus, West Nile virus, and dengue virus by inhibiting the early step(s) of replication. Plays a key role in the antiproliferative action of IFN-gamma either by inhibiting the ERK activation or by arresting cell growth in G1 phase in a p53- dependent manner. Implicated in the control of cell growth. Component of a multimeric complex involved in the transduction of antiproliferative and homotypic adhesion signals.
interferon-induced transmembrane protein 1
, interferon induced transmembrane protein 1 (9-27)
, interferon induced transmembrane protein 1
, dispanin subfamily A member 2a
, interferon-induced protein 17
, interferon-inducible protein 9-27
, leu-13 antigen
, fragilis protein 2
, ifitm-like protein 2
, interferon induced transmembrane protein 2 like
, interferon-induced membrane protein Leu-13/9-27
, interferon-induced transmembrane protein 1 (9-27)
, interferon-induced transmembrane protein 1 (9-27) isoform 1