anti-Interferon-Induced Transmembrane Protein 3 (IFITM3) Antibodies

Mouse (Murine) Interferon-Induced Transmembrane Protein 3 (IFITM3) interaction partners

1. Study in influenza virus infection mouse models found that Ifitm3 is rapidly up-regulated by T cells following their activation and this occurred independently of type I and II interferon and the interferon regulatory factors 3 and 7. Up-regulation of Ifitm3 on effector T cells protected these cells from virus infection and imparted a survival advantage at sites of virus infection.

2. this study shows that IFITM3 drives type 2 T helper cell differentiation and exacerbate allergic airway inflammation

3. the role of IFITM3 in colonic epithelial homeostasis, inflammation and colitis-associated tumorigenesis using IFITM3-deficient mice, was investigated.

4. The extracellular level of Fstl1 is regulated by Ifitm3 in astrocytes, which could be involved in polyI:C-induced neurodevelopmental impairment.

5. contrary to its role in enhancing DNA virus replication, LSD1 limits RNA virus replication by demethylating and activating IFITM3 which is a host restriction factor for many RNA viruses

6. IFITM1 and IFITM3 inhibit Zika virus infection early in the viral life cycle.

7. ZMPSTE24 is a downstream effector of IFITM3 and is important for interferon-induced transmembrane antiviral activity.

8. IFITM3 represents a checkpoint regulator of antiviral immunity that controls cytokine production to restrict viral pathogenesis.

9. Collectively, the data define an antiviral role for Ifitm3 in restricting infection of multiple alphaviruses.

10. Ifitm3 plays a role in mouse primordial germ cell homing and repulsion by enhancing the regionalization of PGCs.

11. Ifitm3 does not impact on the restriction or pathogenesis of bacterial (Salmonella typhimurium, Citrobacter rodentium, Mycobacterium tuberculosis) or protozoan (Plasmodium berghei) pathogens, despite in vitro evidence.

12. results suggest that modification of Tyr(20) may serve in a cellular checkpoint controlling IFITM3 trafficking and degradation and demonstrate the complexity of posttranslational regulation of IFITM3

13. It acts as a defence factor for virus infection, though, it also suppress endocytosis of astroglia, which results in neurodevelopmental impairment.(review)

14. Interferon-induced transmembrane protein 3 is a type II transmembrane protein.

15. results revealed diverse, yet consistent, profiles of IFITM3 localization throughout the gastrula

16. Induction of IFITM3 expression in astrocytes leads to brain dysfunction by impairing neurite development and other non-cell autonomous effects such as increasing mRNA levels of inflammatory cytokines.

17. Jin Chai antiviral capsule exerts antiviral effects against influenza virus by raised expression of IFITM3.

18. lung TRM cells were programmed to retain IFITM3 expression, which facilitated their survival and protection from viral infection during subsequent exposures

19. A central role for Ifitm3 in limiting acute influenza in vivo.

20. IFITM3 is essential for defending the host against influenza A virus in vivo; mice lacking Ifitm3 display fulminant viral pneumonia when challenged with a normally low-pathogenicity influenza virus, mirroring the destruction inflicted by the highly pathogenic 1918 'Spanish' influenza

Human Interferon-Induced Transmembrane Protein 3 (IFITM3) interaction partners

1. Study determined that IFITM3 mutants are essentially packaged into virions proportionally to their intracellular levels of expression. Most mutations were found to concomitantly affect both antiviral properties of IFITM3 against HIV-1, but one CTD mutant exhibited a divergent behavior, possibly highlighting a novel regulatory role for this domain.

2. IFITM3 was constitutively associated with IRF3 and regulated the homeostasis of IRF3 by mediating the autophagic degradation of IRF3. These findings suggest a novel inhibitory function of IFITM3 on the RNA-virus-triggered production of type I IFNs and cellular antiviral responses.

3. Studied the role of interferon induced transmembrane protein 3 (IFITM3) in human metapneumovirus infection.

4. The authors show that full-length IFITM3 mRNA is dominantly expressed (>99%) across all rs12252 genotypes.

5. Role of IFITM3 in vaccinia virus infection was investigated at cellular level and observed that vaccinia virus did not trigger the transcription of IFITM3 or even down regulated IFITM3 expression by an IRF3-independent manner. Silencing of endogenous IFITM3 did not exert any significant effect on virus infection, but it regulated the antiviral activity of type Iota IFN and modulated the vaccinia virus-induced cell death.

6. overexpression of IFITM1, 2 and 3 suppressed entry of CXCR4 and CCR5 tropic viruses; entry of transmitted founder HIV-1 in U87 cells is more sensitive to inhibition by IFITM2 and IFITM3 than by IFITM1

7. The patients with HCC had a significantly higher proportion of IFITM3 rs12252-CC as compared with the patients with chronic HBV infection or liver cirrhosis. Moreover, the distribution of CC genotype in HCC patients with low differentiation was significantly higher than that in those with high differentiation. Furthermore, the patients with CC genotype were found with bigger tumor size.

8. Study showed that IFITM3 was upregulated in hepatocellular carcinoma (HCC) tissues and associated with HCC tumor size, tumor multifocal, and venous invasion. Furthermore, IFITM3 was identified as a new functional target gene of miR29a which expression was negatively correlated with that of IFITM3 in HCC tissues. These results indicated that IFITM3 play a critical role in the development and progression of HCC.

9. a functional convergence between the mTOR pathway and IFITM3 proteins at endolysosomal membranes.

10. 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

11. rs12252 C polymorphism of interferon-induced transmembrane protein 3 (IFITM3) is associated mild flu in Iranian population. Carriers of the rs12252 C allele (CT + CC genotypes) showed 5.92 folds increase in the risk of mild flu comparing to the T allele homozygotes. There is a significant positive association between rs12252 C allele heterozygote and mild flu but not in C allele homozygote group.

12. A significant association between the IFITM3 rs12252 polymorphism and the risk of influenza in both the White and East Asian populations (meta-analysis).

13. contrary to its role in enhancing DNA virus replication, LSD1 limits RNA virus replication by demethylating and activating IFITM3 which is a host restriction factor for many RNA viruses

14. study predicts IFITM3 secondary structures and identifes a highly conserved, short amphipathic helix within a hydrophobic region of IFITM3 previously thought to be a transmembrane domain; show this helix and its amphipathicity are required for IFITM3-dependent inhibition of influenza virus, Zika virus vesicular stomatitis virus, Ebola virus and HIV infections

15. frequencies of the CC genotype and the C allele in the IFITM3 polymorphism were higher in the Korean population than in the European populations but not in Chinese and Japanese populations; the rs12252 polymorphism of the IFITM3 gene did not significantly correlate with the disease severity of influenza A virus infection

16. IFITM3 rs12252 CC genotype was associated with severity rather than susceptibility of IVI in Chinese population, and this strong effect was observed in all subtypes of seasonal influenza infection

17. Identification of three distinct mutations that converted IFITM1 or IFITM3 from inhibitors to enhancers of MERS-CoV or SARS-CoV spike protein-mediated entry revealed key structural motifs or residues determining the biological activities of IFITM proteins.

18. Results demonstrate that IFITM3 expression has a close relationship with prognosis in esophageal squamous cell carcinoma (ESCC) patients. Its overexpression may predict poor prognosis in stage IIA ESCC patients after Ivor Lewis esophagectomy.

19. Study demonstrated, for the first time, that IFITM3 is expressed at a much higher level in lung cancer than in control tissues. Its knockdown could suppress lung cancer cell proliferation, invasion, and migration while inducing lung cancer cell cycle arrest and apoptosis.

20. IFITM3 is upregulated in patient-derivedbrain tumor-propagating cells (BTPCs) upon irradiation but does not affect brain tumor formation or progression in vivo.