Disease relevance of IFIT1

• Protein interaction for an interferon-inducible systemic lupus associated gene, IFIT1 [1].

High impact information on IFIT1

• These profiles showed many similarities to reported interferon-gamma-induced gene expression in normal CD34+ cells; indeed the 2 most up-regulated genes, IFIT1 and IFITM1, are interferon-stimulated genes (ISGs) [2].
• Up-regulation of IFIT1 is a potential diagnostic marker for MDS [2].
• The regions of several genes (IFI-56K, HLA-A3, HLA-DR and 6-16) containing the (putative) ISRE (Interferon Stimulatable Response Element) were tested for their ability to be recognized by HeLa cells nuclear extract proteins [3].
• At 12 h postinfection, there is a striking up-regulation between 10- and 30-fold in the expression of the G1P2, IFIT1, and IFIT2 cellular immune response genes compared to mock-infected cells [4].
• Steady-state levels of IFI56, ISG12, GBP-2, and Wnt7a mRNAs increased in the ovine uterine endometrium between d 10 and 16 of pregnancy but not during the estrous cycle [5].

Biological context of IFIT1

• In addition, evidence is given for the presence of a pseudogene homologous to IFI-56K on chromosome 13 [6].
• The IFI-54K gene promoter region was isolated, from which a 520-base-pair segment was sequenced and compared with the promoter region of the IFI-56K gene that we had previously sequenced [7].
• This conserved sequence might be responsible for the coordinate induction of the IFI-56K and IFI-54K genes by interferon, poly(rI).poly(rC) and viruses [7].
• The human 2',5'-oligoadenylate synthetase-like gene (OASL) encoding the interferon-induced 56-kDa protein maps to chromosome 12q24.2 in the proximity of the 2',5'-OAS locus [8].
• The interferon- and virus-inducible IFI-56K and IFI-54K genes are located on human chromosome 10 at bands q23-q24 [9].

Anatomical context of IFIT1

• Several interferon-resistant cell lines were investigated for the inducibility of both the IFI-56K and IFI-54K genes by interferons, poly(rI).poly(rC) and viruses (which are the natural inducers of interferon-alpha and -beta) [7].
• GBP-2 and IFI56 mRNAs were expressed only in endometrial stroma, ISG12 in both LE and GE, and Wnt7a only in LE of the ovine uterus [5].
• Interesting new microglia markers included interferon-induced protein with tetratricopeptide repeat (ifit), immune responsive gene-1 (irg-1) and thymidylate kinase family LPS-inducible member (tyki) [10].

Associations of IFIT1 with chemical compounds

• We have previously shown that the IFI-56K gene is in addition directly induced by poly(rI).poly(rC), and inducer of interferon-beta [7].
• An IFIT1 protein- protein interaction study showed that IFIT1 may interact with Rho/Rac guanine nucleotide exchange factor [1].

Other interactions of IFIT1

• (2) Interferon (IFN)-inducible anti-viral proteins, including IFIT1, OAS1 and Mx1, and Th1 chemoattractant IP-10, were up-regulated predominantly 6 to 24 hours after stimulation [11].
• Three genes, tissue inhibitor of metalloproteinases 1 (TIMP-1), nm23-H4, and interferon-induced 56K protein (IFI-56K) were strongly overexpressed in all ALCL cell lines compared with stimulated T cells [12].

Analytical, diagnostic and therapeutic context of IFIT1

• IFIT1 (interferon-induced with tetratricopeptide repeats 1) was one of these genes, and overexpression of its mRNA was confirmed independently by real-time PCR in a larger population (40 SLE patients and 29 normal controls) [1].
• Using in situ hybridization, we show here that both IFI-54K and IFI-56K genes map to 10q23-q24 [9].
• Molecular cloning and characterization of two related and interferon-induced 56-kDa and 30-kDa proteins highly similar to 2'-5' oligoadenylate synthetase [13].

References