Ifit2 Reference Search Result - Rat Genome Database

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RGD ID	Title	Citation	Abstract	PubMed	Pub Date
1556487	IFI60/ISG60/IFIT4, a new member of the human IFI54/IFIT2 family of interferon-stimulated genes.	de Veer MJ, etal., Genomics 1998 Dec 1;54(2):267-77.	We report the cloning and sequencing of a full-length cDNA encoding a new member of the human IFI54 (HGMW-approved symbol IFIT2) gene family, designated IFI60 (HGMW-approved symbol IFIT4). The upstream regulatory region of IFI60 shows conservation in structure w ... (more) ith that of the IFI54 and IFI56 (HGMW-approved symbol IFIT1) genes, each containing two interferon-stimulated response elements upstream of a conserved TATA box. We have established a partial gene map of the IFI54 gene family by analysis of YAC library clones. All four members of the human family are clustered together at chromosome 10q23.3. It is proposed that the four members of the IFI54 gene family evolved by a series of duplication events from a common gene of origin.	9828129	1998-10-01
11536274	Cox4i2, Ifit2, and Prdm11 Mutant Mice: Effective Selection of Genes Predisposing to an Altered Airway Inflammatory Response from a Large Compendium of Mutant Mouse Lines.	Horsch M, etal., PLoS One. 2015 Aug 11;10(8):e0134503. doi: 10.1371/journal.pone.0134503. eCollection 2015.	We established a selection strategy to identify new models for an altered airway inflammatory response from a large compendium of mutant mouse lines that were systemically phenotyped in the German Mouse Clinic (GMC). As selection criteria we included published gene functional data, as well as immun ... (more) ological and transcriptome data from GMC phenotyping screens under standard conditions. Applying these criteria we identified a few from several hundred mutant mouse lines and further characterized the Cox4i2tm1Hutt, Ifit2tm1.1Ebsb, and Prdm11tm1.1ahl lines following ovalbumin (OVA) sensitization and repeated OVA airway challenge. Challenged Prdm11tm1.1ahl mice exhibited changes in B cell counts, CD4+ T cell counts, and in the number of neutrophils in bronchoalveolar lavages, whereas challenged Ifit2tm1.1Ebsb mice displayed alterations in plasma IgE, IgG1, IgG3, and IgM levels compared to the challenged wild type littermates. In contrast, challenged Cox4i2tm1Hutt mutant mice did not show alterations in the humoral or cellular immune response compared to challenged wild type mice. Transcriptome analyses from lungs of the challenged mutant mouse lines showed extensive changes in gene expression in Prdm11tm1.1ahl mice. Functional annotations of regulated genes of all three mutant mouse lines were primarily related to inflammation and airway smooth muscle (ASM) remodeling. We were thus able to define an effective selection strategy to identify new candidate genes for the predisposition to an altered airway inflammatory response under OVA challenge conditions. Similar selection strategies may be used for the analysis of additional genotype-envirotype interactions for other diseases.	26263558	1000-09-01
11552700	Long non-coding RNA LINC00161 sensitises osteosarcoma cells to cisplatin-induced apoptosis by regulating the miR-645-IFIT2 axis.	Wang Y, etal., Cancer Lett. 2016 Sep 5;382(2):137-146. doi: 10.1016/j.canlet.2016.08.024.	Chemotherapeutic insensitivity remains a major obstacle to osteosarcoma treatment. Recently, increasing evidence has suggested that long non-coding RNAs (lncRNAs) play an essential role in tumourigenesis. However, the potential biological roles and regulatory mechanisms of novel lncRNAs in response ... (more) to cisplatin treatment are poorly understood. Here, we found that lncRNA LINC00161 was induced by cisplatin in osteosarcoma cells. Elevated LINC00161 increased cisplatin-induced apoptosis and reversed the cisplatin-resistant phenotype of osteosarcoma cells by upregulating IFIT2. Further mechanistic studies revealed that LINC00161 could sponge endogenous miR-645 and inhibit its activity leading to IFIT2 increase. In addition, we identified that LINC00161 enhanced cisplatin-induced apoptosis through regulation of the miR-645-IFIT2 pathway. Thus, these findings demonstrate that LINC00161 is an essential regulator in cisplatin-induced apoptosis, and the LINC00161-miR-645-IFIT2 signalling axis plays an important role in reducing osteosarcoma chemoresistance.	27609068	2016-10-01