Relevant bibliographies by topics / IFI207

Academic literature on the topic 'IFI207'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "IFI207"

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Cao, Yanhong, Lishi Wang, Cong-Yi Wang, Jicheng Ye, Ying Wang, Tiantian Li, Franklin Garcia-Godoy, Dianjun Sun, Weikuan Gu, and Arnold E. Postlethwaite. "Sex Differences in Correlation with Gene Expression Levels between Ifi200 Family Genes and Four Sets of Immune Disease-Relevant Genes." Journal of Immunology Research 2018 (August 28, 2018): 1–12. http://dx.doi.org/10.1155/2018/1290814.

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Background. The HIN-200 family genes in humans have been linked to several autoimmune diseases—particularly to systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Recently, its human counterpart gene cluster, the Ifi200 family in mice, has been linked to spontaneous arthritis disease (SAD). However, many immune-mediated diseases (including RA and SLE) show gender difference. Understanding whether or not and how these genes play a role in sex difference in immune-mediated diseases is essential for diagnosis/treatment. Methods. This study takes advantage of the whole genome gene expression profiles of recombinant inbred (RI) strain populations from female and male mice to analyze potential sex differences in a variety of genes in disease pathways. Expression levels and regulatory QTL of Ifi200 family genes between female and male mice were first examined in a large mouse population, including RI strains derived from C57BL/6J, DBA/2J (BXD), and classic inbred strains. Sex similarities and differences were then analyzed for correlations with gene expression levels between genes in the Ifi200 family and four selected gene sets: known immune Ifi200 pathway-related genes, lupus-relevant genes, osteoarthritis- (OA-) and RA-relevant genes, and sex hormone-related genes. Results. The expression level of Ifi202b showed the most sex difference in correlation with known immune-related genes (the P value for Ifi202b is 0.0004). Ifi202b also showed gender difference in correlation with selected sex hormone genes, with a P value of 0.0243. When comparing coexpression levels between Ifi200 genes and lupus-relevant genes, Ifi203 and Ifi205 showed significant sex difference (P values: 0.0303 and 0.002, resp.). Furthermore, several key genes (e.g., Csf1r, Ifnb1, IL-20, IL-22, IL-24, Jhdm1d, Csf1r, Ifnb1, IL-20, IL-22, IL-24, and Tgfb2 that regulate sex differences in immune diseases) were discovered. Conclusions. Different genes in the Ifi200 family play different roles in sex difference among dissimilar pathways of these four gene groups.
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Zhang, Ke, Daniel Kagan, Wendy DuBois, Richard Robinson, Valery Bliskovsky, William C. Vass, Shuling Zhang, and Beverly A. Mock. "Mndal, a new interferon-inducible family member, is highly polymorphic, suppresses cell growth, and may modify plasmacytoma susceptibility." Blood 114, no. 14 (October 1, 2009): 2952–60. http://dx.doi.org/10.1182/blood-2009-01-198812.

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The human HIN-200 gene cluster and its mouse counterpart, the interferon inducible-200 (Ifi200) family, both on Chr 1, are associated with several diseases, including solid tumors and lupus. Our study was initiated to identify the modifier gene(s) encoded by the Pctm locus, in which mouse B-cell plasmacytomas induced by pristane are associated with heterozygosity of Chr 1 genes near the Ifi200 cluster. A screen for differentially expressed genes in granulomatous tissues induced by pristane in resistant and susceptible strains identified a new Ifi200 member whose expression was 1000-fold higher in the strain carrying the resistant allele of Pctm and was the most highly expressed Ifi200 gene. The gene, designated Mndal (for MNDA-like, myeloid nuclear differentiation antigen-like), was absent in the susceptible genome, as were genomic sequences upstream of Ifi203, the gene adjacent to Mndal. Ectopic expression of MNDAL suppressed cell growth, which, together with the disease susceptibility of heterozygotes at the Pctm locus, suggests that Mndal, perhaps with Ifi203, acts as a tumor suppressor and display(s) haploinsufficiency. Mndal is highly polymorphic among inbred mouse strains, because it is absent in 10 of 24 strains. This polymorphism may have implications for other disease modifiers mapping to the same region.
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Wang, H., G. Chatterjee, J. J. Meyer, C.-J. Liu, N. A. Manjunath, P. Bray-Ward, and P. Lengyel. "Characteristics of Three Homologous 202 Genes (Ifi202a, Ifi202b, and Ifi202c) from the Murine Interferon-Activatable Gene 200 Cluster." Genomics 60, no. 3 (September 1999): 281–94. http://dx.doi.org/10.1006/geno.1999.5923.

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Ghosh, Sreya, Susan Carpenter, and Katherine Fitzgerald. "The PYHIN family member IFI205 regulates immune signaling via transcriptional regulation of the inflammasome adapter ASC (P1280)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 116.18. http://dx.doi.org/10.4049/jimmunol.190.supp.116.18.

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Abstract Members of the PYHIN protein family such as AIM2 and IFI16, function as DNA sensors in innate immunity. Here we investigated the role of Ifi205, a murine PYHIN family member in innate immunity by generating murine macrophages lacking Ifi205 and monitoring immune signaling in these cells. Macrophages lacking Ifi205 had abrogated caspase-1 dependent processing and production of the pro-inflammatory cytokine IL-1β in response to cytosolic double stranded DNA and Nigericin, that activate the AIM2 and NLRP3 inflammasomes, respectively. Surprisingly, expression of the inflammasome adapter ASC was completely abolished at both the protein and mRNA levels in all Ifi205 knockdown cells generated. Reconstitution of the knockdown cells with ASC rescued IL-1β production attributing the knockdown phenotype to the loss of ASC expression. We observed a similar defect in ASC expression in cell lines lacking Ifi205 by targeting the 3’-UTR of the ifi205 gene. Reconstitution of these cells with Ifi205 rescued ASC mRNA expression. We also found that ectopic expression of Ifi205 augmented the activation of an ASC promoter-luciferase reporter gene in a dose-dependent manner in HEK 293T cells. The data suggest that ASC expression might be controlled at the transcriptional level. Thus, Ifi205 regulates inflammasome activation by controlling transcriptional regulation of ASC.
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Li, Tuoyang, Junyi Zhou, Yingming Jiang, Yandong Zhao, Jintuan Huang, Weiyao Li, Zhenze Huang, et al. "The Novel Protein ADAMTS16 Promotes Gastric Carcinogenesis by Targeting IFI27 through the NF-κb Signaling Pathway." International Journal of Molecular Sciences 23, no. 19 (September 20, 2022): 11022. http://dx.doi.org/10.3390/ijms231911022.

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A disintegrin and metalloproteinase with thrombospondin motifs 16 (ADAMTS16) has been reported to be involved in the pathogenesis of solid cancers. However, its role in gastric cancer (GC) is unclear. In this study, the role of ADAMTS16 in gastric cancer was investigated. The effects of ADAMTS16 on cell migration, invasion, and proliferation were investigated by functional experiments in vivo and in vitro. Downstream signal pathways of ADAMTS16 were confirmed by using bioinformatics analysis, co-immunoprecipitation, and immunofluorescence. Meanwhile, bioinformatics analysis, qRT-PCR, western blot, and dual-luciferase reporter gene analysis assays were used to identify ADAMTS16 targets. The expression of ADAMTS16 in GC was analyzed in public datasets. The expression of ADAMTS16 and its correlations with the clinical characteristics of GC were investigated by immunohistochemistry. Ectopic ADAMTS16 expression significantly promoted tumor cell migration, invasion, and growth. Bioinformatics analysis and western blot showed that ADAMTS16 upregulated the IFI27 protein through the NF-κb pathway, which was confirmed by immunofluorescence and western blot. Dual-luciferase reporter gene analysis identified a binding site between P65 and IFI27 that may be directly involved in the transcriptional regulation of IFI27. IFI27 knockdown reversed the promoting effect of ADAMTS16 on cell invasion, migration, and proliferation indicating that ADAMTS16 acts on GC cells by targeting the NF-κb/IFI27 axis. ADAMTS16 was associated with poor prognosis in clinical characteristics. ADAMTS16 promotes cell migration, invasion, and proliferation by targeting IFI27 through the NF-κB pathway and is a potential progressive and survival biomarker of GC.
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Xu, Lin, Tingjian Zu, Tao Li, Min Li, Jun Mi, Fuxiang Bai, Guanyi Liu, et al. "ATF3 downmodulates its new targets IFI6 and IFI27 to suppress the growth and migration of tongue squamous cell carcinoma cells." PLOS Genetics 17, no. 2 (February 4, 2021): e1009283. http://dx.doi.org/10.1371/journal.pgen.1009283.

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Activating transcription factor 3 (ATF3) is a key transcription factor involved in regulating cellular stress responses, with different expression levels and functions in different tissues. ATF3 has also been shown to play crucial roles in regulating tumor development and progression, however its potential role in oral squamous cell carcinomas has not been fully explored. In this study, we examined biopsies of tongue squamous cell carcinomas (TSCCs) and found that the nuclear expression level of ATF3 correlated negatively with the differentiation status of TSCCs, which was validated by analysis of the ATGC database. By using gain- or loss- of function analyses of ATF3 in four different TSCC cell lines, we demonstrated that ATF3 negatively regulates the growth and migration of human TSCC cells in vitro. RNA-seq analysis identified two new downstream targets of ATF3, interferon alpha inducible proteins 6 (IFI6) and 27 (IFI27), which were upregulated in ATF3-deleted cells and were downregulated in ATF3-overexpressing cells. Chromatin immunoprecipitation assays showed that ATF3 binds the promoter regions of the IFI6 and IFI27 genes. Both IFI6 and IFI27 were highly expressed in TSCC biopsies and knockdown of either IFI6 or IFI27 in TSCC cells blocked the cell growth and migration induced by the deletion of ATF3. Conversely, overexpression of either IFI6 or IFI27 counteracted the inhibition of TSCC cell growth and migration induced by the overexpression of ATF3. Finally, an in vivo study in mice confirmed those in vitro findings. Our study suggests that ATF3 plays an anti-tumor function in TSCCs through the negative regulation of its downstream targets, IFI6 and IFI27.
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KIMOTO, OSAMU, JIN SAWADA, KUMIKO SHIMOYAMA, DAISUKE SUZUKI, SATOKI NAKAMURA, HIDEHARU HAYASHI, and NORIYOSHI OGAWA. "Activation of the Interferon Pathway in Peripheral Blood of Patients with Sjögren’s Syndrome." Journal of Rheumatology 38, no. 2 (November 15, 2010): 310–16. http://dx.doi.org/10.3899/jrheum.100486.

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Objective.DNA microarray analysis and quantitative real-time polymerase chain reaction (PCR) were performed to identify key target genes in peripheral blood from patients with Sjögren’s syndrome (SS).Methods.DNA microarray analysis was performed in 19 patients with SS (all women) and 10 healthy controls (5 men and 5 women) using a low-density DNA microarray system with 778 genes. For confirmation, the expression of upregulated genes was analyzed by quantitative real-time PCR in another 37 SS patients (35 women and 2 men) and 9 healthy controls (8 women and 1 man). Relationships between gene signatures and various clinical measures, such as disease duration, symptoms and signs, complications, immunological findings, and salivary and lacrimal functions, were analyzed.Results.Interferon-α (IFN-α)-inducible protein 27 (IFI27) showed the most significant difference between SS patients and controls in the microarray screening. We performed quantitative RT-PCR for IFI27. IFI27 gene expression level was increased in patients with SS compared with controls (p < 0.01) by real-time PCR, supporting our observations from the microarray data. The level of IFI27 was significantly correlated with serum IgG levels (r = 0.462, p < 0.01) and ß2-microglobulin (r = 0.385, p < 0.05), soluble interleukin 2 receptor (r = 0.473, p < 0.01), erythrocyte sedimentation rate (r = 0.333, p < 0.05), and antinuclear antibody titer (speckled pattern; r = 0.445, p < 0.01).Conclusion.Our results suggest that upregulation of IFN-inducible genes in SS patients is a systemic phenomenon, and IFN may play an important role in the pathogenesis of SS. The expression level of IFI27 could be an effective and specific biomarker associated with SS.
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Lei, Hongxing. "A two-gene marker for the two-tiered innate immune response in COVID-19 patients." PLOS ONE 18, no. 1 (January 17, 2023): e0280392. http://dx.doi.org/10.1371/journal.pone.0280392.

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For coronavirus disease 2019 (COVID-19), a pandemic disease characterized by strong immune dysregulation in severe patients, convenient and efficient monitoring of the host immune response is critical. Human hosts respond to viral and bacterial infections in different ways, the former is characterized by the activation of interferon stimulated genes (ISGs) such as IFI27, while the latter is characterized by the activation of anti-bacterial associated genes (ABGs) such as S100A12. This two-tiered innate immune response has not been examined in COVID-19. In this study, the activation patterns of this two-tiered innate immune response represented by IFI27 and S100A12 were explored based on 1421 samples from 17 transcriptome datasets derived from the blood of COVID-19 patients and relevant controls. It was found that IFI27 activation occurred in most of the symptomatic patients and displayed no correlation with disease severity, while S100A12 activation was more restricted to patients under severe and critical conditions with a stepwise activation pattern. In addition, most of the S100A12 activation was accompanied by IFI27 activation. Furthermore, the activation of IFI27 was most pronounced within the first week of symptom onset, but generally waned after 2–3 weeks. On the other hand, the activation of S100A12 displayed no apparent correlation with disease duration and could last for several months in certain patients. These features of the two-tiered innate immune response can further our understanding on the disease mechanism of COVID-19 and may have implications to the clinical triage. Development of a convenient two-gene protocol for the routine serial monitoring of this two-tiered immune response will be a valuable addition to the existing laboratory tests.
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Tang, Benjamin M., Maryam Shojaei, Grant P. Parnell, Stephen Huang, Marek Nalos, Sally Teoh, Kate O'Connor, et al. "A novel immune biomarker IFI27 discriminates between influenza and bacteria in patients with suspected respiratory infection." European Respiratory Journal 49, no. 6 (June 2017): 1602098. http://dx.doi.org/10.1183/13993003.02098-2016.

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Host response biomarkers can accurately distinguish between influenza and bacterial infection. However, published biomarkers require the measurement of many genes, thereby making it difficult to implement them in clinical practice. This study aims to identify a single-gene biomarker with a high diagnostic accuracy equivalent to multi-gene biomarkers.In this study, we combined an integrated genomic analysis of 1071 individuals with in vitro experiments using well-established infection models.We identified a single-gene biomarker, IFI27, which had a high prediction accuracy (91%) equivalent to that obtained by multi-gene biomarkers. In vitro studies showed that IFI27 was upregulated by TLR7 in plasmacytoid dendritic cells, antigen-presenting cells that responded to influenza virus rather than bacteria. In vivo studies confirmed that IFI27 was expressed in influenza patients but not in bacterial infection, as demonstrated in multiple patient cohorts (n=521). In a large prospective study (n=439) of patients presented with undifferentiated respiratory illness (aetiologies included viral, bacterial and non-infectious conditions), IFI27 displayed 88% diagnostic accuracy (AUC) and 90% specificity in discriminating between influenza and bacterial infections.IFI27 represents a significant step forward in overcoming a translational barrier in applying genomic assay in clinical setting; its implementation may improve the diagnosis and management of respiratory infection.
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Wieland, Karen, Andrew Woo, Thomas Akie, and Alan B. Cantor. "Increased Interferon-αa Signaling During Megakaryocyte Ontogeny: Implications for the Spontaneous Resolution of Down Syndrome Transient Myeloproliferative Disorder." Blood 114, no. 22 (November 20, 2009): 1272. http://dx.doi.org/10.1182/blood.v114.22.1272.1272.

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Abstract Abstract 1272 Poster Board I-294 About ten percent of infants with Down syndrome (DS) are born with a transient myeloproliferative disorder (DS-TMD), which spontaneously resolves within the first few months of life. However, the basis for this resolution remains unknown. Acquired mutations leading to exclusive production of a short isoform of the transcription factor GATA-1 (GATA-1s) occur in all cases of DS-TMD, and knock-in mice that exclusively produce GATA-1s have hyperproliferation of megakaryocytes during early fetal liver hematopoiesis, but not during later developmental stages. In this study, we found striking upregulation of the interferon-αa (IFN-αa) receptor and multiple IFN-αa responsive genes, including Ifi203, Ifi205, Irf-1, Irf-8, and Ifitm6, in immunophenotypically isolated megakaryocyte progenitor cells (MkPs) from bone marrow versus embryonic day 13.5 (e13.5) fetal liver of wild type mice. These differences were confirmed at the protein level in megakaryocytes by in situ immunohistochemistry. Addition of IFN-αa to GATA-1s containing e13.5 fetal liver MkPs reduces their hyperproliferation in vitro in a dose-dependent manner. Conversely, injection of neutralizing IFN-αa/β antibodies, but not control IgG, into adult GATA-1s mice markedly increases the percentage of bone marrow CD41+ cells and morphologically recognizable megakaryocytes, in contrast to wild type mice. We propose that increases in IFN-αa signaling during megakaryocyte ontogeny may account for the developmental stage-specific effects of GATA-1s on megakaryocyte hyperproliferation, and possibly the spontaneous resolution of DS-TMD. Interestingly, the genes encoding the IFN-αa/β receptor are located on human chromosome 21 and are expressed at 1.6 times that in trisomy versus disomy 21 cells. We speculate that increased interferon alpha signaling during embryogenesis may be the basis for the strong selective pressure for GATA-1s producing mutations in trisomy 21 fetuses in the first place. Disclosures No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "IFI207"

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Hertrich, Anna Carola [Verfasser]. "Untersuchung zur Regulation der Interferonexpression durch das murine Interferon-induzierbare Protein IFI203 / Anna Carola Hertrich." Bonn : Universitäts- und Landesbibliothek Bonn, 2019. http://d-nb.info/1188906526/34.

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Sim, Helena Y. (Helena Yin Yee) 1973. "A study of human interferon-induced IFI60 protein and STAT1 gene regulation." Monash University, Dept. of Biochemistry and Molecular Biology, 2002. http://arrow.monash.edu.au/hdl/1959.1/8448.

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Hsieh, Wan Ling, and 謝宛伶. "Regulation of EGF-activated CDC25B and IFI27 in epidermal keratinocytes and the potential to be an anti-psoriatic target." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/55030790130712837846.

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Book chapters on the topic "IFI207"

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Appleton, Kathryn M., Ian Cushman, Yuri K. Peterson, Balachandran Manavalan, Shaherin Basith, Sangdun Choi, Akihiro Kimura, et al. "IFI10." In Encyclopedia of Signaling Molecules, 891. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100636.

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"IFI10." In Encyclopedia of Signaling Molecules, 2511. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101801.

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"IFI30." In Encyclopedia of Signaling Molecules, 2511. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_105278.

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Bilger, Andrea, Elizabeth Poli, Andrew Schneider, Rebecca Baus, and Norman Drinkwater. "The Hcs7 Mouse Liver Cancer Modifier Maps to a 3.3 Mb Region Carrying the Strong Candidate Ifi202b." In Liver Tumors. InTech, 2012. http://dx.doi.org/10.5772/32529.

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Conference papers on the topic "IFI207"

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Zimmerman, Mary A., and Kebin Liu. "Abstract LB-207: IFN-Γ directly regulates ifi202B expression to maintain CTL proliferation potential and tumor rejection efficacy." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-207.

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