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Characterizing a transcriptional control region within the Type I interferon gene cluster

表征 I 型干扰素基因簇内的转录控制区域

基本信息

批准号：
10624947
负责人：
Benjamin R. tenOever
金额：
$ 21.19万
依托单位：
NEW YORK UNIVERSITY SCHOOL OF MEDICINE
依托单位国家：
美国
项目类别：
财政年份：
2022
资助国家：
美国
起止时间：
2022-05-19 至 2024-04-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10624947
关键词：
Alveolar Autoimmunity Bacterial Infections Biological Biology CRISPR/Cas technology Cell Lineage Cells Chronic Clinical Clustered Regularly Interspaced Short Palindromic Repeats Conflict (Psychology)Dermal Disease Enabling Factors Ensure Epigenetic Process Epithelium Event Family Family member Fibroblasts Gene Cluster Genes Genetic Genetic Transcription Grant Homeostasis Human Immune Immune System Diseases Immunity Infection Inflammatory Innate Immune Response Interferon Suppression Interferon Type I Interferon alpha Interferon-beta Interferons Knock-out Measures Mediating Microbe Molecular Mus Phenocopy Phenotype Physiological Play Population Production Recording of previous events Regulation Repression Research Role Signal Transduction Site Somatic Cell System Transcription Repressor Transcriptional Regulation Vertebrate Biology Vertebrates Viral Viral Proteins Virus Virus Diseases adaptive immune response adaptive immunity autoimmune pathogenesis cell type combat cytokine gene conservation gene induction gene product gene repression genomic locus immunoregulation member microbiome novel pathogen prevent programs response transcriptome sequencing

项目摘要

PROJECT SUMMARY Type I interferons (IFN-I) provide the first line of defense against viruses and play a pivotal role in coordinating the innate and adaptive immune responses. The presence of infectious viruses triggers a cascade of events leading to the activation of IFN-I genes that further induce the expression of a large battery of antiviral proteins. This antiviral program is something that must be selectively induced only when appropriate as chronic signaling is associated with severe inflammatory phenotypes and autoimmunity. These so called ‘interferonopathies’ are a clinically heterogenic group of diseases that are becoming increasingly recognized and speak to the importance of silencing the IFN-I locus in the absence of infection. Here we propose to define how a conserved gene called Kelch-Like Family Member 9 (KLHL9), which is found in the center of the IFN-I gene cluster, ensures the transcriptional repression of the region in the absence of virus infection. This proposed research will advance the understanding of how the IFN system functions at the center of immune and inflammatory diseases, and should also lead to a better understanding as to the molecular cause of at least a subset of interferonopathies.

项目总结