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LncRNA CHROME regulates the interferon response to viral challenge [COVID]

ABSTRACT: Long non-coding RNAs (lncRNAs) are important regulators of the immune response. Here we identify a novel function for the primate-specific lncRNA, CHROME. We established that CHROME is most highly transcribed in human macrophages treated with influenza virus and/or polyIC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE191238 | GEO | 2022/08/23

REPOSITORIES: GEO

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LncRNA CHROME regulates the interferon response to viral challenge [RNA-Seq]

Project description:Long non-coding RNAs (lncRNAs) are important regulators of the immune response. Here we identify a novel function for the primate-specific lncRNA, CHROME. We established that CHROME is most highly transcribed in human macrophages treated with influenza virus and/or polyIC.

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Project description:Long non-coding RNAs (lncRNAs) are important regulators of the immune response. Here we identify a novel function for the primate-specific lncRNA, CHROMR. We established that CHROME is most highly transcribed in human macrophages treated with influenza virus and/or polyIC.

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LncRNA CHROME regulates the interferon response to viral challenge

Project description:This SuperSeries is composed of the SubSeries listed below.

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Expression analysis of genes modulated after knock-down of lncRNA CHROME.

Project description:Thousands of long non-coding RNAs (lncRNAs) have been identified in the human genome, many of which are not conserved in lower mammals. The majority of these lncRNAs remain functionally uncharacterized and may have important implications in human physiology and disease. Here, we identify a primate-specific lncRNA, CHROME, which is increased in the plasma and atherosclerotic plaques of individuals with coronary artery disease compared to healthy controls. Using a loss-of-function approach, we show that CHROME functions as a competing endogenous RNA of microRNAs and regulates the concentration and biological functions of target genes.

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2017-07-31 | GSE101760 | GEO

Dynamic responses of primary human bronchial epithelial cells to influenza virus, viral RNA and interferon-beta

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Macrophages control pathological interferon responses during viral respiratory infection

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