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The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans

ABSTRACT: The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans

PROVIDER: PRJNA607243 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11100814_1.fastq.gz	Fastqsanger.gz
	SRR11100814_2.fastq.gz	Fastqsanger.gz
	SRR11100815_1.fastq.gz	Fastqsanger.gz
	SRR11100815_2.fastq.gz	Fastqsanger.gz
	SRR11100816_1.fastq.gz	Fastqsanger.gz

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The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans (LPS dataset)

Project description:The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans (LPS dataset)

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The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans (IAV and HSV dataset)

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The long non-coding RNA LUCAT1 is a negative feedback regulator of interferon responses in humans.

Project description:Long non-coding RNAs are important regulators of biological processes including immune responses. The immunoregulatory functions of lncRNAs have been revealed primarily in murine models with limited understanding of lncRNAs in human immune responses. Here, we identify lncRNA LUCAT1 which is upregulated in human myeloid cells stimulated with lipopolysaccharide and other innate immune stimuli. Targeted deletion of LUCAT1 in myeloid cells increases expression of type I interferon stimulated genes in response to LPS. By contrast, increased LUCAT1 expression results in a reduction of the inducible ISG response. In activated cells, LUCAT1 is enriched in the nucleus where it associates with chromatin. Further, LUCAT1 limits transcription of interferon stimulated genes by interacting with STAT1 in the nucleus. Together, our study highlights the role of the lncRNA LUCAT1 as a post-induction feedback regulator which functions to restrain the immune response in human cells.

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The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans (LPS dataset)

Project description:Long non-coding RNAs (lncRNAs) are important regulators of biological processes including immune responses. In the immune system, the immunoregulatory functions of lncRNAs have been revealed in murine studies with limited understanding of lncRNAs and the immune response in humans. Here, we identified lncRNA LUCAT1 as amongst the most dynamically regulated non-coding transcripts in human myeloid cells stimulated with lipopolysaccharide (LPS) and other activators of the innate immune response.

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The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans (IAV and HSV dataset)

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The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans

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The Cul5 E3 Ligase Complex Is a Key Negative Feedback Regulator of TCR/IL2 Signaling and Anti-Tumor Activity in CD8+ T Cells

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Project description:The RIG-I-like receptors (RLRs) form filaments to activate type-I interferon (IFN-I) and NF-KB signaling through their adaptor protein MAVS and downstream cascades. These filaments are recognized and regulated by cell-encoded machinery for correct activation. Here, we identified the stress-sensitive heat shock protein, HSPA6, was induced to express upon RLR-MAVS activation to act as a negative regulator of IFN-I signaling. Interestingly, by using MAVS-KO cells, we showed that HSPA6 was upregulated dependent on the presence of IFN-competent RLRs but not MAVS. Gene knockout (KO) tests indicated that the E3 ligases, stress granules (SGs), and transcription factors IRF1 and AP1 were all shared to induce HSPA6 and the canonical IFNb. Kinetic analysis showed that HSPA6 upregulated slower than IFNb, implicating these two genes competed machinery for transcription activation. Further tests suggested the induced HSPA6 bound to IFN-competent MDA5 to dissolve the filaments and downregulated IFN induction. Thus, our study uncovered a new gene activation mechanism by the IFN-competent RLRs to serve as negative feedback, arguing for a gene regulatory role of functional filaments of innate immunity.

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