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Inflammation drives alternative first exon usage of critical immune genes including Aim2 [nanopore]

ABSTRACT: Inflammation drives alternative first exon usage of critical immune genes including Aim2 [nanopore]

PROVIDER: PRJNA594614 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10620239_1.fastq.gz	Fastqsanger.gz
	SRR10620240_1.fastq.gz	Fastqsanger.gz
	SRR10620241_1.fastq.gz	Fastqsanger.gz
	SRR10620242_1.fastq.gz	Fastqsanger.gz
	SRR10620243_1.fastq.gz	Fastqsanger.gz

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Inflammation drives alternative first exon usage of critical immune genes including Aim2

Project description:Inflammation drives alternative first exon usage of critical immune genes including Aim2

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Inflammation drives alternative first exon usage of critical immune genes including Aim2 [RNA-seq]

Project description:Inflammation drives alternative first exon usage of critical immune genes including Aim2 [RNA-seq]

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Inflammation drives alternative first exon usage of critical immune genes including Aim2 [nanopore]

Project description:Macrophage cells are essential components of the innate immune system and contain toll-like receptors (TLRs) that intiate the immune response when pathogen-associated molecular pattern molecules (PAMPs) are recognized. In this experiment, we stimulate TLR4 in bone marrow-derived macrophage cells with lipopolysaccharide (LPS) for 6 hours to simmulate inflammation and study the resulting differential splicing landscape and gene expression.

2021-06-02 | GSE141750 | GEO

Inflammation drives alternative first exon usage of critical immune genes including Aim2

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

2021-06-01 | GSE141754 | GEO

Inflammation drives alternative first exon usage of critical immune genes including Aim2 [RNA-seq]

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Neuronal activity regulates alternative exon usage

Project description:Neuronal activity regulates alternative exon usage

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Inflammation drives alternative first exon usage to regulate immune genes including a novel iron-regulated isoform of Aim2.

Project description:Determining the layers of gene regulation within the innate immune response is critical to our understanding of the cellular responses to infection and dysregulation in disease. We identified a conserved mechanism of gene regulation in human and mouse via changes in alternative first exon (AFE) usage following inflammation, resulting in changes to the isoforms produced. Of these AFE events, we identified 95 unannotated transcription start sites in mice using a de novo transcriptome generated by long-read native RNA-sequencing, one of which is in the cytosolic receptor for dsDNA and known inflammatory inducible gene, Aim2. We show that this unannotated AFE isoform of Aim2 is the predominant isoform expressed during inflammation and contains an iron-responsive element in its 5'UTR enabling mRNA translation to be regulated by iron levels. This work highlights the importance of examining alternative isoform changes and translational regulation in the innate immune response and uncovers novel regulatory mechanisms of Aim2.

| S-EPMC8260223 | biostudies-literature

KIS counteracts PTBP2 and regulates alternative exon usage in neurons

Project description:Alternative RNA splicing is an essential and dynamic process in neuronal differentiation and synapse maturation, and dysregulation of this process has been associated with neurodegenerative diseases. Recent studies have revealed the importance of RNA-binding proteins in the regulation of neuronal splicing programs. However, the molecular mechanisms involved in the control of these splicing regulators are still unclear. Here we show that KIS, a kinase upregulated in the developmental brain, imposes a genome-wide alteration in exon usage during neuronal differentiation. KIS contains a protein-recognition domain common to spliceosomal components and phosphorylates PTBP2, counteracting the role of this splicing factor in exon exclusion. At the molecular level, phosphorylation of unstructured domains within PTBP2 causes its dissociation from two co-regulators, Matrin3 and hnRNPM, and hinders the RNA-binding capability of the complex. Furthermore, KIS and PTBP2 display strong and opposing functional interactions in synaptic spine emergence and maturation. Taken together, our data uncover a post-translational control of splicing regulators that link transcriptional and alternative exon usage programs in neuronal development.

2024-04-25 | PXD050320 | Pride

AIM2-responsive genes in colorectal tumor cells

Project description:Absent in Melanoma 2 (AIM2) is a member of the HIN-200 family of hematopoietic, IFN-inducible nuclear proteins associated with infection defense and tumor pathology. Recently, AIM2 was found to act as a DNA sensor in innate immunity. In addition, a high frequency of AIM2-alterations was observed in microsatellite unstable tumors. To elucidate AIM2 function in colorectal tumors, we here addressed AIM2-responsive genes by microarray. Among genes up-regulated by AIM2, there were a number of interferon-stimulated genes (ISGs: IFIT1, IFIT2, IFIT3, IFI6, IRF7, ISG15, HLA-DRA, HLA-DRB, TLR3 and CIITA) as well as genes involved in intercellular adhesion and matrix remodeling. Expression of ISGs correlated with expression of AIM2 in ten different IFN-γ treated colorectal cancer cell lines. Moreover, knock-down of AIM2 resulted in reduced expression of HLA-DRA, HLA-DRB, and CIITA in IFN-γ treated cells. IFN-γ independent induction of HLA-DR genes and their encoded proteins was also demonstrated upon transient induction of AIM2. STAT-signaling was not involved in IFN-γ independent induction of ISGs, arguing against participation of cytokines released in an autocrine manner. Our data indicate that AIM2 mediates IFN-γ dependent and independent induction of several Interferon stimulated genes (ISGs) including genes encoding the MHC II antigens HLA-DRα and β. we used microarray techniques to define genes responsive to AIM2 expression in colorectal tumor cells. HCT116 is a colorectal tumour cell line with no evidence for AIM2 expression which served as background for gene transfection. B8 and D1 were transfected subclones with persisting expression of AIM2. Gene expression of B8 and D1 was compared with that of mock transfected control cells.

2012-12-13 | E-GEOD-24155 | biostudies-arrayexpress

AIM2-responsive genes in colorectal tumor cells

2012-12-13 | GSE24155 | GEO