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Manipulation of NR3C1 on the expression of inflammatory transcription factors and their alternative splicing patterns

ABSTRACT: Manipulation of NR3C1 on the expression of inflammatory transcription factors and their alternative splicing patterns

PROVIDER: PRJNA783789 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17043013_1.fastq.gz	Fastqsanger.gz
	SRR17043013_2.fastq.gz	Fastqsanger.gz
	SRR17043014_1.fastq.gz	Fastqsanger.gz
	SRR17043014_2.fastq.gz	Fastqsanger.gz
	SRR17043015_1.fastq.gz	Fastqsanger.gz

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Manipulation of NR3C1 on the expression of inflammatory transcription factors and their alternative splicing patterns

Project description:NR3C1-encoding glucocorticoid receptors have dual roles as RNA-binding protein and transcription factor. Recent studies revealed that NR3C1 might play an important role in the pathogenesis of PTSD (Post-traumatic stress disorder). However, its molecular mechanism remained unclear. In the present study, a neuronal cell model was constructed by transfecting a NR3C1-overexpressing plasmid pIRES-hrGFP-1a-NR3C1 or empty vector into HT22 cells. The changes in global transcription levels and alternative splicing events in HT22 cells after NR3C1 overexpression were analyzed by RNA sequencing. Compared with the empty vector control, the expression of inflammatory factors were differentially regulated by NR3C1, including genes involved in chemokine signal pathway, PI3K-Akt signal pathway, cytokine receptor interaction, neural ligand-receptor interaction and so on. In addition, NR3C1 regulated the alternative splicing of many genes involved in immune response, axon formation, stress response and inflammation. This study was the first to perform a transcriptome analysis of differential gene expression and alternative splicing in a NR3C1-overexpressing HT22 cell model. Our results suggested that NR3C1 could manipulate the expression of inflammatory transcription factors and their alternative splicing patterns, subsequently affecting the expression of downstream targets, leading to the onset of PTSD. This study will provide new insights in the NR3C1-mediated gene regulation in relation to PTSD.

2024-11-26 | GSE189587 | GEO

Lifestyle-induced changes in alternative splicing patterns in mice

Project description:Lifestyle-induced changes in alternative splicing patterns in mice

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Lifestyle-induced changes in alternative splicing patterns in mice [adipose]

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MBNL1 regulates essential alternative RNA splicing patterns in MLL-rearranged leukemia

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Lifestyle-induced changes in alternative splicing patterns in mice [skeletal muscle]

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PRMT5 and CDK4/6 inhibition result in distinctive patterns of alternative splicing

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p38 SAPK and SKIIP induced changes in alternative splicing patterns upon osmostress

Project description:p38 SAPK and SKIIP induced changes in alternative splicing patterns upon osmostress

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Aurora-A phosphorylates splicing factors and regulates alternative splicing

Project description:Aurora-A phosphorylates splicing factors and regulates alternative splicing

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The Impact of Pro-Inflammatory Cytokines on Alternative Splicing Patterns in Human Islets

Project description:The Impact of Pro-Inflammatory Cytokines on Alternative Splicing Patterns in Human Islets

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The Glycogen Synthase Kinase-3 Phosphoproteome: GSK-3 Phosphorylates Multiple Splicing Factors and Regulates Alternative Splicing

Project description:Glycogen Synthase Kinase-3 (GSK-3) is a constitutively active, ubiquitously expressed protein kinase that regulates multiple signaling pathways. Over 100 putative GSK-3 substrates have been reported in diverse cell types based on in vitro kinase assays or genetic and pharmacological manipulation of GSK-3. Many more have been predicted based on a recurrent GSK-3 consensus motif, but this prediction has not been tested by analyzing the GSK-3 phosphoproteome. We used stable isotope labeling of amino acids in culture (SILAC) and mass spectrometry to analyze the repertoire of GSK-3 dependent substrates in mouse embryonic stem cells (ESCs). A comparison of wild-type and Gsk3a;Gsk3b knockout (DKO) ESCs revealed prominent GSK-3-dependent phosphorylation of multiple splicing factors and regulators of RNA biosynthesis, as well as proteins that regulate transcription, translation, and cell division. We demonstrate direct, GSK-3-dependent phosphorylation of the splicing factors RBM8A and PSF as well as the nucleolar protein NPM1. RNA sequencing to compare the transcriptomes of wild-type and Gsk3 DKO ESCs identified more than 210 genes that are alternatively spliced in a GSK-3-dependent manner, supporting a broad role for GSK-3 in regulating alternative splicing. Overall, this study provides the first unbiased analysis of the GSK-3 phosphoproteome and strong evidence for GSK-3 as a regulator of alternative splicing.

2017-08-24 | GSE90921 | GEO

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