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Effect of CLK2 overexpression on alternative splicing

ABSTRACT: Effect of CLK2 overexpression on alternative splicing

PROVIDER: PRJNA946311 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23908407_1.fastq.gz	Fastqsanger.gz
	SRR23908407_2.fastq.gz	Fastqsanger.gz
	SRR23908408_1.fastq.gz	Fastqsanger.gz
	SRR23908408_2.fastq.gz	Fastqsanger.gz
	SRR23908409_1.fastq.gz	Fastqsanger.gz

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Effect of CLK2 overexpression on alternative splicing

Project description:To investigate the function CLK2 in the regulation of alternative splicing, we established HeLa cells overexpressing GFP, CLK2 (WT), or (T343A). We then performed alternative splicing analysis using data obtained from RNA-seq of the three cell lines.

2023-11-09 | GSE227673 | GEO

Effect of CLK2 expression in the regulation of intron retention during heat shock [RNA-seq]

Project description:Intron retention (IR) constitutes a less explored form of alternative splicing, wherein introns are retained within mature mRNA transcripts. Our investigation demonstrates that the CDC-like kinase 2 (CLK2) undergoes liquid-liquid phase separation (LLPS) within nuclear speckles in response to heat shock (HS). The formation of CLK2 condensates depends on the intrinsically disordered region (IDR) located within the N-terminal amino acids 1-148. Phosphorylation at residue T343 sustains CLK2 kinase activity and facilitates autophosphorylation, thus inhibiting the LLPS activity of the IDR. These CLK2 condensates initiate the reorganization of nuclear speckles, transforming them into larger, rounded structures. Moreover, these condensates facilitate the recruitment of splicing factors into these compartments, potentially restricting their access to mRNA for intron splicing. Consequently, the formation of CLK2 condensates promotes the IR.

2024-07-15 | GSE271918 | GEO

Effect of CLK2 expression in the regulation of intron retention during heat shock

Project description:We established the HeLa cells expressing the GFP (control) or CLK2 (WT) and subjected them to heat shock. These cells were subjected to RNA-seq for the alternative splicing analysis.

2023-11-09 | GSE247417 | GEO

Effect of the intrinsically disordered region (IDR) within the CLK2 (T343A) mutant in the regulation of intron retention

Project description:We established the HeLa cells expressing the GFP (control) or CLK2 (T343A) with deletion of the IDR [T343A (dIDR)]. These cells were subjected to RNA-seq for the alternative splicing analysis.

2023-11-09 | GSE247419 | GEO

Proteins that interact with CLK2 (WT) or CLK2 (T343A)

Project description:Our results show that CLK2 undergoes liquid-liquid phase separation (LLPS) in response to heat shock stress. Phosphorylation of CLK2 at T343 prevents the LLPS of CLK2. To identify the proteins that recruited to the CLK2 condensates, we immunoprecipitated CLK2 (WT) or (T343A) proteins with FLAG antibody and performed mass spectrometry to detect the interacting proteins.

2023-11-06 | PXD040997 | Pride

The effect of progerin expression on alternative splicing in keratinocytes of HGPS mice

Project description:Exon level expression analysis for the HGPS pathological aging study data set to analyze the effect of progerin expression on alternative splicing in keratinocytes of HGPS mice. Analysis of the effect of pathological aging (transgenic progerin expression) on alternative splicing (AS) using exon microarrays to interrogate the differential exon usage of the entire genome of HGPS mice (postnatal day 24 and 35) and their wild-type litter mates. Our results suggests that early expression of progerin impairs developmental splicing but that as progerin accumulates, the number of genes with AS increases, similar to what is observed in aging wild-type mice. This dataset is one of the 2 datasets in the overall study. An additional data set series is available with exon expression analysis of aging wild-type mice to analyze the effect of age on alternative splicing during physiological aging. The two datasets are linked together in the SuperSeries GSE67289. A link to the SuperSeries is available at the bottom of this page. 16 skin keratinocyte samples from 2 different age groups: postnatal day 24 and postnatal day 35, from 8 HGPS samples and 8 genotype negative (wild-type) littermates.

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Overexpression of splicing factor SRSF6 in mouse skin

Project description:Many biological processes involve post-transcriptional regulation of gene expression by alternative pre-mRNA splicing. Here, we show that an alternative splicing factor SRSF6 affects tissue homeostasis of the skin. In this dataset, we study effects on gene expression and alternative splicing upon SRSF6 overexpression (+doxycycline) in mouse skin using inducible R26-rtTA+/-, ColA1-TREtight-SRSF6+/- transgenic mice 4 mixed-background strain samples (2 SRSF6-induced skin samples and 2 uninduced skin control samples)

2014-01-19 | E-GEOD-52458 | biostudies-arrayexpress

The effect of progerin expression on alternative splicing in keratinocytes of HGPS mice

2015-11-01 | GSE67288 | GEO

Overexpression of splicing factor SRSF6 in mouse skin

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Aurora-A phosphorylates splicing factors and regulates alternative splicing

Project description:The goal of this study is to identify the effect of inhibition of Aurora-A kinase activity on gene expression and RNA splicing. The perturbation of Aurora-A is well known to affect cell cycle distribution. Therefore, we coupled the inhibition of Aurora-A with cell synchronization procedure in order to avoid the indirect effect of cell cycle perturbation on splicing changes. The mRNA -seq libraries were prepared and subjected to paired-end sequencing on Illumina HiSeq 2500 lanes. Differential gene expression and splicing analysis were carried using the edgeR tool and VAST-tools respectively. The RNA seq analysis identified that pharmacological inhibition of Aurora-A affects alternative splicing of 505 genes while having a marginal effect on gene expression. Overall our work identified Aurora-A as a novel splicing kinase and for the first time, describes a broad role of Aurora-A in regulating alternative splicing.

2024-11-21 | GSE160733 | GEO

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