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Genome wide gene-expression and mRNA splicing profile in human cardiomyocytes differentiated from Wt and QKI mutant embryonic stem cells

ABSTRACT: Genome wide gene-expression and mRNA splicing profile in human cardiomyocytes differentiated from Wt and QKI mutant embryonic stem cells

PROVIDER: PRJNA602488 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10919400_1.fastq.gz	Fastqsanger.gz
	SRR10919400_2.fastq.gz	Fastqsanger.gz
	SRR10919401_1.fastq.gz	Fastqsanger.gz
	SRR10919401_2.fastq.gz	Fastqsanger.gz
	SRR10919402_1.fastq.gz	Fastqsanger.gz

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Genome wide gene-expression and mRNA splicing profile in human cardiomyocytes differentiated from Wt and QKI mutant embryonic stem cells

Project description:We sequenced mRNA from cardiomyocytes derived from hESCS in vitro. By using the Cas9n, we generated the QKI null hESCs. The gene expression level and alternative splicing events were compared between 4 control and 4 QkI KO samples. Here, we applied a widely used cardiomyocyte differentiation protocol that was reported to produce a population of more than 90% cardiac troponin T (TNNT2)-positive cardiomyocytes. And we are able to demonstrate that QKI is indespensible to cardiac sarcomerogenesis and cardiac function through its regulation of alternative splicing in genes involved in Z-disc formation, such as ACTN2, NEBL, ABLIM1, and PDLIM5.

2020-10-19 | GSE144008 | GEO

Genomewide analysis of QKI-dependent alternative splicing

Project description:To identify QKI targets, we performed QKI knockdown in BEAS2B cells and analyzed alternative splicing patterns by high-throughput RNA sequencing. The mRNA profiles of control- and QKI-knockdown BEAS2B cells were generated by deep sequencing using Illumina GAIIx sequencer.

2014-04-14 | E-GEOD-55215 | biostudies-arrayexpress

Single-Cell sequence profile in human cardiomyocytes differentiated from Wt and QKI mutant embryonic stem cells

Project description:Single-Cell sequence profile in human cardiomyocytes differentiated from Wt and QKI mutant embryonic stem cells

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Single-Cell sequence profile in human cardiomyocytes differentiated from Wt and QKI mutant embryonic stem cells

Project description:Transcriptomic profiling of WT and QKI KO hESC derived cardiomyocyte on Day 6 and 15 via Single cell RNA-seq.

2020-10-19 | GSE144009 | GEO

Genomewide analysis of QKI-dependent alternative splicing

Project description:To identify QKI targets, we performed QKI knockdown in BEAS2B cells and analyzed alternative splicing patterns by high-throughput RNA sequencing.

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QKI regulated splicing required for cell polarity

Project description:QKI regulated splicing required for cell polarity

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Analysis of gene expression in QKI knockdown CG-4 cells

Project description:QKI is required for myelin formation in the verterbrate brain. It functions by binding RNA and regulating its stability, translation, and/or aternative splicing. We have used Affymetrix exon arrays to assess changes in gene expression in response to QKI knockdown on an exon level in rat CG-4 oligodendrocyte precursor cells. Knockdown cells were compared to control cells. Knockdown groups included QKI siRNA transfection, QKI shRNA stable transfection, and hnRNP A1 transient transfection. Control groups consisted of untransfected, control siRNA transfection, control shRNA stable transfection. Each group was analyzed in triplicate.

2011-01-20 | E-GEOD-26716 | biostudies-arrayexpress

QKI regulated splicing required for cell polarity

Project description:the RNA binding protein QKI is a post-transcriptional regulator of polarity proteins in muscle stem cells

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WT and Hira-null undifferentiated mESCs and day15 differentiated cardiomyocytes

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The RNA binding protein QKI guides a pro-mesenchymal splicing program driving a subtype switch and limiting outcome in pancreatic cancer [PANC-1 and HPAF-II]

Project description:Transcriptomic analyses have identified two molecular PDAC subtypes, one of which, namely basal-like subtype, is associated with chemoresistance and worse clinical outcomes. Splicing dysregulation is known to contribute to PDAC malignancy. Functional studies in PDAC cells lines identified the splicing factor QKI as a key determinant of a basal-like splicing signature associated with increased tumor aggressiveness. Our studies demonstrate that QKI represses splicing events associated with the classical subtype and improved clinical outcome, while promoting basal-like events associated with shorter survival.

2024-02-05 | GSE234737 | GEO

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