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

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

PROVIDER: PRJNA602493 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10919407_1.fastq.gz	Fastqsanger.gz
	SRR10919407_2.fastq.gz	Fastqsanger.gz
	SRR10919408_1.fastq.gz	Fastqsanger.gz
	SRR10919408_2.fastq.gz	Fastqsanger.gz
	SRR10919409_1.fastq.gz	Fastqsanger.gz

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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

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

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

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

| PRJNA602488 | ENA

WT and Hira-null undifferentiated mESCs and day15 differentiated cardiomyocytes

Project description:WT and Hira-null undifferentiated mESCs and day15 differentiated cardiomyocytes

| PRJNA438521 | ENA

QKI and miR-155 in inflammation and leukemogenesis

Project description:Transcription profiling by array of siRNA against Quaking (QKI) transcripts to identify transcripts that are modulated by QKI activity. MiR-155 is an oncogene and we report here that it targets QKI transcripts. Therefore, we believe that QKI acts as a tumor suppressor gene in different leukemias. We ablated the expression of QKI transcripts using siRNAs in order to further elucidate the effects of QKI in leukemogenesis, and how miR-155 and QKI functionally interact with each other.

2016-01-17 | E-MTAB-2375 | biostudies-arrayexpress

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

WT and Hira-null undifferentiated mESCs and day15 differentiated cardiomyocytes

Project description:Purpose: The goals of this study are to compare transcriptome profiling (RNA-seq) resulting from the knockout of Hira in undifferentiated mouse embryonic stem cells (mESCs) and in day 15 differentiated cardiomyocytes.Methods: RNA extraction was done in duplicate from WT and Hira-null mESCs at day0 and day15 using TRIzol reagent. RNAseq was done onIllumina Nextseq500 and processed by the ICH genomics facility, reads were aligned and normalised using BOWTIE and DEseq R2 package. Gene lists were filtered using adjusted p-value ≤ 0.05 and absolute fold change ≥ 2. Results:We identified 1680 transcripts changed in the absence of HIRA in day 15 differentiated cardiomyocytes. GO term cardiovascular system development was the most downregulated gene set(p-value ≤ 0.01 and FDR ≤0.1. Conclusion: this study analysis the role of HIRA in early cardiac mesoderm development usinf an invitro mESCs model.

2019-04-01 | GSE111910 | GEO

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

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.

2014-04-14 | GSE55215 | GEO

Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP: QKI data

Project description:To assess whether the transcripts identified by PAR-CLIP are regulated by the RNA-binding protein (RBP) Quaking (QKI), we analyzed the mRNA levels of mock-transfected and QKI-specific siRNA-transfected cells with microarrays. Transcripts crosslinked to QKI were significantly upregulated upon siRNA transfection, indicating that QKI negatively regulates bound mRNAs (Figure 3H of PMID 20371350), consistent with previous reports of QKI being a repressor. The RBP QKI was depleted by siRNAs and the expression level was compared to mock-transfected HEK 293 cells.

2010-05-27 | E-GEOD-21574 | biostudies-arrayexpress

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