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Cardiac transcriptome analysis of RKIP-transgenic and GRK2-transgenic mice by NGS

ABSTRACT: Cardiac transcriptome analysis of RKIP-transgenic and GRK2-transgenic mice by NGS

PROVIDER: PRJNA790970 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17281334.fastq.gz	Fastqsanger.gz
	SRR17281335.fastq.gz	Fastqsanger.gz
	SRR17281336.fastq.gz	Fastqsanger.gz
	SRR17281337.fastq.gz	Fastqsanger.gz
	SRR17281338.fastq.gz	Fastqsanger.gz

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Similar Datasets

Cardiac transcriptome analysis of RKIP-transgenic and GRK2-transgenic mice by NGS

Project description:The RAF kinase inhibitor protein, RKIP, is a dual inhibitor of the RAF1 kinase and the G-protein-coupled receptor kinase 2 (GRK2). By inhibition of the proto-oncogenic and pro-survival RAF1-MAPK pathway, the RAF kinase inhibitor protein, RKIP, acts as a tumor suppressor, which enhances cardiomyocyte death and promotes the development of symptoms of heart failure. To elucidate pathomechanisms of heart failure induced by RKIP, the study determined the cardiac transcriptomes of eight-month-old, male, transgenic mice with cardiac-specific expression of RKIP (PEBP1) under control of the myocardium-specific, alpha-MHC promoter. In addition, the study determined the cardiac transcriptomes of GRK2-transgenic mice. Tg-GRK2 mice have a slightly increased transgenic expression of GRK2. According to NGS data, cardiac GRK2-Grk2 transcript levels of Tg-GRK2 mice are 1.59±0.10-fold higher than those of non-transgenic FVB hearts. In Tg-GRK2 mice, transgenic GRK2 is expressed under control of the ubiquitous CMV immediate-early promoter/enhancer. The non-transgenic control group are age-matched, male, nontransgenic FVB/N mice. NGS data of this study document transcriptome changes underlying the heart failure phenotype induced by transgenic RKIP expression and cardiac degeneration induced by GRK2 expression.

2021-12-27 | GSE191316 | GEO

Whole genome cardiac gene expression profiling of transgenic mice with myocardium-specific expression of RKIP (PEBP1), kinase-inactive GRK2-K220R (ADRBK1-K220R), SCD1, and UCP1

Project description:The raf kinase inhibitor protein, RKIP, is up-regulated on cadiac biopsy specimens of heart failure patients. To investigate the in vivo role of an increased cardiac content of RKIP, we generated transgenic mice with myocardium-specific expression of RKIP (PEBP1; phosphatidylethanolamine binding protein 1) under control of the alpha-MHC promoter in B6 (C57BL/6J) background. Because RKIP is a dual-specific GRK2 and Raf kinase inhibitor, RKIP-transgenic mice were compared to transgenic mice with myocardium-specific expression of the GRK2 inhibitor, GRK2-K220R, which is a kinase-inactive GRK2 (ADRBK1) mutant with dominant-negative function. In frame of our studies, we found that RKIP-transgenic mice developed signs of heart failure and cardiotoxic lipid load at an age of 8 months. In contrast, transgenic expression of GRK2-K220R improved cardiac function and protected against chronic pressure overload-induced symptoms of heart failure. To identify genes related to cardiotoxic lipid load, we further determined the cardiac gene expression profile of Tg-SCD1 mice with mypcardium-specific expression of SCD1 (stearoyl-CoA desaturase-1) and Tg-UCP1 mice with heart-specific expression of UCP1 (uncoupling protein 1).

2018-09-18 | GSE120020 | GEO

Microarray gene expression profiling of transgenic mice with myocardium-specific expression of RKIP or a GRK-specific peptide inhibitor

Project description:The Raf kinase inhibitor protein (RKIP) is a dual inhibitor of the Raf kinase and the G-protein-coupled receptor kinase 2 (GRK2). GRK2 is an indispensable kinase, which exerts a major role in the pathogenesis of heart failure, and inhibition of GRK2 is cardioprotective in experimental models of heart failure. To investigate the cardiac function of RKIP as GRK2 inhibitor, we generated transgenic mice with myocardium-specific expression of RKIP under control of the alpha-MHC promoter. For comparison, mice with myocardium-specific expression of a GRK-specific peptide inhibitor (GRK-Inh) were also generated. Two different transgenic mouse models were established. Transgenic RKIP mice and transgenic GRK-Inh mice were born at Mendelian frequencey and grew to adulthood normally. Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) RKIP-transgenic mice, (ii) GRK-Inh-transgenic mice, and (iii) B6 control mice.

2012-12-06 | E-GEOD-42753 | biostudies-arrayexpress

Microarray gene expression profiling of transgenic mice with myocardium-specific expression of RKIP or a GRK-specific peptide inhibitor

2012-12-06 | GSE42753 | GEO

Cardiac transcriptome analysis of BBLN-transgenic mice by NGS

Project description:The study applied NGS to determine the cardiac transcriptomes of BBLN-transgenic mice with FVB/N background in comparison to those of non-transgenic FVB/N mice at an age of 8 months. The BBLN (Bublin coiled-coil protein) is the chromosome 9 open reading frame, C9orf16, with largely unknown function. To investigate the cardiac phenotype of increased cardiac BBLN transcript levels we generated BBLN-transgenic (Tg-BBLN) mice. Echocardiography documented that Tg-BBLN mice developed features of heart failure at an age of 8 months. To elucidate pathomechanisms of heart failure induced by BBLN, we performed NGS of the cardiac transcriptomes of eight-month-old, male, BBLN-transgenic mice with cardiac-specific expression of BBLN under control of the myocardium-specific, alpha-MHC promoter. The non-transgenic control group are age-matched, male, nontransgenic FVB/N mice. NGS data of this study document transcriptome changes underlying the heart failure phenotype induced by transgenic BBLN expression.

2023-09-18 | GSE241161 | GEO

Cardiac transcriptome analysis of BBLN-transgenic mice by NGS

Project description:Cardiac transcriptome analysis of BBLN-transgenic mice by NGS

| PRJNA1006663 | ENA

Cardiac transcriptome analysis of right and left ventricular heart specimens of BBLN-transgenic mice by NGS

Project description:The study performed NGS to investigate the cardiac transcriptomes of right and left ventricular heart specimens of 3-4-month-old BBLN-transgenic mice with FVB/N background in comparison to those of non-transgenic FVB/N mice. BBLN-transgenic (Tg-BBLN) mice with myocardium-specific BBLN expression were generated to investigate the cardiac phenotype of increased cardiac BBLN transcript levels because the function of BBLN (Bublin coiled-coil protein), which is the chromosome 9 open reading frame(C9orf16), is largely unknown. Tg-BBLN mice with increased cardiac BBLN levels developed features of heart failure with increasing age. Pathomechanisms of heart failure induced by BBLN were investigated by NGS of right and left ventricular heart specimens of male, BBLN-transgenic mice (age: 3-4 months). NGS data reveal transcriptome changes in right and left ventricular heart specimens induced by increased expression of BBLN in the heart.

2023-09-18 | GSE241022 | GEO

Whole genome cardiac gene expression profiling of transgenic mice with myocardium-specific expression of RKIP (PEBP1), kinase-inactive GRK2-K220R (ADRBK1-K220R), SCD1, and UCP1

Project description:Whole genome cardiac gene expression profiling of transgenic mice with myocardium-specific expression of RKIP (PEBP1), kinase-inactive GRK2-K220R (ADRBK1-K220R), SCD1, and UCP1

| PRJNA491406 | ENA

Cardiac transcriptome analysis of right and left ventricular heart specimens of BBLN-transgenic mice by NGS

Project description:Cardiac transcriptome analysis of right and left ventricular heart specimens of BBLN-transgenic mice by NGS

| PRJNA1006067 | ENA

MicroRNA expression array for 1833 cells expressing RKIP vs. control

Project description:RKIP has been implicated in suppression of breast tumor metastasis. Identification of microRNAs regulated by RKIP helps us to understand how RKIP suppresses tumor metastasis via its downstream target mircoRNAs and genes. Total RNA was extracted from 1833 cells expressing RKIP or control, respectively. Exiqon miRCURY LNA array v.11.0. was performed to identify the microRNAs regulated by RKIP.

2014-07-01 | E-GEOD-47366 | biostudies-arrayexpress

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