Transformants NGS
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB12451 | ENA |
REPOSITORIES: ENA
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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.
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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.
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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.
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