Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: RNA-seq from heart ventricular tissues of cardiomyocyte-specific NAMPT knockout mice

PROVIDER: PRJNA1141531 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30026237_1.fastq.gz	Fastqsanger.gz
	SRR30026237_2.fastq.gz	Fastqsanger.gz
	SRR30026238_1.fastq.gz	Fastqsanger.gz
	SRR30026238_2.fastq.gz	Fastqsanger.gz
	SRR30026239_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

GNPS - Cardiomyocyte-specific NAMPT Knockout Mice: Untargeted Metabolomics from Heart Ventricle Tissues (dataset1)

Project description:Untargeted metabolomics from heart ventricular tissues of wild-type (WT) and cardiomyocyte-specific conditional NAMPT knockout (KO) mice, harvested at 8-weeks post-NAMPT deletion. Mass spectrometer was operated in both negative (NEG, 70 to 1000 m/z) and positive (POS, 50 to 117.9 m/z) ion mode with the HILIC 25-minute method for the detection of metabolites.

2024-08-06 | MSV000095529 | GNPS

GNPS - Cardiomyocyte-specific NAMPT Knockout Mice: Untargeted Metabolomics from Heart Ventricle Tissues (dataset2)

Project description:Untargeted metabolomics from heart ventricular tissues of wild-type (WT) and cardiomyocyte-specific conditional NAMPT knockout (cNKO) mice untreated or treated with nicotinamide riboside (cNKO-NR), harvested at 8-weeks post-NAMPT deletion. Mass spectrometer was operated in both negative (NEG, 70 to 1000 m/z) and positive (POS, 50 to 117.9 m/z) ion mode with the HILIC 25-minute method for the detection of metabolites.

2024-07-02 | MSV000095223 | GNPS

GNPS - Cardiomyocyte-specific NAMPT Knockout Mice: Targeted Metabolomics for NAD Derivatives from Heart Ventricle Tissues

Project description:Targeted metabolomics for NAD-related metabolites from heart ventricular tissues of wild-type (WT) and cardiomyocyte-specific conditional NAMPT (cNKO) mice untreated or treated with nicotinamide riboside (cNKO-NR), harvested at 8-weeks post-NAMPT deletion. Mass spectrometer was operated in two positive-mode scans (SCAN1 at 118.5 to 800 m/z and SCAN2 at 70 to 117.5 m/z) with the HILIC 20-minute method for the detection of NAD derivatives.

2024-07-03 | MSV000095229 | GNPS

PKN2 deficiency leads both to prenatal ‘congenital’ cardiomyopathy and defective angiotensin II stress responses

Project description:Background: The protein kinase PKN2 is required for embryonic development, and PKN2 knockout mice die as a result of failure in expansion of mesoderm tissues, cardiac development and neural tube closure. In the adult, cardiomyocyte PKN2 and PKN1 (in combination) are required for cardiac adaptation to pressure-overload. The role of PKN2 in contractile cardiomyocytes during development and its role in the adult heart remain to be fully established. Methods: We used mice with cardiomyocyte-directed knockout of PKN2 or global PKN2 haploinsufficiency. Cardiac function and dimensions were assessed with high resolution episcopic microscopy, MRI, micro-CT and echocardiography. Biochemical and histological changes were assessed. Results: Cardiomyocyte-directed PKN2 knockout embryos displayed striking abnormalities in the compact myocardium, with frequent myocardial clefts and diverticula, ventricular septal defects and abnormal heart shape. The sub-Mendelian homozygous knockout survivors developed cardiac failure. RNASeq data showed upregulation of PKN2 in patients with dilated cardiomyopathy, suggesting an involvement in adult heart disease. Given the rarity of homozygous survivors with cardiomyocyte-specific deletion of PKN2, this was explored using mice with constitutive heterozygous PKN2 knockout. Cardiac hypertrophy resulting from hypertension induced by angiotensin II was reduced in haploinsufficient PKN2 mice relative to wild-type littermates, with suppression of cardiomyocyte hypertrophy and cardiac fibrosis. Conclusions: Cardiomyocyte PKN2 is essential for heart development and formation of compact myocardium, and is also required for cardiac hypertrophy in hypertension. Thus, PKN signalling may offer therapeutic options for managing congenital and adult heart diseases.

2022-06-24 | GSE206779 | GEO

GNPS - Cardiomyocyte-specific NAMPT Knockout Mice: Metabolomics of Heart Ventricle Tissues at 2-weeks Post-Deletion

Project description:Metabolomics from heart ventricular tissues of wild-type (WT) and cardiomyocyte-specific conditional NAMPT knockout (cNKO) mice untreated or treated with nicotinamide riboside (cNKO-NR), harvested at 2-weeks post-NAMPT deletion (post-tamoxifen). For untargeted metabolomic running, mass spectrometer was operated in both negative (NEG, 70 to 1000 m/z) and positive (POS, 50 to 117.9 m/z) ion mode with the HILIC 25-minute method for the detection of metabolites. For targeted metabolomic running, mass spectrometer was operated in two positive-mode scans (SCAN1 at 118.5 to 800 m/z and SCAN2 at 70 to 117.5 m/z) with the HILIC 20-minute method for the detection of NAD derivatives.

2024-07-26 | MSV000095445 | GNPS

Thioredoxin-1 (Trx1) maintains mitochondria function via mTOR signaling in the heart

Project description:To investigate the role of Trx1 in the heart, cardiomyocyte-specific Trx1 knockout mice were generated. RNA-sequencing was performed with RNA extracted from the heart.

2020-01-15 | GSE129286 | GEO

PRDM16 is required for proper specification of the working ventricular myocardium by suppressing alternative cardiomyocyte cell fates.

Project description:PRDM16 is a transcription factor with histone methyltransferase activity expressed at the earliest stages of cardiac development. Pathogenic mutations in humans lead to cardiomyopathy, conduction abnormalities and heart failure. PRDM16 is specifically expressed in ventricular but not atrial cardiomyocytes and declines in expression postnatally. Since in other tissues PRDM16 is best known for its role in binary cell fate decisions, we hypothesized a similar decision-making function in cardiomyocytes. Here, we demonstrated that cardiomyocyte-specific deletion of Prdm16 during cardiac development results in contractile dysfunction and abnormal electrophysiology of the postnatal heart, resulting in premature death. By combined RNA+ATAC single-cell sequencing we found that PRDM16 favors ventricular working cardiomyocyte identity, by opposing the activity of master regulators of atrial and ventricular conduction fate. Myocardial loss of Prdm16 during development resulted in hyperplasia of the ventricular conduction system. Hence, PRDM16 plays an indispensable role during cardiac development by driving ventricular working cardiomyocyte identity.

2024-09-18 | GSE255382 | GEO

Single nuclei RNA-seq and snATAC-seq multiome performed in WT and Dhx36 conditional KO hearts at postnatal day 7 (PD7)

Project description:In these experiments, we aimed to investigate the role of cardiomyocyte-specific deletion of the G-quadruplex resolvase Dhx36 in heart development and cardiomyocyte differentiation. To achieve this, we conducted multi-omics analysis using single-nuclei RNA sequencing (RNA-seq) and ATAC sequencing (ATAC-seq) on hearts from postnatal day 7 (PD7) wild-type (WT) and Dhx36 conditional knockout (cKO) mice. Our findings reveal that Dhx36 plays a critical role in the development of the cardiac conduction system (CCS) and in the differentiation of both CCS and working cardiomyocytes

2024-09-15 | E-MTAB-14441 | biostudies-arrayexpress

Single nuclei RNA-seq and snATAC-seq multiome performed in WT and Dhx36 conditional KO hearts at postnatal day 7 (PD7)

2024-09-15 | E-MTAB-14442 | biostudies-arrayexpress

Gene expression in mouse heart

Project description:Growth and expansion of ventricular chambers is essential during cardiogenesis and is achieved by proliferation of cardiac progenitors that are not fully differentiated. Disruption of this process can lead to prenatal lethality. In contrast, adult cardiomyocytes achieve growth through hypertrophy rather than hyperplasia. Although epicardial-derived signals may contribute to the proliferative process in myocytes, the factors and cell types responsible for development of the ventricular myocardial thickness are unclear. Moreover, the function of embryonic cardiac fibroblasts, derived from epicardium, and their secreted factors are largely unknown. Using a novel co-culture system, we found that embryonic cardiac fibroblasts induced proliferation of cardiomyocytes, in contrast to adult cardiac fibroblasts that promoted myocyte hypertrophy. We identified fibronectin, collagen and heparin-binding EGF-like growth factor as embryonic cardiac fibroblast-specific signals that collaboratively promoted cardiomyocyte proliferation in a paracrine fashion. b1 integrin was required for this proliferative response, and ventricular cardiomyocyte-specific deletion of b1 integrin in mice resulted in reduced myocardial proliferation and impaired ventricular compaction. These findings reveal a previously unrecognized paracrine function of embryonic cardiac fibroblasts in regulating cardiomyocyte proliferation. This SuperSeries is composed of the following subset Series: GSE14411: Gene expression in b1-integrin wild-type and knockout mouse heart GSE14412: Gene expression in mouse embyonic cardiomyocytes, fibroblasts and adult cardiac fibroblasts Refer to individual Series

2009-01-14 | E-GEOD-14414 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data