Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of cardiac-specific Cdk1 knockout mice at 3 weeks after experimental myocardial infarction

ABSTRACT: Biological Relevance and Intent of the Experiment: The objective of this study is to elucidate the role of Cdk1 in cardiac function, specifically its contribution to cardiomyocyte proliferation and response to injury. Using a heart-specific Cdk1 knockout mouse model, we investigate the molecular and cellular impact of Cdk1 deficiency in the context of myocardial infarction (MI). Cdk1 is known for its regulatory functions in cell cycle progression, and its absence may significantly affect cardiac repair mechanisms post-MI. This research aims to explore whether the lack of Cdk1 impairs cardiomyocyte regeneration or promotes maladaptive remodeling, leading to compromised cardiac function.

INSTRUMENT(S): Illumina HiSeq 2000

ORGANISM(S): Mus musculus domesticus

SUBMITTER: Ludger Hauck

PROVIDER: E-MTAB-14508 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

RNA-seq of cardiac-specific Cdk1 knockout mice at 4 days after experimental myocardial infarction

Project description:Biological Relevance and Intent of the Experiment: The objective of this study is to elucidate the role of Cdk1 in cardiac function, specifically its contribution to cardiomyocyte (CM) proliferation and response to injury. Using a heart-specific Cdk1 knockout mouse model, we investigate the molecular and cellular impact of Cdk1 deficiency in the context of myocardial infarction (MI). Cdk1 is known for its regulatory functions in cell cycle progression, and its absence may significantly affect cardiac repair mechanisms post-MI. This research aims to explore whether the lack of Cdk1 impairs CM regeneration or promotes maladaptive remodeling, leading to compromised cardiac function. Overview of the Experimental Workflow: We performed RNA-sequencing (RNA-seq) on heart tissue collected from both wild-type (WT) and cardiac-specific Cdk1 knockout mice subjected to experimental MI. Heart samples were collected 4 days to capture dynamic transcriptional changes associated with Cdk1 loss. Comparative transcriptomic analysis between WT and knockout samples will reveal differentially expressed genes and signaling pathways involved in cardiomyocyte proliferation, apoptosis, and fibrosis. These insights may uncover key pathways driving heart regeneration or degeneration in the absence of Cdk1.

2024-10-31 | E-MTAB-14505 | biostudies-arrayexpress

Analysis of cardiac miRNA expression in the early neonatal period

Project description:The regenerative capacity of the mammalian heart is lost quickly after birth when cardiomyocytes stop dividing and undergo cell cycle arrest. Thus, the adult mammalian heart lacks the ability to heal itself to any appreciable amount after ischemic injury such as myocardial infarction. Heart growth begins during fetal life with the first phase of DNA synthesis that is exclusively associated with cardiomyocyte proliferation. This process proceeds until 12 hours after birth and is defined as 0 days in our submitted samples. Cardiomyocytes division is undetectable at neonatal day 1. To analyze the molecular mechanisms responsible for cessation of cardiomyocyte proliferation, we performed genome-wide miRNA microarray profiling by comparing postnatal days 0 vs 1d.This revealed a profile of 8 significantly downregulated miRNAs in the proliferative DKO hearts (versus vehicle-injected control), that were enriched for mRNA targets involved in cell cycle regulation. In vitro studies have demonstrated that knockdown of these 8 miRNAs in neonatal rat cardiomyocytes can increase the occurrence of cytokinetic events. Ultimately, we aim to inject antagomirs targeting these miRNAs into mice post-myocardial infarction to determine the effect of these miRNAs on heart function and cardiomyocyte proliferation in vivo.

2022-01-30 | E-MTAB-9256 | biostudies-arrayexpress

Epigenetic activation of a subset of mRNAs identified using polyribosome microarray analysis

Project description:Background: Translation deregulation is an important mechanism that causes aberrant cell growth, proliferation and survival. eIF4E, the mRNA 5 prime capâ??binding protein, plays a major role in translational control. To understand how eIF4E affects cellular proliferation and cell survival, we identified mRNA targets that are translationally responsive to eIF4E. Methodology/ principal findings: Microarray analysis of polysomal mRNA from an eIF4E-inducible NIH 3T3 cell line was performed. Induction of eIF4E expression resulted in increased translation of a defined set of mRNAs; many of the mRNAs are novel targets, including those that encode large- and small-subunit ribosomal proteins and cell growthâ??related factors. eIF4E overexpression also led to augmented translation of mRNAs encoding anti-apoptotic proteins, which conferred resistance to endoplasmic reticulumâ??mediated apoptosis. Conclusions/ significance: Our results shed new light on the mechanisms by which eIF4E prevents apoptosis and transforms cells. Downregulation of eIF4E and its downstream targets is a therapeutic option for the development of novel anti-cancer drugs. Keywords: time course Comparison of total and polysomal RNA upon eIF4E iinduction in NIH3T3/parental and NIH3T3/eIF4E cells Each of the following pairs were generated from one hybridization: GSM153931 GSM153932 GSM153933 GSM153934 GSM153935 GSM153936 GSM153937 GSM153938 GSM153939 GSM153940 GSM153941 GSM153942 GSM153943 GSM153944 GSM153945 GSM153946 GSM153947 GSM153948 GSM153949 GSM153950 GSM153951 GSM153952 GSM153953 GSM153954 GSM153955 GSM153956 GSM153957 GSM153958 GSM153959 GSM153960 GSM153961 GSM153962

2010-06-11 | E-GEOD-6639 | biostudies-arrayexpress

Targeted MIP sequencing for healthy samples

Project description:We developed Del-Read, an algorithm targeting medium-sized deletions (6-100 BPs) in short-reads, which are challenging for current variant callers relying on alignment. Our focus was on Micro-Homology mediated End Joining deletions (MMEJ-dels), prevalent in myeloid malignancies. MMEJ-dels follow a distinct pattern, occurring between two homologies, allowing us to generate a comprehensive list of MMEJ-dels in the exome. Using Del-Read, we identified numerous novel germline and somatic MMEJ-dels in Beat AML and TCGA-breast datasets. Validation in 500 healthy individuals confirmed their presence.

2023-09-20 | E-MTAB-13306 | biostudies-arrayexpress

Functional and Molecular Single-Cell Analyses Implicate PRDM14 in the Initiation of a Novel B-1 Cell Malignancy - Single Cell RNA sequencing experiments

Project description:Description: Molecular mechanisms underlying high-risk subtypes of leukemia remain elusive. PR domain-containing 14 (Prdm14) is a potent oncogene implicated in the initiation of many cancers, including leukemia. Here, we interrogate the heterogeneity of Prdm14-expressing cell types in a mouse model of T-cell acute lymphoblastic leukemia (T-ALL). We identified an abnormal B-1 cell-like population in pre-leukemic bone marrow. B-1 cells are a self-renewing population of unconventional B cells established during embryonic development. This dataset contains single-cell transcriptomic profiling of four samples. Cells from R26PR;Mx1-cre mice were sorted on GFP expression (“GFP+” and “GFP-” samples) or on a pro-B-1-like immunophenotype of CD11b- CD19+ CD127+ Sca-1+ (“Pre-leukemia” sample). As a control, immunophenotype-matched cells from R26PR mice were analyzed by scRNA-seq after sorting on CD11b- CD19+ CD127+ Sca-1+ (“Control” sample) (Supplemental Figure 2). Accordingly, we conducted scRNA-seq of four total samples: “GFP+”, “GFP-“, “Pre-leukemia”, and “Control”. The GFP+ and GFP- samples provide the cellular context to the bone marrow samples.

2024-06-29 | E-MTAB-13160 | biostudies-arrayexpress

Transcription profiling of wild type and arp8 mutant yeast after hyperosmolarity stress treatment

Project description:Hyperosmolarty stress treatment of wild type and arp8 mutant Saccharomyces cerevisiae cells

2008-07-15 | E-MEXP-1445 | biostudies-arrayexpress

Transcription profiling of wild type and Pdr1 and Pdr3 knock-out yeast treated with detergents DCP (2-4-dichlorophenol) and POELE (polyoxyethylen-9-laurylether)

Project description:DCP (2-4-dichlorophenol; 0,3mM) and POELE (polyoxyethylen-9-laurylether; 0,1mM)treatment on Saccharomyces cerevisiae W303-1A wild-type cells. Further investigation of the involvement of the transcripton factors Pdr1 and Pdr3 in DCP treated cells. Cells were growing in early exponential phase in rich medium.

2007-10-09 | E-MEXP-865 | biostudies-arrayexpress

Candida glabrata oxidative stress

Project description:Investigating the oxidative stress response: Candida glabrata strains were stressed with hydrogen peroxide and menadione (causing oxygen radicals) to induce the oxidative stress regulon, which is thought to be upregulated during the oxidative burst inside of phagocytic cells.

2011-01-01 | E-MEXP-2915 | biostudies-arrayexpress

Transcription profiling of Candida glabrata after environmental stress

Project description:Characterization of Environmental Stress Response of Candida glabrata

2008-06-20 | E-MEXP-1427 | biostudies-arrayexpress

metal stress 1

Project description:Effect of mild metal ion-stress (40µM AgNO3, 200µM AsCl3, 2µM CdCl2, 100µM CoCl2, 30µM HgCl2, 1.5mM MnCl2, 1.5mM NiSO4) on cellular metabolism, resp. on transcription - 30min incubation in yeast Saccharomyces cerevisiae

2011-01-01 | E-MEXP-2985 | 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