Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

30 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Analysis of miR-1_133a function

ABSTRACT: Effect of the loss of both miR-1/133a clusters on the embryonic heart. Please note: dKO means it is a double KO of the two miR-1/133a clusters in the mouse. Control means we do not use just WT but also some heterozygous animals to compare to dKOs, however these controls do not have a phenotype. Transgene negative: these are littermates of the myocd transgenic animals that do not carry a transgene.

ORGANISM(S): Mus musculus

SUBMITTER: Thomas Boettger

PROVIDER: E-MEXP-3873 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

miR-1/133a clusters cooperatively specify the cardiomyogenic lineage by adjustment of myocardin levels during embryonic heart development.

Wystub Katharina K Besser Johannes J Bachmann Angela A Boettger Thomas T Braun Thomas T

PLoS genetics 20130919 9

miRNAs are small RNAs directing many developmental processes by posttranscriptional regulation of protein-coding genes. We uncovered a new role for miR-1-1/133a-2 and miR-1-2/133a-1 clusters in the specification of embryonic cardiomyocytes allowing transition from an immature state characterized by expression of smooth muscle (SM) genes to a more mature fetal phenotype. Concomitant knockout of miR-1-1/133a-2 and miR-1-2/133a-1 released suppression of the transcriptional co-activator myocardin, a ...[more]

PMID: 24068960

Similar Datasets

NIH3T3 transfected with myocardin

Project description:NIH3T3 cell transiently transfected with myocardin-EGFP or EGFP. Transfection: Lipofectamine 2000 according to the manufacturers instructions (Invitrogen).

2013-11-15 | E-MEXP-3869 | biostudies-arrayexpress

Adult cardiomyocyte specific loss of myostatin

Project description:Inhibition of myostatin signaling induces strong skeletal muscle growth making it an attractive target to treat muscle wasting and sarcopenia. However, the biological function of myostatin in the heart is barely understood. We demonstrate that conditional inactivation of myostatin in the adult murine heart leads to cardiac hypertrophy, heart failure and increased lethality. To induce cardiomyocyte specific loss of myostatin a conditionally active Mstn^fl/fl allele was generated by insertion of loxP elements upstream and downstream of exons 1 and 2 of the mouse myostatin gene. The selection cassette was removed in vivo by flp-recombination. To inactivate myostatin, mice were mated to alphaMyHC-MCM mice (Sohal, DS, et al. (2001) Circulation Research 89, 20-25). Cre-recombination was achieved by intraperitoneal administration of Tamoxifen (40 mg/kg) for 5 consecutive days. The respective control alphaMyHC-MCM animals were equally treated.

2014-05-16 | E-MEXP-3744 | biostudies-arrayexpress

Title: Aging-associated changes in microRNA expression profile of internal anal sphincter smooth muscle: Role of microRNA-133a

Project description:A comprehensive –omic, computational, and physiological approach was employed to examine the (previously unexplored) role of microRNAs (miRNAs) as regulators of IAS smooth muscle contractile phenotype and basal tone. MicroRNA profiling, genome wide expression, validation and network analyses were employed to assess changes in mRNA and miRNA expression in IAS smooth muscles from young vs. aging rats. Multiple miRNAs, including rno-miR-1, rno-miR-340-5p, rno-miR-185, rno-miR-199a-3p, rno-miR-200c, rno-miR-200b, rno-miR-31, rno-miR-133a and rno-miR-206 were found to be up-regulated in aging IAS. qRT-PCR confirmed the up-regulated expression of these miRNAs and down regulation of multiple, predicted targets (Eln, Col3a1, Col1a1, Zeb2, Myocd, SRF, Smad1, Smad2, RhoA/ROCK2, Fn1, Sm22-v2, Klf4, and Acta2) involved in regulation of SM contractility. Subsequent studies demonstrated an aging-associated increase in the expression of miR-133a, corresponding decreases in RhoA, ROCK2, MYOCD, SRF and SM22α protein expression, RhoA-signaling, and a decrease in basal and agonist (U-46619 (thromboxane A2 analog))-induced increase in the IAS tone. Moreover, in vitro transfection of miR-133a caused a dose-dependent increase of IAS tone in strips, which was reversed by anti-miR-133a. Lastly, in vivo perianal injection of anti-miR-133a reversed the loss of IAS tone associated with age. This work establishes the important regulatory effect of miRNA-133a on basal and agonist-stimulated IAS tone. Moreover, reversal of age-associated loss of tone via anti-miR delivery strongly implicates miR dysregulation as a causal factor in the aging-associated decrease in IAS tone, and suggests miR-133a is feasible therapeutic target in aging-associated rectoanal incontinence.

2016-10-28 | GSE79350 | GEO

Transcription profiling of mouse heart from mice with a SMYD2 heart-specific deletion

Project description:Effect of Smyd2 cardiac deficiency was analyzed in mouse heart

2010-04-12 | E-MEXP-2542 | biostudies-arrayexpress

Transcription profiling by array of mouse kidney from Slc4a5 knock-out and wild type mice

Project description:Transcriptional profiling of kidney total RNA extracted from Slc4a5 knock-out and WT mice

2011-11-23 | E-MEXP-2692 | biostudies-arrayexpress

Cardiac mtDNA and oxidative stress

Project description:Overexpression of twinkle protects cardiomyocytes from genotoxic stress caused by SOD2 heterozygocity

2013-11-01 | E-MEXP-3983 | biostudies-arrayexpress

Rat heart developmental hypertrophy

Project description:Transcriptional profiling of rat hearts at different developmental stages

2012-03-20 | E-MEXP-3590 | biostudies-arrayexpress

Transcription profiling of mouse kidney wild type and Slc4a11 knock-out

Project description:Effect of the loss of Slc4a11 an transcriptional profile of kidney

2010-03-03 | E-MEXP-2568 | biostudies-arrayexpress

miRNA-1/133a clusters regulate adrenergic control of cardiac repolarization

Project description:Analysis of the function of miR-1/133a clusters in Physiology of the adult heart. Analysis of transcriptome was perfromed for heart tissue isolated from WT (n=7), miR-1-1/133a KO (mouse chromosome 2; n=4) and miR-1-2/133a-1 KO (mouse chromosome 18; n=5) animals.

2014-11-24 | E-MTAB-2727 | biostudies-arrayexpress

numb and numblike deleted by Nkx2.5Cre

Project description:The ventricular wall of the heart is composed of trabeculated and compactlayers, which are separated by yet unknown processes during embryonic development. Notch signaling plays important roles in cardiac development. Mutations in Notch signaling components are related to human congenital heart diseases Two homologues, Numb and Numblike (Numbl), are expressed in mammals, which also act as inhibitors of Notch signaling Here we investigate the role of Notch2 and Numb/Numblike during myocardial trabeculation and compaction. The aim of the experiment is to analyze whether Numb/Numblike are involved in inhibition of Notch activity in the developing heart.

2013-01-17 | E-MEXP-3490 | 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