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Links from GEO DataSets

Items: 8

1.

Cardiac muscle ring finger-1 increases susceptibility to heart failure by inhibiting creatine kinase activity in vivo

(Submitter supplied) Muscle ring finger-1 (MuRF1) is a muscle-specific protein implicated in the regulation of cardiac myocyte size and contractility. MuRF2, a closely related family member, redundantly interacts with protein substrates, and hetero-dimerizes with MuRF1. Mice lacking either MuRF1 or MuRF2 are phenotypically normal whereas mice lacking both proteins develop a spontaneous cardiac and skeletal muscle hypertrophy indicating cooperative control of muscle mass by MuRF1 and MuRF2. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL2876
19 Samples
Download data: GPR
Series
Accession:
GSE11661
ID:
200011661
2.

Muscle Ring Finger 1 (MuRF1) and MuRF2 are Necessary but Functionally Redundant During Developmental Cardiac Growth and Regulate E2F1-Mediated Gene Expression In Vivo

(Submitter supplied) Muscle ring finger (MuRF) proteins have been implicated in the transmission of mechanical forces to nuclear cell signaling pathways through their association with the sarcomere. We recently reported that MuRF1, but not MuRF2, regulated pathologic cardiac hypertrophy in vivo. This was surprising since MuRF1 and MuRF2 interact redundantly with sarcomeric proteins in yeast two hybrid studies, and form both homo- and hetero-dimers with each other. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL7202
16 Samples
Download data: TXT
Series
Accession:
GSE14512
ID:
200014512
3.

Muscle Ring Finger-1 regulation of right-sided heart transcriptional responses to hypoxia in vivo.

(Submitter supplied) To determine the role of cardiomyocyte muscle ring finger-1 (MuRF1) in vivo, we employed whole genome microarray expression profiling as a discovery platform to identify genes differentially regulated by MuRF1 using MuRF1-/- and alphaMHC (cardiomyocyte-specific) MuRF1 transgenic mice in a model of pulmonary hypertension-induced right sided heart failure. Mice were placed in hypoxia chambers set at 10.0% oxygen (partial pressure of oxygen roughly 65 mmHg in Albuquerque) and monitored both by the digital feedback control system (Biospherix, Colorado) as well as by a secondary O2/CO2 monitor (O2Cap, OxiGraf, Inc.; Mountain View, CA). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL4134
17 Samples
Download data: TXT
Series
Accession:
GSE82345
ID:
200082345
4.

MuRF1-dependent regulation of systemic carbohydrate metabolism as revealed from transgenic mouse studies

(Submitter supplied) Under various pathophysiological muscle-wasting conditions like diabetes and starvation, a family of ubiquitin ligases, including MuRF1 (Muscle specific RING-Finger protein 1), are induced to target muscle proteins for degradation via ubiquitination. In an attempt to identify the in vivo targets of MuRF1 we have generated transgenic mouse lines overexpressing MuRF1 in a skeletal muscle specific fashion. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6526
4 Samples
Download data: CEL
Series
Accession:
GSE10626
ID:
200010626
5.

MuRF1 regulation of Fenofibrate’s induction of spontaneous cardiac hypertrophy in vivo.

(Submitter supplied) MuRF1 -/- w/ Fenofibrate treatment leads to the reduction of proteolytic and fibrolytic enzymes, increasing hypertrophy
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL7202
20 Samples
Download data: TXT
Series
Accession:
GSE68480
ID:
200068480
6.

Analysis of Akt1 activation in transgenic mouse hearts show expression profiles associated with hypertrophy and failure

(Submitter supplied) To investigate molecular mechanisms involved in the development of cardiac hypertrophy and heart failure, a tetracycline-regulated transgenic system to conditionally switch a constitutively-active form of the Akt1 protein kinase on or off in the adult heart was developed. Short-term activation (2 weeks) of Akt1 resulted in completely reversible hypertrophy with maintained contractility. In contrast, chronic Akt1 activation (6 weeks) induced extensive cardiac hypertrophy, severe contractile dysfunction, and massive interstitial fibrosis. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Datasets:
GDS2304 GDS2308
Platforms:
GPL339 GPL340
36 Samples
Download data
Series
Accession:
GSE3383
ID:
200003383
7.
Full record GDS2308

Akt1 serine-threonine protein kinase activation effect on the heart (MG-430B)

Analysis of hearts after acute or chronic induction of a transgenic Akt1 kinase. Acute activation results in reversible hypertrophy, while chronic activation induces transition to failure. Results provide insight into the mechanisms involved in the development of cardiac hypertrophy and failure.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 5 protocol sets
Platform:
GPL340
Series:
GSE3383
18 Samples
Download data
DataSet
Accession:
GDS2308
ID:
2308
8.
Full record GDS2304

Akt1 serine-threonine protein kinase activation effect on the heart (MG-430A)

Analysis of hearts after acute or chronic induction of a transgenic Akt1 kinase. Acute activation results in reversible hypertrophy, while chronic activation induces transition to failure. Results provide insight into the mechanisms involved in the development of cardiac hypertrophy and failure.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 5 protocol sets
Platform:
GPL339
Series:
GSE3383
18 Samples
Download data
DataSet
Accession:
GDS2304
ID:
2304
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