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Molecular profiles of dystrophin-deficient and normal murine muscle

ABSTRACT: Expression profiles of six skeletal muscle types in mdx, mdx5cv and wildtype mice. Keywords: other

ORGANISM(S): Mus musculus

PROVIDER: GSE897 | GEO | 2004/04/12

SECONDARY ACCESSION(S): PRJNA87907

REPOSITORIES: GEO

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Transcription profiling of six skeletal muscle types in dystrophin-deficient mice mdx, mdx5cv and wildtype mice.

Project description:Expression profiles of six skeletal muscle types in mdx, mdx5cv and wildtype mice.

2007-12-13 | E-GEOD-897 | biostudies-arrayexpress

Molecular profiles (HG-U95A) of dystrophin-deficient and normal human muscle

Project description:Molecular profiles of dystophin-deficient patients and normal human skeletal muscles on Affymetrix HG-U95A arrays Keywords = DMD Keywords = Duchenne muscular dystrophy Keywords = dystrophin Keywords = Affymetrix U95A array Keywords = skeletal muscle Keywords = gene expression profiles Keywords: other

2004-01-29 | GSE1004 | GEO

Molecular profiles (HG-U95A) of dystrophin-deficient and normal human muscle

2004-01-29 | E-GEOD-1004 | biostudies-arrayexpress

Molecular profiles(HG-U95B,C,D,E) of dystrophin-deficient and normal human skeletal muscle

Project description:molecular profiles (HG-U95B,C,D,E) of biopsy skeletal muscle samples obtained from 10 normal individuals and 10 DMD patients Keywords = gene expression profiles of normal human skeletal muscles Keywords = gene expression profiles of DMD patients' skelatal muscle samples Keywords = Affymetrix HG-U95B Keywords = Affymetrix HG-U95C Keywords = Affymetrix HG-U95D Keywords = Affymetrix HG-U95E Keywords: other

2004-02-04 | GSE1007 | GEO

Molecular profiles(HG-U95B,C,D,E) of dystrophin-deficient and normal human skeletal muscle

2004-02-04 | E-GEOD-1007 | biostudies-arrayexpress

Array profiling of dystrophin-deficient mice with a secondary glycosylation defect

Project description:A deletion in the CMAH gene in humans occurred approximately 3.5 million years ago. This resulted in the inactivation of the CMP-Neu5Ac hydroxylase enzyme, and hence, in the specific deficiency in N-glycolylneuraminic acid (Neu5Gc), a form of sialic acid, in all modern humans. Although there is evidence that this molecular milestone in the origin of humans may have led to the evolution of human-specific pathogens, how deficiency in Neu5Gc might alter progression of non-infectious human diseases remains unanswered. Here, we have investigated cardiac and skeletal muscle gene expression changes in mdx mice, a model of Duchenne muscular dystrophy (DMD), that do or do not carry the human-like inactivating mutation in the mouse Cmah gene. We have evidence that Neu5Gc-deficiency in humans might explain some of the discrepancies in the disease phenotype between mdx mice and DMD patients. The study had four groups of mice: 1) Wild type, 2) Cmah KO (mice carrying a human-like mutation in the Cmah gene and hence have human-like deficiency in Neu5Gc sialic acid), 3) mdx (mouse model for Duchenne Muscular Dystrophy), and 4) mdx mice deficient in Cmah. Gene expression was studied in heart and gastrocnemius muscle samples. Three replicates per group/tissue.

2010-07-31 | E-GEOD-16438 | biostudies-arrayexpress

Dystrophin-deficient and dystrophin and utrophin double-deficient mice crossed with mice with full-length hDMD genes

Project description:Crossing of hDMD mice that contain the full-length 2.3 Mb hDMD gene were crossed with dystrophin-deficient mdx mice and dystrophin and utrophin double-deficient mdx x utrn-/- mice resulted in a full rescue of the dystrophic features of these mice, as concluded from histological analysis. Analysis on Affymetrix gene chips demonstrated that also expression profiles of the dystrophic mice were normalized by crossing with transgenic hDMD mice. This confirms the full functionality of the hDMD transgene in mice. Keywords: disease state analysis

2007-12-13 | GSE6790 | GEO

Array profiling of dystrophin-deficient mice with a secondary glycosylation defect

2010-07-31 | GSE16438 | GEO

Transcription profiling of 16-week-old mdx mouse muscles to characterize transcriptional changes induced by dystrophin deficiency.

Project description:Despite over 3,000 articles published on dystrophin in the last 15 years, the reasons underlying the progression of the human disease, differential muscle involvement, and disparate phenotypes in different species are not understood. The present experiment employed a screen of 12,488 mRNAs in 16-wk-old mouse mdx muscle at a time when the skeletal muscle is avoiding severe dystrophic pathophysiology, despite the absence of a functional dystrophin protein. A number of transcripts whose levels differed between the mdx and human Duchenne muscular dystrophy were noted. A fourfold decrease in myostatin mRNA in the mdx muscle was noted. Differential upregulation of actin-related protein 2/3 (subunit 4), beta-thymosin, calponin, mast cell chymase, and guanidinoacetate methyltransferase mRNA in the more benign mdx was also observed. Transcripts for oxidative and glycolytic enzymes in mdx muscle were not downregulated. These discrepancies could provide candidates for salvage pathways that maintain skeletal muscle integrity in the absence of a functional dystrophin protein in mdx skeletal muscle.

2007-11-06 | E-GEOD-466 | biostudies-arrayexpress

Transcription profiling of mouse dystrophin-deficient and dystrophin and utrophin double-deficient animalse crossed with mice with full-length hDMD genes

2008-06-15 | E-GEOD-6790 | biostudies-arrayexpress

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