Constitutive upregulations of titin-based signalling proteins in KY deficient muscles
Copyright policy )Constitutive upregulations of titin-based signalling proteins in KY deficient muscles
An increase in the expression of stretch/stress response elements in fast and slow muscles has been previously described in a transcriptional profiling of KY deficient muscles. Here, we have characterized the induction of this titin-based family of signalling proteins in ky/ky muscles at the protein level. Changes in expression of MLP, MARP2 and Xin have been related to the onset of dystrophic and adaptive changes that operate in ky/ky muscles. Our results indicate that induction of this set of genes is an early consequence of the interference caused by the absence of the KY protein. A search of muscle profiles of mouse models revealed such molecular hallmark only in muscles subjected to a single bout of eccentric contractions and specific titin mutants. Based on the role of this family as titin-based stress response molecules, it is suggested that titin structural/signalling instability is common to ky and titin mouse mutants and eccentric contractions.
- Charité - University Medicine Berlin Germany
- University of Helsinki Finland
- University of Bonn Germany
- University of Oxford United Kingdom
Transcription, Genetic, Muscle Proteins, Nuclear Proteins, LIM Domain Proteins, Muscular Dystrophy, Animal, Adaptation, Physiological, Mice, Mutant Strains, Protein Structure, Tertiary, Up-Regulation, DNA-Binding Proteins, Mice, Animals, Connectin, Muscle, Skeletal, Protein Kinases, Oligonucleotide Array Sequence Analysis, Peptide Hydrolases, Signal Transduction
Transcription, Genetic, Muscle Proteins, Nuclear Proteins, LIM Domain Proteins, Muscular Dystrophy, Animal, Adaptation, Physiological, Mice, Mutant Strains, Protein Structure, Tertiary, Up-Regulation, DNA-Binding Proteins, Mice, Animals, Connectin, Muscle, Skeletal, Protein Kinases, Oligonucleotide Array Sequence Analysis, Peptide Hydrolases, Signal Transduction
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