ArticleTransgenic research2003
Transgenic and tissue culture analyses of the muscle creatine kinase enhancer Trex control element in skeletal and cardiac muscle indicate differences in gene expression between muscle types.
Article in Transgenic research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Metabolic Basis of Creatine in Health and Disease: A Bioinformatics-Assisted Review.Nutrients · 2021Review
- Of rAAV and Men: From Genetic Neuromuscular Disorder Efficacy and Toxicity Preclinical Studies to Clinical Trials and Back.Journal of personalized medicine · 2020Review
- Ectopic overexpression of porcine DGAT1 increases intramuscular fat content in mouse skeletal muscle.Transgenic research · 2013Article
- Constitutive expression of Yes-associated protein (Yap) in adult skeletal muscle fibres induces muscle atrophy and myopathy.PloS one · 2013Article
- Differentiation and fiber type-specific activity of a muscle creatine kinase intronic enhancer.Skeletal muscle · 2011Article
- TEAD-1 overexpression in the mouse heart promotes an age-dependent heart dysfunction.The Journal of biological chemistry · 2010Article
- UTX mediates demethylation of H3K27me3 at muscle-specific genes during myogenesis.The EMBO journal · 2010Article
- Overexpression of TEAD-1 in transgenic mouse striated muscles produces a slower skeletal muscle contractile phenotype.The Journal of biological chemistry · 2008Article
- Article
- Quantitative proteomic identification of MAZ as a transcriptional regulator of muscle-specific genes in skeletal and cardiac myocytes.Molecular and cellular biology · 2008Article
- Quantitative proteomic identification of six4 as the trex-binding factor in the muscle creatine kinase enhancer.Molecular and cellular biology · 2004Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The muscle creatine kinase (MCK) gene is expressed at high levels only in differentiated skeletal and cardiac muscle. The activity of the cloned enhancer-promoter has previously been shown to be dependent on the Trex element which is specifically bound by a yet unidentified nuclear factor, TrexBF. We have further characterized the function of the Trex site by comparing wild-type and Trex-mutated MCK transgenes in five mouse skeletal muscles: quadriceps, extensor digitorum longus (EDL), soleus, diaphragm, and distal tongue, as well as in heart ventricular muscle. Several types of statistical analysis including analysis of variance (ANOVA) and rank sum tests were used to compare expression between muscle types and between constructs. Upon mutation of the Trex site, median transgene expression levels decreased 3- to 120-fold in the muscles examined, with statistically significant differences in all muscles except the EDL. Expression in the largely slow soleus muscle was more affected than in the EDL, and expression in the distal tongue and diaphragm muscles was affected more than in soleus. Median expression of the transgene in ventricle decreased about 18-fold upon Trex mutation. Transfections into neonatal rat myocardiocytes confirmed the importance of the Trex site for MCK enhancer activity in heart muscle, but the effect is larger in transgenic mice than in cultured cells.
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Registered trials
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