ArticleMolecular and cellular biology1996
E-box sites and a proximal regulatory region of the muscle creatine kinase gene differentially regulate expression in diverse skeletal muscles and cardiac muscle of transgenic mice.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.
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- Expression and function of four AAV-based constructs for dystrophin restoration in the mdx mouse model of Duchenne muscular dystrophy.Biology open · 2023Article
- A Muscle Hybrid Promoter as a Novel Tool for Gene Therapy.Molecular therapy. Methods & clinical development · 2019Article
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- Twist2 amplification in rhabdomyosarcoma represses myogenesis and promotes oncogenesis by redirecting MyoD DNA binding.Genes & development · 2019Article
- Systemic AAV Micro-dystrophin Gene Therapy for Duchenne Muscular Dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Review
- Incorporation of a skeletal muscle-specific enhancer in the regulatory region of Igf1 upregulates IGF1 expression and induces skeletal muscle hypertrophy.Scientific reports · 2018Article
- β-Sarcoglycan gene transfer decreases fibrosis and restores force in LGMD2E mice.Gene therapy · 2016Article
- Treatment of hypophosphatasia by muscle-directed expression of bone-targeted alkaline phosphatase via self-complementary AAV8 vector.Molecular therapy. Methods & clinical development · 2016Article
- Human α7 Integrin Gene (ITGA7) Delivered by Adeno-Associated Virus Extends Survival of Severely Affected Dystrophin/Utrophin-Deficient Mice.Human gene therapy · 2015Article
- AAV1.NT-3 gene therapy for charcot-marie-tooth neuropathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2014Article
- Plasmapheresis eliminates the negative impact of AAV antibodies on microdystrophin gene expression following vascular delivery.Molecular therapy : the journal of the American Society of Gene Therapy · 2014Article
- AAV-mediated overexpression of human α7 integrin leads to histological and functional improvement in dystrophic mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- Non-passaged muscle precursor cells from 32-month old rat skeletal muscle have delayed proliferation and differentiation.Cell proliferation · 2013Article
- Gene therapy for muscular dystrophy: lessons learned and path forward.Neuroscience letters · 2012Review
- An adeno-associated virus vector efficiently and specifically transduces mouse skeletal muscle.Molecular biotechnology · 2011Article
- Differentiation and fiber type-specific activity of a muscle creatine kinase intronic enhancer.Skeletal muscle · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Previous analysis of the muscle creatine kinase (MCK) gene indicated that control elements required for transcription in adult mouse muscle differed from those required in cell culture, suggesting that distinct modes of muscle gene regulation occur in vivo. To examine this further, we measured the activity of MCK transgenes containing E-box and promoter deletions in a variety of striated muscles. Simultaneous mutation of three E boxes in the 1,256-bp MCK 5' region, which abolished transcription in muscle cultures, had strikingly different effects in mice. The mutations abolished transgene expression in cardiac and tongue muscle and caused a reduction in expression in the soleus muscle (a muscle with many slow fibers) but did not affect expression in predominantly fast muscles: quadriceps, abdominals, and extensor digitorum longus. Other regulatory sequences with muscle-type-specific activities were found within the 358-bp 5'-flanking region. This proximal region conferred relatively strong expression in limb and abdominal skeletal muscles but was inactive in cardiac and tongue muscles. However, when the 206-bp 5' enhancer was ligated to the 358-bp region, high levels of tissue-specific expression were restored in all muscle types. These results indicate that E boxes and a proximal regulatory region are differentially required for maximal MCK transgene expression in different striated muscles. The overall results also imply that within skeletal muscles, the steady-state expression of the MCK gene and possibly other muscle genes depends on transcriptional mechanisms that differ between fast and slow fibers as well as between the anatomical and physiological attributes of each specific muscle.
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