ArticleFree radical research2009
Sarcolipin and ubiquitin carboxy-terminal hydrolase 1 mRNAs are over-expressed in skeletal muscles of alpha-tocopherol deficient mice.
Article in Free radical research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Introduction of Mature Mast Cells into Bone Marrow Alters Bone Metabolism in Growing Mice.International journal of molecular sciences · 2025Article
- Skeletal Muscle UCHL1 Negatively Regulates Muscle Development and Recovery after Muscle Injury.International journal of molecular sciences · 2024Article
- UCHL1 regulates oxidative activity in skeletal muscle.PloS one · 2020Article
- UCHL1 regulates muscle fibers and mTORC1 activity in skeletal muscle.Life sciences · 2019Article
- Coding sequences of sarcoplasmic reticulum calcium ATPase regulatory peptides and expression of calcium regulatory genes in recurrent exertional rhabdomyolysis.Journal of veterinary internal medicine · 2019Article
- Sarcolipin expression is repressed by endoplasmic reticulum stress in C2C12 myotubes.Journal of physiology and biochemistry · 2017Article
- Ubiquitin C-Terminal Hydrolase L1 regulates myoblast proliferation and differentiation.Biochemical and biophysical research communications · 2017Article
- Sarcolipin: A Key Thermogenic and Metabolic Regulator in Skeletal Muscle.Trends in endocrinology and metabolism: TEM · 2016Review
- Role of callose synthases in transfer cell wall development in tocopherol deficient Arabidopsis mutants.Frontiers in plant science · 2014Article
- Vitamin E in sarcopenia: current evidences on its role in prevention and treatment.Oxidative medicine and cellular longevity · 2014Review
- Evaluation of long-term vitamin E insufficiency or excess on bone mass, density, and microarchitecture in rodents.Free radical biology & medicine · 2013Article
- Chronic vitamin E deficiency promotes vitamin C deficiency in zebrafish leading to degenerative myopathy and impaired swimming behavior.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2013Article
- Article
- Enhanced Ca2+ transport and muscle relaxation in skeletal muscle from sarcolipin-null mice.American journal of physiology. Cell physiology · 2011Article
- Modulation of ozone-sensitive genes in alpha-tocopherol transfer protein null mice.Inhalation toxicology · 2010Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The transcriptome of ataxic muscles from alpha-tocopherol transfer protein deficient (ATTP-KO), 23-month old, mice was compared with that of their normal littermates. Genes encoding sarcolipin (sln) and ubiquitin carboxyl-terminal hydrolase (uchl1) were over-expressed (> or =10-fold) in ataxic muscles. SLN is a 3.2 kDa membrane protein that binds to sarcoplasmic reticulum calcium ATPase, regulates Ca(+ +) transport and muscle relaxation-contraction cycles. UCHL1 is a 24.8 kDa member of proteosome proteins; it is over-expressed in myofibrillar myopathy and is associated with neurodegenerative diseases. Furthermore, six additional transcripts, three encoding thin-filament proteins and three encoding Ca(+ +) sensing proteins that participate in contraction-relaxation cycle, and eight transcripts that encode members of lysosomal proteins were also over-expressed in ataxic muscles. These observations suggest that chronic alpha-tocopherol (AT) deficiency activates critical genes of muscle contractility and protein degradation pathways, simultaneously. The magnitude of induction of sln and uchl1 was lower in asymptomatic, 8-month old, ATTP-KO mice and in 8-month old mice fed an AT-depleted diet. These studies suggest sln and uchl1 genes as novel targets of AT deficiency and may offer molecular correlates of well documented descriptions of neuromuscular dysfunctions in AT-deficient rodents. Since the neuromuscular deficits of ATTP-KO mice appear to be similar to those of patients with ATTP mutations, it is suggested that over-expression of sln and uchl1 may also contribute to AT-sensitive ataxia in humans.
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