ArticleAmerican journal of physiology. Cell physiology2011
Muscle-specific overexpression of NCOATGK, splice variant of O-GlcNAcase, induces skeletal muscle atrophy.
Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- O-GlcNAc participates in the meiosis of aging oocytes by mediating mitochondrial function.Reproduction (Cambridge, England) · 2024Article
- Sustained Increases in Cardiomyocyte ProteinJournal of the American Heart Association · 2023Article
- O-GlcNAcylation of SIRT1 Protects against Cold Stress-Induced Skeletal Muscle Damage via Amelioration of Mitochondrial Homeostasis.International journal of molecular sciences · 2022Article
- ProteinMetabolites · 2022Review
- Review
- Role ofPhysiological reviews · 2021Review
- Increased Glucose Availability Attenuates Myocardial Ketone Body Utilization.Journal of the American Heart Association · 2020Article
- New Insights Into the Biology of Protein O-GlcNAcylation: Approaches and Observations.Frontiers in aging · 2020Article
- Skeletal muscle O-GlcNAc transferase is important for muscle energy homeostasis and whole-body insulin sensitivity.Molecular metabolism · 2018Article
- Involvement of O-GlcNAcylation in the Skeletal Muscle Physiology and Physiopathology: Focus on Muscle Metabolism.Frontiers in endocrinology · 2018Review
- Post-translational modifications of the cardiac proteome in diabetes and heart failure.Proteomics. Clinical applications · 2016Review
- Phospho-GlcNAc modulation of slow MLC2 during soleus atrophy through a multienzymatic and sarcomeric complex.Pflugers Archiv : European journal of physiology · 2014Article
- O-GlcNAcylation, contractile protein modifications and calcium affinity in skeletal muscle.Frontiers in physiology · 2014Review
- Increasing O-GlcNAcylation level on organ culture of soleus modulates the calcium activation parameters of muscle fibers.PloS one · 2012Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The protein O-linked β-N-acetylglucosamine (O-GlcNAc) modification plays an important role in skeletal muscle development and physiological function. In this study, bitransgenic mice were generated that overexpressed NCOAT(GK), an O-GlcNAcase-inactive spliced variant of the O-GlcNAcase gene, specifically in skeletal muscle using the muscle creatine kinase promoter. Expression of the chimeric enhanced green fluorescent protein-NCOAT(GK) transgene caused an increase of cellular O-GlcNAc levels, along with the accumulation and activation of proapoptotic factors in muscles of bitransgenic mice. The consequence of overexpressing the transgene for a 2-wk period was muscle atrophy and, in some cases, resulted in the death of male mice. Muscle atrophy is a common complication of many diseases, some of which correlate markedly with high cellular O-GlcNAc levels, such as diabetes. Our study provides direct evidence linking muscle atrophy and the disruption of O-GlcNAcase activity.
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