ArticleThe Journal of biological chemistry2010
A novel glycerophosphodiester phosphodiesterase, GDE5, controls skeletal muscle development via a non-enzymatic mechanism.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 86 citations in OpenAlex.
- Proteomic and Metabolomic Analysis Reveals Candidate Biomarkers and Meat Quality Differences in Divergent Climatically Adapted Sheep Breeds.Foods (Basel, Switzerland) · 2026Article
- Recent perspectives on biotechnological production, modulation and applications of glycerophosphoryl diester phosphodiesterases.Biodegradation · 2025Review
- Glucosyl Hesperidin Supplementation Prevents Tubulointerstitial Fibrosis and Immune Activation in Diabetic Nephropathy in Mice.Nutrients · 2025Article
- Cellular and organismal function of choline metabolism.Nature metabolism · 2025Review
- Dysregulation of choline metabolism and therapeutic potential of citicoline in Huntington's disease.Aging cell · 2024Article
- AMPK activation induces RALDH+ tolerogenic dendritic cells by rewiring glucose and lipid metabolism.The Journal of cell biology · 2024Article
- EDI3 knockdown in ER-HER2+ breast cancer cells reduces tumor burden and improves survival in two mouse models of experimental metastasis.Breast cancer research : BCR · 2024Article
- GDE5/Gpcpd1 activity determines phosphatidylcholine composition in skeletal muscle and regulates contractile force in mice.Communications biology · 2024Article
- An update on Glycerophosphodiester Phosphodiesterases; From Bacteria to Human.The protein journal · 2024Review
- Gpcpd1-GPC metabolic pathway is dysfunctional in aging and its deficiency severely perturbs glucose metabolism.Nature aging · 2024Article
- A novel insertional allele of theFrontiers in genetics · 2024Article
- Article
- Screening Potential Diagnostic Biomarkers for Age-Related Sarcopenia in the Elderly Population by WGCNA and LASSO.BioMed research international · 2022Article
- Article
- Nucleus Type-Specific DNA Methylomics Reveals Epigenetic "Memory" of Prior Adaptation in Skeletal Muscle.Function (Oxford, England) · 2021Article
- Increased nuclear but not cytoplasmic activities of CELF1 protein leads to muscle wasting.Human molecular genetics · 2020Article
- Insulin Resistance in Apolipoprotein M Knockout Mice is Mediated by the Protein Kinase Akt Signaling Pathway.Endocrine, metabolic & immune disorders drug targets · 2020Article
- Focus on the glycerophosphocholine pathway in choline phospholipid metabolism of cancer.NMR in biomedicine · 2019Review
- GDE5 inhibition accumulates intracellular glycerophosphocholine and suppresses adipogenesis at a mitotic clonal expansion stage.American journal of physiology. Cell physiology · 2019Article
- Exploration of haplotype research consortium imputation for genome-wide association studies in 20,032 Generation Scotland participants.Genome medicine · 2017Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
Mammalian glycerophosphodiester phosphodiesterases (GP-PDEs) have been identified recently and shown to be implicated in several physiological functions. This study isolated a novel GP-PDE, GDE5, and showed that GDE5 selectively hydrolyzes glycerophosphocholine (GroPCho) and controls skeletal muscle development. We show that GDE5 expression was reduced in atrophied skeletal muscles in mice and that decreasing GDE5 abundance promoted myoblastic differentiation, suggesting that decreased GDE5 expression has a counter-regulatory effect on the progression of skeletal muscle atrophy. Forced expression of full-length GDE5 in cultured myoblasts suppressed myogenic differentiation. Unexpectedly, a truncated GDE5 construct (GDE5DeltaC471), which contained a GP-PDE sequence identified in other GP-PDEs but lacked GroPCho phosphodiesterase activity, showed a similar inhibitory effect. Furthermore, transgenic mice specifically expressing GDE5DeltaC471 in skeletal muscle showed less skeletal muscle mass, especially type II fiber-rich muscle. These results indicate that GDE5 negatively regulates skeletal muscle development even without GroPCho phosphodiesterase activity, providing novel insight into the biological significance of mammalian GP-PDE function in a non-enzymatic mechanism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.