ArticleEuropean journal of translational myology2014
The Ubr2 Gene is Expressed in Skeletal Muscle Atrophying as a Result of Hind Limb Suspension, but not Merg1a Expression Alone.
Article in European journal of translational myology, 2014. 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, 18 citations in OpenAlex.
- UBR5: A New Player in Protein Quality Control for Skeletal Muscle Growth and Remodeling.Exercise and sport sciences reviews · 2025Review
- Population-scale gene-based analysis of whole-genome sequencing provides insights into metabolic health.Nature genetics · 2025Article
- ERG1A KScientific reports · 2025Article
- Relationship between DNA methylation changes and skeletal muscle mass.BMC genomic data · 2023Article
- The ERG1A KDiagnostics (Basel, Switzerland) · 2021Article
- Article
- A Key Role for the Ubiquitin Ligase UBR4 in Myofiber Hypertrophy in Drosophila and Mice.Cell reports · 2019Article
- Muscle spindles of the rat sternomastoid muscle.European journal of translational myology · 2018Article
- Chemotherapy-induced muscle wasting: an update.European journal of translational myology · 2018Article
- Revisiting the peculiar regional distribution of muscle fiber types in rat Sternomastoid Muscle.European journal of translational myology · 2018Article
- An innovative way to highlight the power of each polymorphism on elite athletes phenotype expression.European journal of translational myology · 2018Article
- Mobility disorders and pain, interrelations that need new research concepts and advanced clinical commitments.European journal of translational myology · 2017Article
- What Can be Learned from the Time Course of Changes in Low-Frequency Stimulated Muscle?European journal of translational myology · 2017Article
- 2017Spring PaduaMuscleDays, roots and byproducts.European journal of translational myology · 2017Article
- Chronically endurance-trained individuals preserve skeletal muscle mitochondrial gene expression with age but differences within age groups remain.Physiological reports · 2014Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Skeletal muscle (SKM) atrophy is a potentially debilitating condition induced by muscle disuse, denervation, many disease states, and aging. The ubiquitin proteasome pathway (UPP) contributes greatly to the protein loss suffered in muscle atrophy. The MERG1a K(+) channel is known to induce UPP activity and atrophy in SKM. It has been further demonstrated that the mouse ether-a-gogo-related gene (Merg)1a channel modulates expression of MURF1, an E3 ligase component of the UPP, while it does not affect expression of the UPP E3 ligase Mafbx/ATROGIN1. Because the UBR2 E3 ligase is known to participate in SKM atrophy, we have investigated the effect of Merg1a expression and hind limb suspension on Ubr2 expression. Here, we report that hind limb suspension results in a significant 25.6% decrease in mouse gastrocnemius muscle fiber cross sectional area (CSA) and that electro-transfer of Merg1a alone into gastrocnemius muscles yields a 15.3% decrease in CSA after 7 days. More interestingly, we discovered that hind limb suspension caused a significant 8-fold increase in Merg1a expression and a significant 4.7-fold increase in Ubr2 transcript after 4 days, while electro-transfer of Merg1a into gastrocnemius muscles resulted in a significant 6.2-fold increase in Merg1a transcript after 4 days but had no effect on Ubr2 expression. In summary, the MERG1a K(+) channel, known to induce atrophy and MURF1 E3 ligase expression, does not affect UBR2 E3 ligase transcript levels. Therefore, to date, the MERG1a channel's contribution to UPP activity appears mainly to be through up-regulation of Murf1 gene expression.
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