ArticlePloS one2015
Eps 15 Homology Domain (EHD)-1 Remodels Transverse Tubules in Skeletal Muscle.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- A Quarter Century of EHD Protein Research: From Endosomal Recycling to Ciliopathies.Traffic (Copenhagen, Denmark) · 2026Review
- Structures of EHD2 filaments on curved membranes provide a model for caveolar neck stabilization.Nature communications · 2026Article
- Plasma membrane invaginations and their diverse cellular functions.BMC biology · 2026Review
- The role of junctophilin proteins in cellular function.Physiological reviews · 2022Review
- Cellular functions and intrinsic attributes of the ATP-binding Eps15 homology domain-containing proteins.Protein science : a publication of the Protein Society · 2020Review
- Cardiomyocyte damage control in heart failure and the role of the sarcolemma.Journal of muscle research and cell motility · 2019Article
- Recombinant annexin A6 promotes membrane repair and protects against muscle injury.The Journal of clinical investigation · 2019Article
- Requirement of Pitx2 for skeletal muscle homeostasis.Developmental biology · 2019Article
- Role of the EHD Family of Endocytic Recycling Regulators for TCR Recycling and T Cell Function.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Post-Myocardial Infarction T-tubules Form Enlarged Branched Structures With Dysregulation of Junctophilin-2 and Bridging Integrator 1 (BIN-1).Journal of the American Heart Association · 2017Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
We previously showed that Eps15 homology domain-containing 1 (EHD1) interacts with ferlin proteins to regulate endocytic recycling. Myoblasts from Ehd1-null mice were found to have defective recycling, myoblast fusion, and consequently smaller muscles. When expressed in C2C12 cells, an ATPase dead-EHD1 was found to interfere with BIN1/amphiphysin 2. We now extended those findings by examining Ehd1-heterozygous mice since these mice survive to maturity in normal Mendelian numbers and provide a ready source of mature muscle. We found that heterozygosity of EHD1 was sufficient to produce ectopic and excessive T-tubules, including large intracellular aggregates that contained BIN1. The disorganized T-tubule structures in Ehd1-heterozygous muscle were accompanied by marked elevation of the T-tubule-associated protein DHPR and reduction of the triad linker protein junctophilin 2, reflecting defective triads. Consistent with this, Ehd1-heterozygous muscle had reduced force production. Introduction of ATPase dead-EHD1 into mature muscle fibers was sufficient to induce ectopic T-tubule formation, seen as large BIN1 positive structures throughout the muscle. Ehd1-heterozygous mice were found to have strikingly elevated serum creatine kinase and smaller myofibers, but did not display findings of muscular dystrophy. These data indicate that EHD1 regulates the maintenance of T-tubules through its interaction with BIN1 and links T-tubules defects with elevated creatine kinase and myopathy.
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Registered trials
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