ArticleNature communications2023
How myosin VI traps its off-state, is activated and dimerizes.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- GIPC1 governed ferroptosis by regulating DECR1-modulating lipid homeostasis during dilated cardiomyopathy (DCM).Cell death and differentiation · 2026Article
- The High-Altitude Adaptation Characteristics of Microbiota-Host Cross-Talk in Yak Gastrointestinal Track.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Global human myeloid replacement with peripheral progenitors induces interferonopathy and neurodegeneration.Research square · 2025Article
- Role of myosin heavy chain 9 in gastrointestinal tumorigenesis: A comprehensive review.World journal of gastrointestinal oncology · 2025Review
- Cardiolipin membranes drive Myosin VI activation, oligomerization, and processive cargo transport.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- How Omecamtiv Modulates Myosin Motion.Biochemistry · 2025Article
- Motor domain phosphorylation increases nucleotide exchange and turns MYO6 into a faster and stronger motor.Nature communications · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 4 institutions in 3 countries.
Funding
Abstract
Myosin VI (Myo6) is the only minus-end directed nanomotor on actin, allowing it to uniquely contribute to numerous cellular functions. As for other nanomotors, the proper functioning of Myo6 relies on precise spatiotemporal control of motor activity via a poorly defined off-state and interactions with partners. Our structural, functional, and cellular studies reveal key features of myosin regulation and indicate that not all partners can activate Myo6. TOM1 and Dab2 cannot bind the off-state, while GIPC1 binds Myo6, releases its auto-inhibition and triggers proximal dimerization. Myo6 partners thus differentially recruit Myo6. We solved a crystal structure of the proximal dimerization domain, and show that its disruption compromises endocytosis in HeLa cells, emphasizing the importance of Myo6 dimerization. Finally, we show that the L926Q deafness mutation disrupts Myo6 auto-inhibition and indirectly impairs proximal dimerization. Our study thus demonstrates the importance of partners in the control of Myo6 auto-inhibition, localization, and activation.
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What Socratic holds
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 Socratic graph.