ReviewBiology2022
Does the Actin Network Architecture Leverage Myosin-I Functions?
Review in Biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
6 citing papers in PubMed, 7 citations in OpenAlex.
- Myosin Class I Genes Follow a Cell Type-Specific Transcription Pattern in Human Haematopoietic Cell Lines.International journal of molecular sciences · 2026Article
- Conserved Phosphorylation of the Myosin1e TH1 Domain Impacts Membrane Association and Function in Yeast and Worms.Cytoskeleton (Hoboken, N.J.) · 2025Article
- MLC2: Physiological Functions and Potential Roles in Tumorigenesis.Cell biochemistry and biophysics · 2025Review
- Actin-dependent α-catenin oligomerization contributes to adherens junction assembly.Nature communications · 2025Article
- Characterization of early and late events of adherens junction assembly.bioRxiv : the preprint server for biology · 2024Article
- Discovery of the first unconventional myosin:Frontiers in physiology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The actin cytoskeleton plays crucial roles in cell morphogenesis and functions. The main partners of cortical actin are molecular motors of the myosin superfamily. Although our understanding of myosin functions is heavily based on myosin-II and its ability to dimerize, the largest and most ancient class is represented by myosin-I. Class 1 myosins are monomeric, actin-based motors that regulate a wide spectrum of functions, and whose dysregulation mediates multiple human diseases. We highlight the current challenges in identifying the "pantograph" for myosin-I motors: we need to reveal how conformational changes of myosin-I motors lead to diverse cellular as well as multicellular phenotypes. We review several mechanisms for scaling, and focus on the (re-) emerging function of class 1 myosins to remodel the actin network architecture, a higher-order dynamic scaffold that has potential to leverage molecular myosin-I functions. Undoubtfully, understanding the molecular functions of myosin-I motors will reveal unexpected stories about its big partner, the dynamic actin cytoskeleton.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.