ArticleThe Journal of cell biology2012
Myo1c facilitates G-actin transport to the leading edge of migrating endothelial cells.
Article in The Journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 60 citations in OpenAlex.
- Liraglutide Promotes Diabetic Wound Healing via Myo1c/Dock5.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Myosin-1C augments endothelial secretion of von Willebrand factor by linking contractile actomyosin machinery to the plasma membrane.Blood advances · 2024Article
- A noncanonical E3 ubiquitin ligase RNF41-mediated MYO1C stability promotes prostate cancer metastasis by inducing actin remodeling.Oncogene · 2024Article
- G-actin diffusion is insufficient to achieve F-actin assembly in fast-treadmilling protrusions.Biophysical journal · 2023Article
- Manipulation of microvillar proteins duringFrontiers in cellular and infection microbiology · 2023Article
- SMOC2 promotes aggressive behavior of fibroblast-like synoviocytes in rheumatoid arthritis through transcriptional and post-transcriptional regulating MYO1C.Cell death & disease · 2022Article
- Class I Myosins, molecular motors involved in cell migration and cancer.Cell adhesion & migration · 2022Article
- Responsible Genes for Neuronal Migration in the Chromosome 17p13.3: BeyondBrain sciences · 2021Review
- SH3BGRL3 binds to myosin 1c in a calcium dependent manner and modulates migration in the MDA-MB-231 cell line.BMC molecular and cell biology · 2021Article
- Mechanoresponsive metabolism in cancer cell migration and metastasis.Cell metabolism · 2021Review
- Targeting myosin 1c inhibits murine hepatic fibrogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2021Article
- Loss of Motor Protein MYO1C Causes Rhodopsin Mislocalization and Results in Impaired Visual Function.Cells · 2021Article
- Myosins, an Underestimated Player in the Infectious Cycle of Pathogenic Bacteria.International journal of molecular sciences · 2021Review
- Downregulation of MYO1C mediated by cepharanthine inhibits autophagosome-lysosome fusion through blockade of the F-actin network.Journal of experimental & clinical cancer research : CR · 2019Article
- The motor protein Myo1c regulates transforming growth factor-β-signaling and fibrosis in podocytes.Kidney international · 2019Article
- Reconsidering an active role for G-actin in cytoskeletal regulation.Journal of cell science · 2018Review
- The fungal myosin I is essential for Fusarium toxisome formation.PLoS pathogens · 2018Article
- Rho Kinase Regulates Aortic Vascular Smooth Muscle Cell Stiffness Via Actin/SRF/Myocardin in Hypertension.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2017Article
- Model of turnover kinetics in the lamellipodium: implications of slow- and fast- diffusing capping protein and Arp2/3 complex.Physical biology · 2016Article
- G-actin guides p53 nuclear transport: potential contribution of monomeric actin in altered localization of mutant p53.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Addition of actin monomer (G-actin) to growing actin filaments (F-actin) at the leading edge generates force for cell locomotion. The polymerization reaction and its regulation have been studied in depth. However, the mechanism responsible for transport of G-actin substrate to the cell front is largely unknown; random diffusion, facilitated transport via myosin II contraction, local synthesis as a result of messenger ribonucleic acid localization, or F-actin turnover all might contribute. By tracking a photoactivatable, nonpolymerizable actin mutant, we show vectorial transport of G-actin in live migrating endothelial cells (ECs). Mass spectrometric analysis identified Myo1c, an unconventional F-actin-binding motor protein, as a major G-actin-interacting protein. The cargo-binding tail domain of Myo1c interacted with G-actin, and the motor domain was required for the transport. Local microinjection of Myo1c promoted G-actin accumulation and plasma membrane ruffling, and Myo1c knockdown confirmed its contribution to G-actin delivery to the leading edge and for cell motility. In addition, there is no obvious requirement for myosin II contractile-based transport of G-actin in ECs. Thus, Myo1c-facilitated G-actin transport might be a critical node for control of cell polarity and motility.
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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.