ArticleJournal of muscle research and cell motility2005
Localization of myosin phosphatase target subunit and its mutants.
Article in Journal of muscle research and cell motility, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 32 citations in OpenAlex.
- Enhanced RHO-ROCK signaling is associated with CRELD2 production and fibroblast recruitment in cutaneous squamous cell carcinoma.Cytoskeleton (Hoboken, N.J.) · 2024Article
- Development and Application of an Optogenetic Manipulation System to Suppress Actomyosin Activity inInternational journal of molecular sciences · 2023Article
- Complex Transcriptional Profiles of theCells · 2022Article
- Optogenetic relaxation of actomyosin contractility uncovers mechanistic roles of cortical tension during cytokinesis.Nature communications · 2021Article
- TIMAP inhibits endothelial myosin light chain phosphatase by competing with MYPT1 for the catalytic protein phosphatase 1 subunit PP1cβ.The Journal of biological chemistry · 2019Article
- Article
- Diversity and plasticity in signaling pathways that regulate smooth muscle responsiveness: Paradigms and paradoxes for the myosin phosphatase, the master regulator of smooth muscle contraction.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2017Review
- Role of myosin light chain phosphatase in cardiac physiology and pathophysiology.Journal of molecular and cellular cardiology · 2016Review
- Inhibition of MLC20 phosphorylation downstream of Ca2+ and RhoA: A novel mechanism involving phosphorylation of myosin phosphatase interacting protein (M-RIP) by PKG and stimulation of MLC phosphatase activity.Cell biochemistry and biophysics · 2014Article
- Nuclear localization of CPI-17, a protein phosphatase-1 inhibitor protein, affects histone H3 phosphorylation and corresponds to proliferation of cancer and smooth muscle cells.Biochemical and biophysical research communications · 2013Article
- Myosin phosphatase is inactivated by caspase-3 cleavage and phosphorylation of myosin phosphatase targeting subunit 1 during apoptosis.Molecular biology of the cell · 2013Article
- Site-specific phosphorylation of protein phosphatase 1 regulatory subunit 12A stimulated or suppressed by insulin.Journal of proteomics · 2012Article
- LATS1/WARTS phosphorylates MYPT1 to counteract PLK1 and regulate mammalian mitotic progression.The Journal of cell biology · 2012Article
- Molecular characterization of myosin phosphatase in endothelium.Journal of cellular physiology · 2012Article
- Myosin phosphatase-targeting subunit 1 regulates mitosis by antagonizing polo-like kinase 1.Developmental cell · 2008Article
- Myosin phosphatase target subunit: Many roles in cell function.Biochemical and biophysical research communications · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Transient transfection of NIH3T3 cells with various constructs of myosin phosphatase target subunit (MYPT1) and GFP showed distinct cellular localizations. Constructs containing the N-terminal nuclear localization signals (NLS), i.e. full-length MYPT1 and N-terminal MYPT1 fragments, were concentrated in the nucleus. Full-length chicken and human MYPT1-GFP showed discrete nuclear foci. Deletion of the N-terminal NLS or use of central or C-terminal MYPT1 fragments did not show unique nuclear distributions (C-terminal NLS are present). Transient transfection of NIH3T3 cells (in the presence of serum) with full-length MYPT1-GFP caused a marked decrease in number of attached cells, an apparent block in the cell cycle prior to M phase and signs of increased apoptosis. Under conditions of serum starvation the unique nuclear localization of MYPT1-GFP was not found and there was no marked decrease in the number of attached cells (after 48 h). Stable transfection of HEK 293 cells with GFP-MYPT1 was obtained. MYPT1 and its N-terminal mutants bound to retinoblastoma protein (Rb), raising the possibility that Rb is implicated in the effects caused by overexpression of MYPT1.
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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.