ArticleProceedings of the National Academy of Sciences of the United States of America2000
Creatine kinase, an ATP-generating enzyme, is required for thrombin receptor signaling to the cytoskeleton.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 79 citations in OpenAlex.
- Protease-activated receptors act as a liaison between metabolism and inflammation.Inflammopharmacology · 2026Review
- CKB inhibits epithelial-mesenchymal transition and prostate cancer progression by sequestering and inhibiting AKT activation.Neoplasia (New York, N.Y.) · 2021Article
- Coagulation Signaling through PAR1 as a Therapeutic Target in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2021Review
- Metabolic Basis of Creatine in Health and Disease: A Bioinformatics-Assisted Review.Nutrients · 2021Review
- The bioenergetics of neuronal morphogenesis and regeneration: Frontiers beyond the mitochondrion.Developmental neurobiology · 2020Review
- Gonadotropin regulation of ankyrin-repeat and SOCS-box protein 9 (ASB9) in ovarian follicles and identification of binding partners.PloS one · 2019Article
- Review
- Creatine kinase in ischemic and inflammatory disorders.Clinical and translational medicine · 2016Review
- Protease-activated receptors (PARs)--biology and role in cancer invasion and metastasis.Cancer metastasis reviews · 2015Review
- Article
- Energy dysfunction in Huntington's disease: insights from PGC-1α, AMPK, and CKB.Cellular and molecular life sciences : CMLS · 2012Review
- A novel unbiased proteomic approach to detect the reactivity of cerebrospinal fluid in neurological diseases.Molecular & cellular proteomics : MCP · 2011Article
- Proteomic changes in the heart of diet-induced pre-diabetic mice.Journal of proteomics · 2011Article
- RANKL up-regulates brain-type creatine kinase via poly(ADP-ribose) polymerase-1 during osteoclastogenesis.The Journal of biological chemistry · 2010Article
- Monoclonal antibody 4C5 prevents activation of MMP2 and MMP9 by disrupting their interaction with extracellular HSP90 and inhibits formation of metastatic breast cancer cell deposits.BMC cell biology · 2010Article
- Signal transduction by protease-activated receptors.British journal of pharmacology · 2010Review
- Zyxin is involved in thrombin signaling via interaction with PAR-1 receptor.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Article
- Involvement of creatine kinase B in hepatitis C virus genome replication through interaction with the viral NS4A protein.Journal of virology · 2009Article
- Adenylate kinase and AMP signaling networks: metabolic monitoring, signal communication and body energy sensing.International journal of molecular sciences · 2009Review
- Article
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 2 institutions in 1 country.
Funding
Abstract
Thrombin orchestrates cellular events after injury to the vascular system and extravasation of blood into surrounding tissues. The pathophysiological response to thrombin is mediated by protease-activated receptor-1 (PAR-1), a seven-transmembrane G protein-coupled receptor expressed in the nervous system that is identical to the thrombin receptor in platelets, fibroblasts, and endothelial cells. Once activated by thrombin, PAR-1 induces rapid and dramatic changes in cell morphology, notably the retraction of growth cones, axons, and dendrites in neurons and processes in astrocytes. The signal is conveyed by a series of localized ATP-dependent reactions directed to the actin cytoskeleton. How cells meet the dynamic and localized energy demands during signal transmission is unknown. Using the yeast two-hybrid system, we identified an interaction between PAR-1 cytoplasmic tail and the brain isoform of creatine kinase, a key ATP-generating enzyme that regulates ATP within subcellular compartments. The interaction was confirmed in vitro and in vivo. Reducing creatine kinase levels or its ATP-generating potential inhibited PAR-1-mediated cellular shape changes as well as a PAR-1 signaling pathway involving the activation of RhoA, a small G protein that relays signals to the cytoskeleton. Thrombin-stimulated intracellular calcium release was not affected. Our results suggest that creatine kinase is bound to PAR-1 where it may be poised to provide bursts of site-specific high-energy phosphate necessary for efficient receptor signal transduction during cytoskeletal reorganization.
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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.