The DOI matches its Crossref record; 288 of the 288 references it cites were found in a registry or an index.
Protease-Activated Receptors: Contribution to Physiology and Disease
Abstract
Ossovskaya, Valeria S., and Nigel W. Bunnett. Protease-Activated Receptors: Contribution to Physiology and Disease. Physiol Rev 84: 579–621, 2004; 10.1152/physrev.00028.2003.—Proteases acting at the surface of cells generate and destroy receptor agonists and activate and inactivate receptors, thereby making a vitally important contribution to signal transduction. Certain serine proteases that derive from the circulation (e.g., coagulation factors), inflammatory cells (e.g., mast cell and neutrophil proteases), and from multiple other sources (e.g., epithelial cells, neurons, bacteria, fungi) can cleave protease-activated receptors (PARs), a family of four G protein-coupled receptors. Cleavage within the extracellular amino terminus exposes a tethered ligand domain, which binds to and activates the receptors to initiate multiple signaling cascades. Despite this irreversible mechanism of activation, signaling by PARs is efficiently terminated by receptor desensitization (receptor phosphorylation and uncoupling from G proteins) and downregulation (receptor degradation by cell-surface and lysosomal proteases). Protease signaling in tissues depends on the generation and release of proteases, availability of cofactors, presence of protease inhibitors, and activation and inactivation of PARs. Many proteases that activate PARs are produced during tissue damage, and PARs make important contributions to tissue responses to injury, including hemostasis, repair, cell survival, inflammation, and pain. Drugs that mimic or interfere with these processes are attractive therapies: selective agonists of PARs may facilitatehealing, repair, and protection, whereas protease inhibitors and PAR antagonists can impede exacerbated inflammation and pain. Major future challenges will be to understand the role of proteases and PARs in physiological control mechanisms and human diseases and to develop selective agonists and antagonists that can be used to probe function and treat disease.
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Cites
2 retracted
Uehara, A., Muramoto, K., Takada, H., & Sugawara, S. (2003) · The Journal of Immunology · doi:10.4049/jimmunol.170.11.5690 · Cited by 157
RetractedUehara, A., Sugawara, S., Muramoto, K., & Takada, H. (2002) · The Journal of Immunology · doi:10.4049/jimmunol.169.8.4594 · Cited by 88
RetractedThe capsaicin receptor: a heat-activated ion channel in the pain pathway
Caterina, M. J., Schumacher, M. A., Tominaga, M., Rosen, T. A., Levine, J. D., & Julius, D. (1997) · Nature · doi:10.1038/39807 · Cited by 9,107
Efficacy and Safety of Recombinant Human Activated Protein C for Severe Sepsis
Bernard, G. R., Vincent, J.-L., Laterre, P.-F., LaRosa, S. P., Dhainaut, J.-F., Lopez-Rodriguez, A., Steingrub, J. S., Garber, G. E., Helterbrand, J. D., Ely, E. W., et al. (2001) · New England Journal of Medicine · doi:10.1056/nejm200103083441001 · Cited by 6,132
Vu, T.-K. H., Hung, D. T., Wheaton, V. I., & Coughlin, S. R. (1991) · Cell · doi:10.1016/0092-8674(91)90261-v · Cited by 2,970
Mitogen-Activated Protein Kinase: Conservation of a Three-Kinase Module From Yeast to Human
WIDMANN, C., GIBSON, S., JARPE, M. B., & JOHNSON, G. L. (1999) · Physiological Reviews · doi:10.1152/physrev.1999.79.1.143 · Cited by 2,729
Molecular mechanisms of nociception
Julius, D., & Basbaum, A. I. (2001) · Nature · doi:10.1038/35093019 · Cited by 2,685 · cited 1×
“TRPV1 is a nonselective cation channel that is activated by protons, elevated temperature, and certain lipids, as well as by exogenous vanilloids such as capsaicin (37, 141).”
BackgroundThrombin signalling and protease-activated receptors
Coughlin, S. R. (2000) · Nature · doi:10.1038/35025229 · Cited by 2,482
Metcalfe, D. D., Baram, D., & Mekori, Y. A. (1997) · Physiological Reviews · doi:10.1152/physrev.1997.77.4.1033 · Cited by 1,724
Prenzel, N., Zwick, E., Daub, H., Leserer, M., Abraham, R., Wallasch, C., & Ullrich, A. (1999) · Nature · doi:10.1038/47260 · Cited by 1,504
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Kettenmann, H., Hanisch, U.-K., Noda, M., & Verkhratsky, A. (2011) · Physiological Reviews · doi:10.1152/physrev.00011.2010 · Cited by 3,547
Neutrophil Elastase, Proteinase 3, and Cathepsin G as Therapeutic Targets in Human Diseases
Korkmaz, B., Horwitz, M. S., Jenne, D. E., & Gauthier, F. (2010) · Pharmacological Reviews · doi:10.1124/pr.110.002733 · Cited by 870
Birder, L., & Andersson, K.-E. (2013) · Physiological Reviews · doi:10.1152/physrev.00030.2012 · Cited by 438
Frontiers in pruritus research: scratching the brain for more effective itch therapy
Paus, R. (2006) · Journal of Clinical Investigation · doi:10.1172/jci28553 · Cited by 373
Structure, function and pathophysiology of protease activated receptors
Adams, M. N., Ramachandran, R., Yau, M.-K., Suen, J. Y., Fairlie, D. P., Hollenberg, M. D., & Hooper, J. D. (2011) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2011.01.003 · Cited by 370
Metadata
- Authors
- OSSOVSKAYA, V. S., & BUNNETT, N. W.
- Venue
- Physiological Reviews
- Publisher
- American Physiological Society
- Published
- 2004-04
- Volume
- 84
- Issue
- 2
- Pages
- 579-621
- ISSN
- 0031-9333 (ISSN-L)
- 1522-1210
- OpenAlex
- W1963938486
- Cited by
- 1,078
- References
- 288
- FWCI
- 8.33
- Type
- journal article
- Language
- en
- Open access
- closed
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