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Books on the topic 'TRPA1'

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Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

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1

Gomtsyan, Arthur, and Connie R. Faltynek, eds. Vanilloid Receptor TRPV1 in Drug Discovery. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470588284.

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2

Malmberg, Annika B., and Keith R. Bley, eds. Turning up the Heat on Pain: TRPV1 Receptors in Pain and Inflammation. Basel: Birkhäuser Basel, 2005. http://dx.doi.org/10.1007/3-7643-7379-2.

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3

Gomtsyan, Arthur. Vanilloid receptor TRPV1 in drug discovery: Targeting pain and other pathological disorders. Hoboken, N.J: Wiley, 2010.

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4

Gomtsyan, Arthur. Vanilloid receptor TRPV1 in drug discovery: Targeting pain and other pathological disorders. Hoboken, N.J: Wiley, 2010.

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5

Gomtsyan, Arthur, and Connie R. Faltynek. Vanilloid Receptor Trpv1 in Drug Discovery. Wiley & Sons, Incorporated, John, 2010.

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6

Sprague, Jared Michael. TRPV1 Sensitization in Primary Sensory Neurons. 2014.

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7

Li, Albert Steven. Structural studies of TRPV1 activation by capsaicin. 2009.

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8

Nagy, Istvan. VR1 in inflammatory thermal hyperalgesia. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0028.

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The landmark paper discussed in this chapter, published by Davis et al. in 2000, describes the role of the capsaicin receptor, which is called transient receptor potential cation channel subfamily vanilloid member 1 (TRPV1), in inflammatory thermal hyperalgesia. Capsaicin, the pungent agent found in hot peppers, has been linked to pain for centuries because it induces a burning pain sensation which, after prolonged application of the agent, turns into analgesia. Because of this, capsaicin has been used to relieve pain, most likely since prehistoric times. The elucidation of the role of TRPV1 in nociceptive processing was heralded as the starting point for the development of agents which would revolutionize pain management. Unfortunately, that promise is yet to be realized and apparently we need a more detailed understanding of the role of TRPV1 in physiological and pathological processes in order to fulfil the analgesic potential of drugs acting on this receptor.

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9

TRP01 - Royal Conservatory Technical Requirements for Piano Level 1 2015 Edition. The Frederick Harris Music Company, 2015.

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10

Vanilloid receptor TRPV1 in drug discovery: Targeting pain and other pathological disorders. Hoboken, N.J: Wiley, 2010.

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11

Gomtsyan, Arthur, and Connie R. Faltynek. Vanilloid Receptor TRPV1 in Drug Discovery: Targeting Pain and Other Pathological Disorders. Wiley & Sons, Incorporated, John, 2010.

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12

Annika B. Malmberg,Keith R. Bley. Turning Up the Heat on Pain: Trpv1 Receptors in Pain and Inflammation. Springer, 2008.

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13

Malmberg, Annika B., and Keith R. Bley. Turning up the Heat on Pain: TRPV1 Receptors in Pain and Inflammation. Springer London, Limited, 2005.

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14

(Editor), Annika B. Malmberg, and Keith R. Bley (Editor), eds. Turning up the Heat on Pain: TRPV1 Receptors in Pain and Inflammation (Progress in Inflammation Research). Birkhäuser Basel, 2005.

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15

MacGregor, Alex, Ana Valdes, and Frances M. K. Williams. Genetics of osteoarthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0044.

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In this chapter we outline the approaches which have been adopted to identify genetic variants predisposing to osteoarthritis (OA), a condition long recognized as having a heritable component. Such routes to their identification include examining mendelian traits in which OA is a feature, candidate gene studies based on knowledge of OA pathobiology, linkage analysis in related individuals, and, more recently, genome-wide association studies in large samples of unrelated individuals. It is increasingly evident that the main symptom deriving from OA—notably joint pain—also has a genetic basis but this is differs from that underlying OA. Variants convincingly shown to predispose to OA lie in the GDF5 and MCF2L genes and in the chr7 cluster mapping to the COG5 gene, in addition to the ASPN gene in Asian populations. Those associated with pain in OA include TRPV1 and PACE4. Epigenetic influences are also being explored in both the pathogenesis of OA and the variation of pain processing.

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