TRP Channels as Therapeutic Targets: From Basic Science to by Arpad Szallasi

By Arpad Szallasi

TRP Channels as healing goals: From uncomplicated technological know-how to scientific Use is authored via specialists throughout academia and undefined, offering readers with a whole photograph of the healing power and demanding situations linked to utilizing TRP channels as drug pursuits.

This booklet deals a special medical process by way of overlaying compounds that focus on TRP channels in pre-clinical and medical stages, additionally delivering a dialogue of TRP channels as biomarkers.

An complete part is dedicated to the unconventional and cutting edge makes use of of those channels throughout various illnesses, providing options that may be used to beat the antagonistic results of first new release TRPV1 antagonists.

Intended for all researchers and clinicians operating towards the improvement of winning medicinal drugs concentrating on TRP channels, this booklet is a necessary source chocked filled with the newest scientific information and findings.

  • Contains finished assurance of TRP channels as healing objectives, from rising scientific symptoms to accomplished medical trials
  • Discusses TRP channels as confirmed goals, starting from weight problems and diabetes via melanoma and breathing issues, kidney illnesses, high blood pressure, neurodegenerative problems, and more
  • Provides severe research of the issues and unwanted side effects that experience surfaced in the course of medical trials, providing evidence-based feedback for overcoming them

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Am J Hum Genet 2009;84:307–15. [78] Camacho N, Krakow D, Johnykutty S, Katzman PJ, Pepkowitz S, Vriens J, et al. Dominant TRPV4 mutations in nonlethal and lethal metatropic dysplasia. Am J Med Genet A 2010;152A:1169–77. [79] Unger S, Lausch E, Stanzial F, Gillessen-Kaesbach G, Stefanova I, Di Stefano CM, et al. Fetal akinesia in metatropic dysplasia: the combined phenotype of chondrodysplasia and neuropathy? Am J Med Genet A 2011;155A:2860–4. [80] Lamande SR, Yuan Y, Gresshoff IL, Rowley L, Belluoccio D, Kaluarachchi K, et al.

Whole genome SNP genotyping and exome sequencing reveal novel genetic variants and putative causative genes in congenital hyperinsulinism. PLoS One 2013;8:e68740. [75] Rock MJ, Prenen J, Funari VA, Funari TL, Merriman B, Nelson SF, et al. Gain-of-function mutations in TRPV4 cause autosomal dominant brachyolmia. Nat Genet 2008;40:999–1003. [76] Nishimura G, Dai J, Lausch E, Unger S, Megarbane A, Kitoh H, et al. Spondylo-epiphyseal dysplasia, Maroteaux type (pseudo-Morquio syndrome type 2), and parastremmatic dysplasia are caused by TRPV4 mutations.

132] Liu H, El Zein L, Kruse M, Guinamard R, Beckmann A, Bozio A, et al. Gain-of-function mutations in TRPM4 cause autosomal dominant isolated cardiac conduction disease. Circ Cardiovasc Genet 2010;3:374–85. [133] Stallmeyer B, Zumhagen S, Denjoy I, Duthoit G, Hebert JL, Ferrer X, et al. Mutational spectrum in the Ca(2+) activated cation channel gene TRPM4 in patients with cardiac conductance disturbances. Hum Mutat 2012;33:109–17. [134] Folgering JH, Sharif-Naeini R, Dedman A, Patel A, Delmas P, Honore E.

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