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TRP-Mediated Cytoskeletal Reorganization: Implications for Disease and Drug Development

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TRP Channels in Drug Discovery

Part of the book series: Methods in Pharmacology and Toxicology ((MIPT))

Abstract

So far the major focus of Transient Receptor Potential (TRP) channels in the context of pathophysiological disorders was centered exclusively on the ionic conductivity mediated by these channels. However, recently the importance of non-ionic functions of TRP channels in different pathophysiological disorders has emerged. Recently several physical and functional interactions of TRP channels with cytoskeletal components have been characterized. These interactions play important roles in executing the non-ionic functions and regulations of TRP channels per se. In the membranous environment, TRP channels form dynamic signaling complexes that include components like microtubule and actin cytoskeleton, other scaffolding and key regulatory components. TRP channels can also regulate the integrity and dynamics of different cytoskeletal systems in complex manner. In many cases, these regulations seem to be independent of Ca2+ influx mediated by these channels and thus have immense significance in the context of pathophysiological disorders. In this review, I highlight the importance of TRP channel interactions and multi-directional regulations with cytoskeletal components in detail. This aspect opens up new avenues to target TRP signaling complexes by pharmacological manners. The strategies to target TRP complexes rather than targeting TRP channel solely might be useful for several clinical purposes.

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Abbreviations

4aPDD:

4a-phorbol-didecanoate

CIRB domain:

Calmodulin- and IP3R-binding region

CMT2:

Charcot–Marie-Tooth disease type 2

DRG neurons:

Dorsal root ganglion neurons

eGFP:

Enhanced green fluorescence protein

EGTA:

Ethylene glycol tetraacetic acid

FRET:

Fluorescence Resonance Energy Transfer

5’I-RTX:

5’-iodoresiniferatoxin

HUVEC:

Human umbilical vein endothelial cell

TRP Channels:

Transient receptor potential channels

PC2:

Polycystin-2

TRPN:

NomPC-like TRP channel

TRPC:

Transient receptor potential canonical

TRPML:

Transient receptor potential mucolipin

MAPs:

Microtubule-associated proteins

MBP:

Maltose-binding protein

NF200:

Neurofilament heavy chain 200 KDa

OAG:

1-oleoyl-2-acetyl-sn-glycerol

PKC:

Protein kinase C

PKD:

Polycystic kidney disease

PKCe:

Protein kinase Ce sub type

RTX:

Resiniferatoxin

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Acknowledgement

This review reflects the views and interpretation of the data available in the literature. The author regrets for not being able to include all the scientific works due to space limitations. The author acknowledges the support and intellectual inputs from Mr. Rakesh Majhi and other lab members. CG acknowledges the support previously obtained from Freie University of Berlin and Max Planck Institute of Molecular Genetics, Berlin. Financial support from NISER, Bhubaneswar is appreciated.

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  1. Institute of Physics, National Institute of Science Education and Research, Bhubaneswar, Orissa, India

    Chandan Goswami

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  1. Chandan Goswami
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Correspondence to Chandan Goswami .

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  1. , Transfusion Services, Monmouth Medical Center, Second Avenue 300, Long Branch, 07740, New Jersey, USA

    Arpad Szallasi

  2. Medical and Health Science Center, Department of Physiology, University of Debrecen, Nagyerdei Krt. 98, Debrecen, 4032, Hungary

    Tamás Bíró

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Goswami, C. (2012). TRP-Mediated Cytoskeletal Reorganization: Implications for Disease and Drug Development. In: Szallasi, A., Bíró, T. (eds) TRP Channels in Drug Discovery. Methods in Pharmacology and Toxicology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-62703-077-9_2

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  • DOI: https://doi.org/10.1007/978-1-62703-077-9_2

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