Abstract
The TRP (transient receptor potential) family of ion channels is a heterogeneous family of calcium permeable cation channels that is subdivided into seven subfamilies: TRPC (“Canonical”), TRPV (“Vanilloid”), TRPM (“Melastatin”), TRPA (“Ankyrin”), TRPN (“NOMPC”), TRPP (“Polycystin”), and TRPML (“Mucolipin”). TRP-mediated ion currents across the cell membrane are determined by the single channel conductance, by the fraction of activated channels, and by the total amount of TRP channels present at the plasma membrane. In many cases, the amount of TRP channels at the plasma membrane is altered in response to physiological stimuli by translocation of channels to and from the plasma membrane. Regulated translocation has been described for channels of the TRPC, TRPV, TRPM, and TRPA family and is achieved by vesicular transport of these channels along cellular exocytosis and endocytosis pathways. This review summarizes the stimuli and signalling cascades involved in the translocation of TRP channels and highlights interactions of TRP channels with proteins of the endocytosis and exocytosis machineries.
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Abbreviations
- 4α-PDD:
-
4α-phorbol 12,13-didecanoate
- AIP4:
-
atropine-1 interacting protein 4
- AMPA-receptor:
-
α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor
- ATP:
-
adenosine-triphosphate
- BAPTA:
-
1,2-bis(o-aminophenoxy) ethane-N,N,N’,N’-tetraacetic acid
- bFGF:
-
basic fibroblast growth factor
- cAMP:
-
cyclic adenosine-monophosphate
- CHO:
-
chinese hamster ovary
- DAG:
-
diacylglycerol
- DHPG:
-
3,5-dihydroxyphenylglycine
- EETs:
-
epoxyeicosatrienoic acids
- EGF:
-
epithelial growth factor
- (e)GFP:
-
(enhanced) green fluorescent protein
- ePKC:
-
eye specific protein kinase C
- ER:
-
endoplasmatic reticulum
- ERK:
-
extracellular-signal-regulated kinase
- fMLP:
-
formyl Met-Leu-Phe
- GTP:
-
guanosine-triphosphate
- HA-tag:
-
haemagglutinin tag
- HEK:
-
human embryonic kidney
- HPAEC:
-
human pulmonary artery endothelial cells
- Hrs:
-
hepatocyte growth factor regulated tyrosine kinase substrate
- IGF-1:
-
insulin-like growth factor 1
- IMCD:
-
inner medullary collecting duct
- INAD:
-
inactivation no afterpotential D
- IP3 :
-
inositol triphosphate
- IP3R:
-
inositol triphosphate receptor
- lysoPC:
-
lysophosphatidylcholine
- NCC:
-
thiazide-sensitive Na-Cl cotransporter
- NGF:
-
nerve growth factor
- NHERF:
-
Na/H exchanger regulatory factor
- OAG:
-
1-oleyl-2-acetyl-sn-glycerol
- OS-9:
-
osteosarcoma amplified 9
- PACS:
-
phosphofurin acidic cluster sorting protein
- PACSIN:
-
protein kinase C and casein kinase substrate in neurons
- PDGF:
-
platelet derived growth factor
- PI(3) kinase:
-
phosphatidylinositide 3 kinase
- PIP:
-
phosphatidylinositol 4-phosphate
- PIP2 :
-
phosphatidylinositol 4,5-bisphosphate
- PIP3 :
-
phosphatidylinositol 3,4,5-trisphosphate
- PKA:
-
protein kinase A
- PKC:
-
protein kinase C
- PKD:
-
polycystic kidney disease
- PLC:
-
phospholipase C
- PTH:
-
parathyroid hormone
- RGA:
-
recombination gene activator
- RNF24:
-
ring finger protein 24
- SGK:
-
serum and glucocorticoid inducible kinase
- SNAP:
-
soluble NSF attachment protein
- snapin:
-
synaptic vesicle-associated protein
- SNARE:
-
soluble NSF attachment protein receptors
- STAM:
-
signal transducing adaptor molecule
- TRP:
-
transient receptor potential
- TRPL:
-
transient receptor potential like
- VAMP2:
-
vesicle-associated membrane protein 2
- WNK:
-
with no K (lysine)
- YFP:
-
yellow fluorescent protein
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Acknowledgments
The authors are grateful to T. Oberacker, C. Oberegelsbacher, and O. Voolstra for helpful comments on the manuscript and to C. Oberegelsbacher for providing the data of Fig. 30.1. Research in the laboratory of the authors is supported by the Deutsche Forschungsgemeinschaft (Hu 839/2-5) and the German-Israeli-Foundation for Research and Development (I 1001-96.13/2008).
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Cerny, A.C., Huber, A. (2011). Regulation of TRP Signalling by Ion Channel Translocation Between Cell Compartments. In: Islam, M. (eds) Transient Receptor Potential Channels. Advances in Experimental Medicine and Biology, vol 704. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-0265-3_30
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