Transient receptor potential proteins

Helliwell RM, Large WA 1997 Alphal-adrenoceptor activation of a non-selective cation current in rabbit portal vein by 1,2-diacyl-sn-glycerol. J Physiol 499 417-428 Hofmann F, Lacinova L, Klugbauer N 1999 Voltage-dependent calcium channels from structure to function. Rev Physiol Biochem Pharmacol 139 33—87 Hofmann T, Schaefer M, Schultz G, Gundermann T 2000 Transient receptor potential channels as molecular substrates of receptor-mediated cation entry. J Mol Med 78 14—25 Inoue R, Okada T, Onoue H et al 2001 The transient receptor potential protein homologue TRP6 is the essential component of vascular aj-adrenoceptor-activated Ca2+-permeable cation channel. Circ Res 88 325—332... 

Okada T, Inoue R, Yamazaki K et al 1999 Molecular and functional characterization of a novel mouse transient receptor potential protein homologue TRP7. Ca2+-permeable cation channel that is constitutively activated and enhanced by stimulation of G protein-coupled receptor. J Biol Chem 274 27359-27370... 

Abbreviations CT, Chorda tympani CTX, Bilateral transection of the chorda tympani nerve DRK, Delayed-rectifying potassium FFA, Free fatty acid GL, Glossopharyngeal GLX, Bilateral transection of the glossopharyngeal nerve GPCR, G-protein-coupled receptor LCFA, Long-chain fatty acid PROP, 6-n-Propylthiouracil PTK, Protein tyrosine kinase PUFA, Polyunsaturated fatty acid NST, Nucleus of the solitary tract TG, Triglyceride TRC, Taste receptor cells TRPM5, Transient receptor potential protein 5... 

A superfamily of cation channels conserved in mammals, flies, worms and yeast. The various TRP-proteins bear-sequence and predicted structural similarities to the founding member of this superfamily, transient receptor-potential (TRP), a light activated cation channel in the Dmsophila photoreceptor. 

The molecules that transduce noxious heat or cold are members of the transient receptor potential (TRP) receptor family. TRP proteins (Table 57-2) form tetra-meric nonselective cation channels within the plasma membrane, allowing sodium and calcium ion influx [4]. The TRPV3 channel is activated at temperatures between 31 and39°C, TRPV1 at43°C, and TRPV2 at 52-55°C. The heat pain threshold in humans is 43°C, suggesting that... 

The molecular entities of VOCCs have been well characterized. Ten distinct genes have so far been cloned, six of which have been identified in smooth muscle (Hofmann et al 1999, Ertel et al 2000). In contrast, the molecular counterparts of ROCCs and CCE have long been elusive, due probably to the lack of specific ligands/blockers and the presence of complex entangled regulatory mechanisms. The transient receptor potential (TRP) protein gene... 

Abstract The transient receptor potential (TRP) channels are a large family of proteins with... 

The carboxyl-terminal 469 amino acids of NompC resemble a class of ion channel proteins called TRP (transient receptor potential) channels. This region includes six putative transmembrane helices with a porelike region between the fifth and sixth helices. The amino-terminal 1150 amino acids consist almost exclusively of 29 ankyrin repeats (Figure 32.35). Ankyrin repeats are structural motifs formed by 33 amino acids folded into a hairpin loop followed by a helix-tum-helix. Importantly, in other proteins, regions with tandem arrays of these motifs mediate protein-protein interactions, suggesting that these arrays couple the motions of other proteins to the activity of the NompC channel. 

Fig. 2 The bitter taste signal transduction cascade. Bitter taste receptors are G-protein-coupled receptors. Activation of TAS2Rs results in the activation of the heterotrimeric G-protein complex a-gustducin (a-gust), 3 or pi, and yl3. The Py-subunits activate phospholipase C P2, (PLCj52) resulting in the production of inositol 1,4,5-trisphosphate (/P3). The IP3-mediated increase of intracellular calcium activates transient receptor potential channel 5 (TRPM5)...

Calcium ions are mostly present in bones or chelated to biological molecules. In blood plasma, only 1% of the calcium ions present are unbound 78% is bound to albumin, 8% to citrate, and 13% to other plasma proteins. The free calcium ions are prevented from precipitating by plasma pyrophosphate. Calcium ions are also stored in the endoplasmic reticulum (ER), mostly chelated to ER-resident proteins and phosphatidylser-ine. Free calcium ions may be released through transient receptor potential channels to the cytosol where it activates numerous physiological processes. If the free calcium ion concentration of blood plasma falls, parathyroid hormone (PTH) is secreted by the parathyroid gland cells. PTH speeds up the transport of demineralized bone products by osteoclasts. In the kidney, it increases the excretion of phosphate and decreases the excretion of calcium. PTH also acts on kidney cells to make calcitriol from vitamin D, which induces calcium transporters in the intestine and osteoclasts. PTH mediates these effects by activating G-protein-coupled receptors in the kidney and osteoclasts. 

Vitamin D is a fat soluble vitamin related to cholesterol. In the skin, sunlight spontaneously oxidizes cholesterol to 7-dehydrocholesterol. 7-Dehydrocholesterol spontaneously isomerizes to cholecalciferol (vitamin D3), which is oxidized in the liver to 25-hydroxy cholecalciferol and, under the influence of PTH in the kidney, to 1,25-dihy-droxy cholecalciferol (calcitriol), the active form of vitamin D. Vitamin D induces the expression of calcium ion transport proteins (calbindins) in intestinal epithelium, osteoclasts, and osteoblasts. Calbindins and transient receptor potential channels (TRPV) are responsible for the uptake of calcium from the diet. In children, the absence of sunlight provokes a deficiency of vitamin D, causing an absence of calbindins and inadequate blood calcium levels. Osteoid tissue cannot calcify, causing skeletal deformities (rickets). In the elderly, there is a loss of intestinal TRPV receptors and decreased calbindin expression by vitamin D. In both cases, the resultant low blood calcium levels cause poor mineralization during bone remodeling (osteomalacia). Rickets is the childhood expression of osteomalacia. Osteoclast activity is normal but the bone does not properly mineralize. In osteoporosis, the bone is properly mineralized but osteoclasts are overly active. 

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