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CA2 — TRPV1

Text-mined interactions from Literome

Tóth et al., Biochem Biophys Res Commun 2002 : However, 45Ca2+ uptake was not detected after thapsigargin treatment, indicating that the emptying of the thapsigargin sensitive intracellular pools of Ca2+ was responsible for the elevated [Ca2+ ] i level rather than the activation of VR-1
Liu et al., J Biol Chem 2003 : Versatile regulation of cytosolic Ca2+ by vanilloid receptor I in rat dorsal root ganglion neurons
Hermann et al., Cell Mol Life Sci 2003 : In this study, we over expressed both receptor types in human embryonic kidney (HEK)-293 cells and investigated the effect of the CB1 agonist HU-210 on the VR1 mediated increase in intracellular Ca2+ ( [ Ca2+ ] i ), a well-known response of the prototypical VR1 agonist capsaicin ... The endogenous agonist of CB1 and VR1 receptors, anandamide, was more efficacious in inducing a VR1 mediated stimulation of [ Ca2+ ] i in CB1-VR1-HEK cells than in VR1-HEK cells, and part of its effect on the former cells was blocked by SR141716A ( 0.5 microM )
Numazaki et al., Proc Natl Acad Sci U S A 2003 : Extracellular Ca2+ dependent desensitization of TRPV1 observed in patch-clamp experiments when using both heterologous expression systems and native sensory ganglia is thought to be one mechanism underlying the paradoxical effectiveness of capsaicin as an analgesic therapy
Kárai et al., J Biol Chem 2004 (Calcium Signaling) : Vanilloid receptor 1 regulates multiple calcium compartments and contributes to Ca2+ induced Ca2+ release in sensory neurons
Amadesi et al., J Neurosci 2004 (Hyperalgesia) : Inhibitors of phospholipase C and protein kinase C ( PKC ) suppressed PAR2 induced sensitization of TRPV1 mediated changes in [Ca2+ ] i and TRPV1 currents
Tominaga et al., Novartis Found Symp 2004 (Inflammation...) : We found that disruption of the calmodulin binding segment prevented TRPV1 desensitization even in the presence of extracellular Ca2+
Mohapatra et al., J Biol Chem 2005 : We conclude that Ca2+ dependent desensitization of TRPV1 might be in part regulated through channel dephosphorylation by calcineurin and channel phosphorylation by PKA possibly involving Thr370 as a key amino acid residue
Vetter et al., Molecular pain 2006 : TRPV1 mediated Ca2+ responses potentiated by the direct PKA activator 8-Br-cAMP and the PKC activator Phorbol-12-myristate-13-acetatewere not modulated by morphine
Lukacs et al., J Neurosci 2007 (Calcium Signaling...) : The PLC inhibitor U73122 and dialysis of PtdIns ( 4,5 ) P2 or PtdIns ( 4 ) P through the patch pipette inhibited desensitization of TRPV1, indicating that Ca2+ induced activation of PLC contributes to desensitization of TRPV1 by depletion of PtdIns ( 4,5 ) P2 and PtdIns ( 4 ) P. Selective conversion of PtdIns ( 4,5 ) P2 to PtdIns ( 4 ) P by a rapamycin-inducible PIP2 5-phosphatase did not inhibit TRPV1 at high capsaicin concentrations, suggesting a significant role for PtdIns ( 4 ) P in maintaining channel activity
Jeske et al., Pain 2008 (Hyperalgesia) : In CHO cells, the PKA RII binding site on AKAP was necessary for PKA enhancement of TRPV1 mediated Ca2+-accumulation