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• W1993431922 endingPage "34" @default.
• W1993431922 startingPage "1744" @default.
• W1993431922 abstract "The transient receptor potential vanilloid type1 (TRPV1) is expressed in nociceptive sensory neurons and is sensitive to phosphorylation. A-Kinase Anchoring Protein 79/150 (AKAP150) mediates phosphorylation of TRPV1 by Protein Kinases A and C, modulating channel activity. However, few studies have focused on the regulatory mechanisms that control AKAP150 association with TRPV1. In the present study, we identify a role for calcium/calmodulin in controlling AKAP150 association with, and sensitization of, TRPV1.In trigeminal neurons, intracellular accumulation of calcium reduced AKAP150 association with TRPV1 in a manner sensitive to calmodulin antagonism. This was also observed in transfected Chinese hamster ovary (CHO) cells, providing a model for conducting molecular analysis of the association. In CHO cells, the deletion of the C-terminal calmodulin-binding site of TRPV1 resulted in greater association with AKAP150, and increased channel activity. Furthermore, the co-expression of wild-type calmodulin in CHOs significantly reduced TRPV1 association with AKAP150, as evidenced by total internal reflective fluorescence-fluorescence resonance energy transfer (TIRF-FRET) analysis and electrophysiology. Finally, dominant-negative calmodulin co-expression increased TRPV1 association with AKAP150 and increased basal and PKA-sensitized channel activity.the results from these studies indicate that calcium/calmodulin interferes with the association of AKAP150 with TRPV1, potentially extending resensitization of the channel." @default.
• W1993431922 created "2016-06-24" @default.
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• W1993431922 creator A5053535369 @default.
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• W1993431922 date "2011-01-01" @default.
• W1993431922 modified "2023-10-05" @default.
• W1993431922 title "AKAP150-Mediated TRPV1 Sensitization is Disrupted by Calcium/Calmodulin" @default.
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• W1993431922 doi "https://doi.org/10.1186/1744-8069-7-34" @default.
• W1993431922 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3113319" @default.
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