Sandbox Reserved 1652: Difference between revisions

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'''Phosphorylation''' of the TRPV1 receptor leads to its sensitization.Phosphorylations occurs on multiple phosphorylation sites at both N-terminal and C-terminal sites of TRPV1 by [https://en.wikipedia.org/wiki/Kinase kinases]. Phosphorylations are either caused by '''PKC''' (IP3 signalling), by '''PKA''' (AMPc signalling) or by '''CamKII'''.<ref>K. W. Ho, N. J. Ward, et D. J. Calkins, « TRPV1: a stress response protein in the central nervous system », Am. J. Neurodegener. Dis., vol. 1, no 1, p. 1‑14, avr. 2012.</ref><ref name="Integrating TRPV1 Receptor Function with Capsaicin Psychophysics">.The phosphorylation of TRPV1 lead to an increase in the expression of TRPV1 at the membrane surface.<ref>K. W. Ho, N. J. Ward, et D. J. Calkins, « TRPV1: a stress response protein in the central nervous system », Am. J. Neurodegener. Dis., vol. 1, no 1, p. 1‑14, avr. 2012.</ref>. The phosphorylation of TRPV1 lead to an increase in the expression of TRPV1 at the membrane surface.<ref>K. W. Ho, N. J. Ward, et D. J. Calkins, « TRPV1: a stress response protein in the central nervous system », Am. J. Neurodegener. Dis., vol. 1, no 1, p. 1‑14, avr. 2012.</ref>. Moreover, phosphorylated TRPV1 would have a reduced channel opening threshold.<ref>G. Bhave et al., « Protein kinase C phosphorylation sensitizes but does not activate the capsaicin receptor transient receptor potential vanilloid 1 (TRPV1) », Proc. Natl. Acad. Sci., vol. 100, no 21, p. 12480‑12485, oct. 2003, doi: 10.1073/pnas.2032100100.</ref>. As a result phosphorylated TRPV1 are more responsive to agonist because they are '''overexpressed''' and because the same quantity of agonist leads to a better openings of ion channels.
'''Phosphorylation''' of the TRPV1 receptor leads to its sensitization.Phosphorylations occurs on multiple phosphorylation sites at both N-terminal and C-terminal sites of TRPV1 by [https://en.wikipedia.org/wiki/Kinase kinases]. Phosphorylations are either caused by '''PKC''' (IP3 signalling), by '''PKA''' (AMPc signalling) or by '''CamKII'''.<ref>K. W. Ho, N. J. Ward, et D. J. Calkins, « TRPV1: a stress response protein in the central nervous system », Am. J. Neurodegener. Dis., vol. 1, no 1, p. 1‑14, avr. 2012.</ref><ref name="Integrating TRPV1 Receptor Function with Capsaicin Psychophysics">.The phosphorylation of TRPV1 lead to an increase in the expression of TRPV1 at the membrane surface.<ref>K. W. Ho, N. J. Ward, et D. J. Calkins, « TRPV1: a stress response protein in the central nervous system », Am. J. Neurodegener. Dis., vol. 1, no 1, p. 1‑14, avr. 2012.</ref>. The phosphorylation of TRPV1 lead to an increase in the expression of TRPV1 at the membrane surface.<ref>K. W. Ho, N. J. Ward, et D. J. Calkins, « TRPV1: a stress response protein in the central nervous system », Am. J. Neurodegener. Dis., vol. 1, no 1, p. 1‑14, avr. 2012.</ref>. Moreover, phosphorylated TRPV1 would have a reduced channel opening threshold.<ref>G. Bhave et al., « Protein kinase C phosphorylation sensitizes but does not activate the capsaicin receptor transient receptor potential vanilloid 1 (TRPV1) », Proc. Natl. Acad. Sci., vol. 100, no 21, p. 12480‑12485, oct. 2003, doi: 10.1073/pnas.2032100100.</ref>. As a result phosphorylated TRPV1 are more responsive to agonist because they are '''overexpressed''' and because the same quantity of agonist leads to a better openings of ion channels.
PKA phosphorylates T370, PKC and CaMKII phosphorylate <scene name='86/868185/Ser502_thr704/1'>S502 and T704</scene>  
PKA phosphorylates <scene name='86/868185/S502_t370/1'>T370 and S502</scene>, PKC and CaMKII phosphorylate <scene name='86/868185/Ser502_thr704/1'>S502 and T704</scene>  


====Desensitization====
====Desensitization====