IndraLab

Statements


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"In tsA-201 cells, expression of N-type channels with human ORL1 resulted in a voltage-dependent G-protein inhibition of the channel that occurred in the absence of nociceptin, the ORL1 receptor agonist."

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"In 5 out of 10 nociceptin-responsive cells tested, I Ba inhibited by nociceptin was facilitated by the prepulse and exhibited slowed activation kinetics, another hallmark o[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"G protein (Gβγ)-mediated voltage-dependent inhibition of N- and P/Q-type Ca 2+ channels contributes to presynaptic inhibition and short-term synaptic plasticity."

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"In this manuscript we have narrowly focused on the contribution of individual amino acids in the Ca v 2.2 I-II linker region to voltage dependent G protein inhibition of the channel."

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"Direct interaction with the β subunit of the heterotrimeric G protein complex causes voltage-dependent inhibition of N-type calcium channels."

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"To articulate the specific scope of the experiments and results, we first review the “willing-reluctant” model of voltage-dependent G-protein inhibition of neuronal calcium channels ( xref ; xref ), a leading mechanistic framework for rationalizing the key functional features of this form of modulation."

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"These alterations in kinetics may help explain the apparent reduced voltage-dependent inhibition by G proteins of the Ca V 2.1 mutant channels."

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"A leading mechanistic framework for such modulation is the “willing-reluctant” model of voltage-dependent G-protein inhibition ( xref ; xref )."

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"Ifproven to be correct, voltage-dependent G-protein inhibition would represent one ofthe rare instances ofion channel modulation bychanges inpermeation as well as in gating (Chen and Huang, 1992)."

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"Reconstitution of Voltage-dependent G-Protein Inhibition of N- and P/Q-type Calcium Channels."

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"From our data it is apparent that either alpha 1A or alpha 1B Ca2+ channels expressed alone are sufficient for voltage-dependent G protein inhibition. alpha 1C Ca2+ channels expressed alone do not exhibit the G protein inhibition seen in alpha 1A and alpha 1B channels."

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"In COS-7 cells, G protein inhibition of N-type Ca 2+ channels was markedly enhanced by coexpressed Ca v βs [ xref ]; in tsA-201 cells, a point mutation in the AID of Ca v 2.2 (W391A) that disrupted Ca v β binding abolished voltage-dependent G protein inhibition [ xref ]."

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"These include reports that the α 1B N-terminus acts as a gated module that enables voltage-dependent G-protein βγ subunit inhibition of Ca V 2.2 channels; xref a role for α 1C N-terminus in protein kinase C modulation of Ca V 1.2 channels; xref that the N-termini of Ca V 1.2 and Ca V 1.3 channels contains a Ca 2+ -CaM binding site (termed NSCaTE for N-terminal spatial Ca 2+ transforming element) that controls local vs. global spatial Ca 2+ selectivity for CaM regulation of Ca V channels; xref and that deleting segments of α 1C N-terminus increases I Ca,L by enhancing channel P o . xref "