The IQ Motif is Crucial for Cav1.1 Function

Ca2+-dependent modulation via calmodulin, with consensus CaM-binding IQ motif playing a key role, has been documented for most high-voltage-activated Ca2+ channels. The skeletal muscle Cav1.1 also exhibits Ca2+-/CaM-dependent modulation. Here, whole-cell Ca2+ current, Ca2+ transient, and maximal, im...

Full description

Bibliographic Details
Main Author: Stroffekova, Katarina
Format: Online
Language:English
Published: Hindawi Publishing Corporation 2011
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3228397/
id pubmed-3228397
recordtype oai_dc
spelling pubmed-32283972011-12-08 The IQ Motif is Crucial for Cav1.1 Function Stroffekova, Katarina Research Article Ca2+-dependent modulation via calmodulin, with consensus CaM-binding IQ motif playing a key role, has been documented for most high-voltage-activated Ca2+ channels. The skeletal muscle Cav1.1 also exhibits Ca2+-/CaM-dependent modulation. Here, whole-cell Ca2+ current, Ca2+ transient, and maximal, immobilization-resistant charge movement (Qmax) recordings were obtained from cultured mouse myotubes, to test a role of IQ motif in function of Cav1.1. The effect of introducing mutation (IQ to AA) of IQ motif into Cav1.1 was examined. In dysgenic myotubes expressing YFP-Cav1.1AA, neither Ca2+ currents nor evoked Ca2+ transients were detectable. The loss of Ca2+ current and excitation-contraction coupling did not appear to be a consequence of defective trafficking to the sarcolemma. The Qmax in dysgenic myotubes expressing YFP-Cav1.1AA was similar to that of normal myotubes. These findings suggest that the IQ motif of the Cav1.1 may be an unrecognized site of structural and functional coupling between DHPR and RyR. Hindawi Publishing Corporation 2011 2011-11-13 /pmc/articles/PMC3228397/ /pubmed/22162637 http://dx.doi.org/10.1155/2011/504649 Text en Copyright © 2011 Katarina Stroffekova. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Stroffekova, Katarina
spellingShingle Stroffekova, Katarina
The IQ Motif is Crucial for Cav1.1 Function
author_facet Stroffekova, Katarina
author_sort Stroffekova, Katarina
title The IQ Motif is Crucial for Cav1.1 Function
title_short The IQ Motif is Crucial for Cav1.1 Function
title_full The IQ Motif is Crucial for Cav1.1 Function
title_fullStr The IQ Motif is Crucial for Cav1.1 Function
title_full_unstemmed The IQ Motif is Crucial for Cav1.1 Function
title_sort iq motif is crucial for cav1.1 function
description Ca2+-dependent modulation via calmodulin, with consensus CaM-binding IQ motif playing a key role, has been documented for most high-voltage-activated Ca2+ channels. The skeletal muscle Cav1.1 also exhibits Ca2+-/CaM-dependent modulation. Here, whole-cell Ca2+ current, Ca2+ transient, and maximal, immobilization-resistant charge movement (Qmax) recordings were obtained from cultured mouse myotubes, to test a role of IQ motif in function of Cav1.1. The effect of introducing mutation (IQ to AA) of IQ motif into Cav1.1 was examined. In dysgenic myotubes expressing YFP-Cav1.1AA, neither Ca2+ currents nor evoked Ca2+ transients were detectable. The loss of Ca2+ current and excitation-contraction coupling did not appear to be a consequence of defective trafficking to the sarcolemma. The Qmax in dysgenic myotubes expressing YFP-Cav1.1AA was similar to that of normal myotubes. These findings suggest that the IQ motif of the Cav1.1 may be an unrecognized site of structural and functional coupling between DHPR and RyR.
publisher Hindawi Publishing Corporation
publishDate 2011
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3228397/
_version_ 1611491192821776384