A Calsequestrin-1 Mutation Associated with a Skeletal Muscle Disease Alters Sarcoplasmic Ca2+ Release

Characterization of Two Human Skeletal Calsequestrin Mutants Implicated in Malignant Hyperthermia and Vacuolar Aggregate Myopathy

(2015) Kevin M. Lewis et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

The couplonopathies: A comparative approach to a class of diseases of skeletal and cardiac muscle

(2015) Eduardo Ríos et al.   JOURNAL OF GENERAL PHYSIOLOGY

ACASQ1founder mutation in three Italian families with protein aggregate myopathy and hyperCKaemia

(2015) Claudia Di Blasi et al.   JOURNAL OF MEDICAL GENETICS

A Mutation in theCASQ1Gene Causes a Vacuolar Myopathy with Accumulation of Sarcoplasmic Reticulum Protein Aggregates

(2014) Daniela Rossi et al.   HUMAN MUTATION

High-capacity Ca2+Binding of Human Skeletal Calsequestrin

(2012) Emiliano J. Sanchez et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

Mice Null for Calsequestrin 1 Exhibit Deficits in Functional Performance and Sarcoplasmic Reticulum Calcium Handling

(2011) Rotimi O. Olojo et al.   PLoS One

Contribution of the central hydrophobic residue in the PXP motif of voltage-dependent K+channels to S6 flexibility and gating properties

(2010) Paola Imbrici et al.   Channels

CONTROL OF MUSCLE RYANODINE RECEPTOR CALCIUM RELEASE CHANNELS BY PROTEINS IN THE SARCOPLASMIC RETICULUM LUMEN

(2008) Nicole A Beard et al.   CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY

The differential expression of low-threshold K+currents generates distinct firing patterns in different subtypes of adult mouse trigeminal ganglion neurones

(2008) Luigi Catacuzzeno et al.   JOURNAL OF PHYSIOLOGY-LONDON