Abstract
Mutation in Cattle Muscle Disease Causes Premature Degradation of Sarco(endo)plasmic Reticulum Ca2+-ATPase Isoform 1♦: Inhibition of Ubiquitin Proteasome System Rescues the Defective Sarco(endo)plasmic Reticulum Ca2+-ATPase (SERCA1) Protein Causing Chianina Cattle Pseudomyotonia
Highlights
A similar disease happens in humans called Brody disease
In this Paper of the Week, a team led by Roberta Sacchetto in collaboration with Dorianna Sandonaat the University of Padova in Italy demonstrated that the mutated SERCA1 is functional in cattle, the protein gets prematurely degraded by the ubiquitin-proteasome system
The investigators showed that treating cultured cells with a proteasome inhibitor helped to maintain calcium homeostasis
Summary
Mutation in Cattle Muscle Disease Causes Premature Degradation of Sarco(endo)plasmic Reticulum Ca2؉-ATPase Isoform 1ࡗ 2014, 289, 33073–33082 Inhibition of Ubiquitin Proteasome System Rescues the Defective Sarco(endo)plasmic Reticulum Ca2؉-ATPase (SERCA1) Protein Causing Chianina Cattle Pseudomyotonia
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