Introduction of CAV3
CAV3, also known as caveolin-3 or M-caveolin, functions as a component of the caveolae plasma membranes which is found in most cell types. CAV3 exists in skeletal and smooth muscle tissue and heart, more recently, in glial cells and early post-natal peripheral nerves. The CAV3 protein is 151 amino acids (aa) long and is divided into five domains: N-terminal, scaffold, transmembrane, C-terminal and a signature sequence involved in N-terminal. These structures fuse with the plasma membrane to form the final caveolae.
|Basic Information of CAV3|
|Organism||Homo sapiens (Human)|
Function of CAV3 Membrane Protein
The caveolar structure is formed by caveolins, a family of proteins composed of three isoforms, caveolin-1 (CAV-1), -2 and -3. All three genes encoding each family member are evolutionary. Conservatively, the CAV1 and CAV3 amino acid sequences show a high degree of homology. In adult muscle fibers, CAV3 is located at a position critical for the electrical transmission of contractile impulses, acting as a platform which concentrates on ion channels, kinases, and signaling molecules. It is important to maintain the physiological levels of CAV3 for normal skeletal muscle development and postnatal function. Most CAV3 mutations cause severe loss of CAV3 protein. The mutations in CAV3 lead to distinct neuromuscular and cardiac disorders such as Limb Girdle Muscular Dystrophy (LGMD) 1-C, idiopathic persistent elevation of serum creatine kinase (H-CK), inherited rippling muscle disease (RMD), distal myopathy (MD) and familial hypertrophic cardiomyopathy (HCM).
Fig.1 CAV3 protein structure. (Kim, 2016)
Application of CAV3 Membrane Protein in Literature
This article finds that a partial deficiency of CAV3 was occasionally detected in the muscles of patients with myasthenia gravis (MG) and that CAV3 overexpression may be required after MG muscle injury.
CAV3 is expressed in smooth and skeletal muscles, and different mutations of CAV3 cause a variety of human muscular diseases. This article characterizes the secondary structure, dynamics, and topology of the monomeric form of the full-length lipidated protein. These provide insight into the structure of CAV3 and set the stage for mechanistic investigations of the effects of pathogenic mutations.
This study characterized the role of the CAV3 gene in patients with limb-girdle muscular dystrophy, hyperCKemia, cardiomyopathies. CAV3 gene involves neuromuscular disorders but no evidence is found in the group of patients with cardiomyopathies.
In the heart, CAV3 is the main component of caveolae and plasma membrane domains that regulate multiple cellular processes highly relevant for cardiac excitability, such as trafficking, calcium homeostasis, signal transduction and cellular response to injury. This article found a new putative CAV3 variant, CAV3 V82I, in a patient with SCD. They suggest that the detrimental effect of CAV3 V82I variant on cell viability may participate in determining the susceptibility to cardiac death.
This article demonstrates the relationship between left ventricular dysfunction and CAV3 levels by mouse experiments and suggests that CAV3 may act as a new target for the treatment of heart failure.
CAV3 Preparation Options
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