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Caveolin 3

caveolin-3, CAV3
This gene encodes a caveolin family member, which functions as a component of the caveolae plasma membranes found in most cell types. Caveolin proteins are proposed to be scaffolding proteins for organizing and concentrating certain caveolin-interacting molecules. Mutations identified in this gene lead to interference with protein oligomerization or intra-cellular routing, disrupting caveolae formation and resulting in Limb-Girdle muscular dystrophy type-1C (LGMD-1C), hyperCKemia or rippling muscle disease (RMD). Alternative splicing has been identified for this locus, with inclusion or exclusion of a differentially spliced intron. In addition, transcripts utilize multiple polyA sites and contain two potential translation initiation sites. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: caveolin-1, CAN, HAD, CACNA1G, V1a
Papers on caveolin-3
Mibefradil suppresses the proliferation of pulmonary artery smooth muscle cells.
Shen et al., Shanghai, China. In J Investig Med, Jan 2016
however, no changes in TRPC1, TRPC3, CAV1.2, and CAV3.2 levels were observed.
Hyperglycemia Abrogates Ischemic Postconditioning Cardioprotection by Impairing AdipoR1/Caveolin-3/STAT3 Signaling in Diabetic Rats.
Xia et al., Hong Kong, Hong Kong. In Diabetes, Jan 2016
Hypoxic postconditioning(HPo)-induced protection against hypoxia/reoxygnation injury was lost in Adipo(-/-) cardiomyocytes but restored by recombinant adiponectin, while this adiponectin beneficial effect was abolished by either specific STAT3 or adiponectin receptor-1(AdipoR1) gene knockdown, or caveolin-3(Cav3) disruption.
No apparent role for T-type Ca(2+) channels in renal autoregulation.
Sorensen et al., Copenhagen, Denmark. In Pflugers Arch, Jan 2016
The role of T- and L-type calcium channels in the response to acute increases in RPP in T-type channel knockout mice (CaV3.1)
Molecular Targets of Cannabidiol in Neurological Disorders.
Whalley et al., Reading, United Kingdom. In Neurotherapeutics, Oct 2015
Of interest and after excluding unlikely and implausible targets, the remaining molecular targets of CBD with plausible evidence for involvement in therapeutic effects in neurological disorders (e.g., voltage-dependent anion channel 1, G protein-coupled receptor 55, CaV3.x, etc.) are associated with either the regulation of, or responses to changes in, intracellular calcium levels.
Targeting caveolin-3 for the treatment of diabetic cardiomyopathy.
Kitmitto et al., Manchester, United Kingdom. In Pharmacol Ther, Jul 2015
Here we review the aetiology of diabetic cardiomyopathy and explore the involvement of the protein caveolin-3 (Cav3).
Protein assemblies of sodium and inward rectifier potassium channels control cardiac excitability and arrhythmogenesis.
Jalife et al., Madrid, Spain. In Am J Physiol Heart Circ Physiol, Jul 2015
Recent findings include compartmentalized regulation of NaV1.5 channel expression and function through a PDZ (postsynaptic density protein, Drosophila disc large tumor suppressor, and zonula occludens-1 protein) domain-binding motif, and interaction of caveolin-3 with Kir2.1 and ankyrin-G as a molecular platform for NaV1.5 signaling.
Caveolin-3 Promotes a Vascular Smooth Muscle Contractile Phenotype.
Frank et al., Tours, France. In Front Cardiovasc Med, 2014
In the present study, we have examined the role of caveolin-3 in the regulation of SM cell phenotype.
A mutation in the low voltage-gated calcium channel CACNA1G alters the physiological properties of the channel, causing spinocerebellar ataxia.
Kawakami et al., Hiroshima, Japan. In Mol Brain, 2014
RESULTS: In this study, we analyzed a Japanese family with autosomal dominant SCA using linkage analysis and exome sequencing, and identified CACNA1G, which encodes the calcium channel CaV3.1, as a new causative gene.
Genetic basis of limb-girdle muscular dystrophies: the 2014 update.
Savarese et al., Napoli, Italy. In Acta Myol, 2014
The dominant forms (LGMD1) are: LGMD1A (myotilin), LGMD1B (lamin A/C), LGMD1C (caveolin 3), LGMD1D (DNAJB6), LGMD1E (desmin), LGMD1F (transportin 3), LGMD1G (HNRPDL), LGMD1H (chr.
The cAMP-binding Popdc proteins have a redundant function in the heart.
Schindler et al., United Kingdom. In Biochem Soc Trans, 2014
Another important Popdc-interacting protein is caveolin 3, and the loss of Popdc1 affects caveolar size.
An inhibitor of transforming growth factor beta type I receptor ameliorates muscle atrophy in a mouse model of caveolin 3-deficient muscular dystrophy.
Sunada et al., Okayama, Japan. In Lab Invest, 2012
We show that a TbetaRI kinase inhibitor, Ki26894, restores impaired myoblast differentiation in vitro caused by activin, myostatin, and TGF-beta1, as well as CAV3(P104L).
Essential role of caveolin-3 in adiponectin signalsome formation and adiponectin cardioprotection.
Ma et al., Taiyuan, China. In Arterioscler Thromb Vasc Biol, 2012
Cav-3 plays an essential role in adiponectin transmembrane signaling and APN anti-ischemic/cardioprotective actions.
Loss of bladder smooth muscle caveolae in the aging bladder.
Sullivan et al., Boston, United States. In Neurourol Urodyn, 2012
caveolin-3 protein expression and immunoreactivity were reduced in bladder smooth muscle at 6, 12 and 19 months of age compared with young animals.
Expression of caveolin-1, caveolin-2 and caveolin-3 in thyroid cancer and stroma.
Koo et al., Seoul, South Korea. In Pathobiology, 2011
Stromal caveolin-3 expression were more frequent in anaplastic carcinoma and diffuse sclerosing variant of papillary carcinoma compared to conventional papillary thyroid carcinoma.
Endolysosomal sorting of ubiquitylated caveolin-1 is regulated by VCP and UBXD1 and impaired by VCP disease mutations.
Meyer et al., Essen, Germany. In Nat Cell Biol, 2011
In patient muscle, muscle-specific caveolin-3 accumulates in sarcoplasmic pools and specifically delocalizes from the sarcolemma.
Caveolin-1, caveolin-3 and VEGF expression in the masticatory muscles of mdx mice.
Spassov et al., Greifswald, Germany. In Folia Histochem Cytobiol, 2010
The expression of caveolin-1 (cav-1), caveolin-3 (cav-3) and VEGF was examined in control and mdx mice.
The role of voltage-gated calcium channels in pancreatic beta-cell physiology and pathophysiology.
Berggren et al., Stockholm, Sweden. In Endocr Rev, 2006
At least six CaValpha1 subunits, including CaV1.2, CaV1.3, CaV2.1, CaV2.2, CaV2.3, and CaV3.1, have been identified in pancreatic beta-cells.
Increased neuronal nitric oxide synthase-derived NO production in the failing human heart.
Heymes et al., Paris, France. In Lancet, 2004
Diseased hearts had a significant increase in nNOS mRNA and protein expression, and activity associated with the translocation of nNOS to the sarcolemma through interactions with caveolin 3. Enhanced nNOS activity counteracted a decrease in eNOS expression and activity.
Amphiphysin 2 (Bin1) and T-tubule biogenesis in muscle.
De Camilli et al., New Haven, United States. In Science, 2002
Caveolin-3 and amphiphysin were implicated in their biogenesis.
Mutations in CAV3 cause mechanical hyperirritability of skeletal muscle in rippling muscle disease.
Kubisch et al., Bonn, Germany. In Nat Genet, 2001
We found missense mutations in positional candidate CAV3 (encoding caveolin 3; ref. 5) in all five families analyzed.
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