ELISA/assay

Rat Caveolin-3 (CAV3) ELISA Kit

MBS7236065

48-Strip-Wells

470 USD

ELISA Kit

Rat Caveolin-3 (CAV3) ELISA Kit

Caveolin-3 (CAV3)

caveolin-3; Caveolin-3; caveolin-3; M-caveolin; caveolin 3; M-caveolin

CAV3

CAV3; CAV3; LQT9; VIP21; LGMD1C; VIP-21

CAV3_HUMAN

Rat

This assay has high sensitivity and excellent specificity for detection of CAV-3. No significant cross-reactivity or interference between CAV-3 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between CAV-3 and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C.

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive. Sensitivity: 0.1 ng/mL.

Intended Uses: This CAV-3 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Rat CAV-3. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Principle of the assay: CAV-3 ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-CAV-3 antibody and an CAV-3-HRP conjugate. The assay sample and buffer are incubated together with CAV-3-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the CAV-3 concentration since CAV-3 from samples and CAV-3-HRP conjugate compete for the anti-CAV-3 antibody binding site. Since the number of sites is limited, as more sites are occupied by CAV-3 from the sample, fewer sites are left to bind CAV-3-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The CAV-3 concentration in each sample is interpolated from this standard curve.

15451860

NP_203123.1

NM_033337.2

17,259 Da

Bacterial Invasion Of Epithelial Cells Pathway (149807); Bacterial Invasion Of Epithelial Cells Pathway (148661); Endocytosis Pathway (102279); Endocytosis Pathway (102181); Focal Adhesion Pathway (198795); Focal Adhesion Pathway (83067); Focal Adhesion Pathway (478); Integrin-mediated Cell Adhesion Pathway (198816); PDGFR-alpha Signaling Pathway (138049); Proteoglycans In Cancer Pathway (782000)

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]

caveolin-3: May act as a scaffolding protein within caveolar membranes. Interacts directly with G-protein alpha subunits and can functionally regulate their activity. May also regulate voltage-gated potassium channels. Plays a role in the sarcolemma repair mechanism of both skeletal muscle and cardiomyocytes that permits rapid resealing of membranes disrupted by mechanical stress. Defects in CAV3 are the cause of limb-girdle muscular dystrophy type 1C (LGMD1C). LGMD1C is a myopathy characterized by calf hypertrophy and mild to moderate proximal muscle weakness. LGMD1C inheritance can be autosomal dominant or recessive. Defects in CAV3 are a cause of hyperCKmia (HYPCK). It is a disease characterized by persistent elevated levels of serum creatine kinase without muscle weakness. Defects in CAV3 are a cause of rippling muscle disease (RMD). RMD is a rare disorder characterized by mechanically triggered contractions of skeletal muscle. In RMD, mechanical stimulation leads to electrically silent muscle contractions that spread to neighboring fibers that cause visible ripples to move over the muscle. Defects in CAV3 are a cause of familial hypertrophic cardiomyopathy (CMH); also designated FHC or HCM. Familial hypertrophic cardiomyopathy is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death. Defects in CAV3 are the cause of long QT syndrome type 9 (LQT9). Long QT syndromes are heart disorders characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to excercise or emotional stress. They can present with a sentinel event of sudden cardiac death in infancy. Defects in CAV3 can be a cause of sudden infant death syndrome (SIDS). SIDS is the sudden death of an infant younger than 1 year that remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of clinical history. Pathophysiologic mechanisms for SIDS may include respiratory dysfunction, cardiac dysrhythmias, cardiorespiratory instability, and inborn errors of metabolism, but definitive pathogenic mechanisms precipitating an infant sudden death remain elusive. Long QT syndromes-associated mutations can be responsible for some SIDS cases. Defects in CAV3 are the cause of myopathy distal Tateyama type (MPDT). A disorder characterized by progressive muscular atrophy and muscle weakness beginning in the hands, the legs, or the feet. Muscle atrophy may be restricted to the small muscles of the hands and feet. Belongs to the caveolin family. Protein type: Dystrophin complex; Cell development/differentiation; Motility/polarity/chemotaxis; Extracellular matrix. Chromosomal Location of Human Ortholog: 3p25. Cellular Component: dystrophin-associated glycoprotein complex; Golgi membrane; cell surface; endoplasmic reticulum; T-tubule; plasma membrane; caveola; neuromuscular junction; Z disc; vesicle; sarcolemma; lipid raft. Molecular Function: protein C-terminus binding; protein binding; sodium channel regulator activity; calcium channel regulator activity; protein complex binding; protein complex scaffold; potassium channel inhibitor activity; nitric-oxide synthase binding; alpha-tubulin binding. Biological Process: negative regulation of MAP kinase activity; muscle development; positive regulation of microtubule polymerization; T-tubule organization and biogenesis; negative regulation of cell size; glucose homeostasis; regulation of heart contraction; cytoplasmic microtubule organization and biogenesis; muscle maintenance; protein localization; elevation of cytosolic calcium ion concentration; regulation of transforming growth factor beta receptor signaling pathway; cardiac muscle cell development; plasma membrane organization and biogenesis; positive regulation of cell proliferation; regulation of skeletal muscle contraction; cell growth; cell differentiation; regulation of nerve growth factor receptor activity; myoblast fusion; negative regulation of calcium ion transport; negative regulation of nitric-oxide synthase activity; negative regulation of MAPKKK cascade; regulation of heart rate; actin filament organization; regulation of protein kinase B signaling cascade; endocytosis; nucleus localization; regulation of membrane potential; cholesterol homeostasis; triacylglycerol metabolic process; plasma membrane repair; negative regulation of protein kinase activity; lipid raft organization and biogenesis. Disease: Creatine Phosphokinase, Elevated Serum; Long Qt Syndrome 9; Rippling Muscle Disease; Muscular Dystrophy, Limb-girdle, Type 1c; Myopathy, Distal, Tateyama Type; Cardiomyopathy, Familial Hypertrophic, 1

48-Strip-Wells

470 USD

96-Strip-Wells

675