Synthetic peptide corresponding to Human Caveolin-3 aa 1-100 conjugated to Keyhole Limpet Haemocyanin (KLH). (Peptide available as ab31791)
ab30750 gave a positive signal in the following tissue lysates:
Skeletal Muscle (Human) - adult normal tissue
Heart (Human) - adult normal tissue
Skeletal Muscle (Mouse)
Skeletal Muscle (Rat) - normal tissue
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use at an assay dependent concentration. PubMed: 21680711
Use at an assay dependent concentration.
Use at an assay dependent concentration.
Use a concentration of 1 µg/ml. Detects a band of approximately 18 kDa (predicted molecular weight: 17 kDa).
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.
Expressed predominantly in muscle.
Defects in CAV3 are the cause of limb-girdle muscular dystrophy type 1C (LGMD1C) [MIM:607801]. 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) [MIM:123320]. 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) [MIM:606072]. 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 cardiomyopathy familial hypertrophic (CMH) [MIM:192600]; 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) [MIM:611818]. 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) [MIM:272120]. 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.
Belongs to the caveolin family.
Golgi apparatus membrane. Cell membrane. Membrane > caveola. Potential hairpin-like structure in the membrane. Membrane protein of caveolae.
Western blot - Anti-Caveolin-3 antibody - Caveolae Marker (ab30750)
All lanes : Anti-Caveolin-3 antibody - Caveolae Marker (ab30750) at 1 µg/ml
Lane 1 : Human skeletal muscle tissue lysate - total protein (ab29330) Lane 2 : Human heart tissue lysate - total protein (ab29431) Lane 3 :Mouse skeletal muscle tissue lysate - total protein (ab29711) Lane 4 : Skeletal Muscle (Rat) Tissue Lysate - normal tissue (ab29376)
Lysates/proteins at 20 µg per lane.
Secondary All lanes : IRDye 680 Conjugated Goat Anti-Rabbit IgG (H+L) at 1/10000 dilution
Performed under reducing conditions.
Predicted band size: 17 kDa Observed band size: 17 kDa Additional bands at: 40 kDa. We are unsure as to the identity of these extra bands.
ICC/IF image of ab30750 stained HepG2 cells. The cells were 100% methanol fixed (5 min) and then incubated in 1%BSA / 10% normal goat serum / 0.3M glycine in 0.1% PBS-Tween for 1h to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with the antibody (ab30750, 5µg/ml) overnight at +4°C. The secondary antibody (green) was ab96899 Dylight® 488 goat anti-rabbit IgG (H+L) used at a 1/250 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red) at a 1/200 dilution for 1h. DAPI was used to stain the cell nuclei (blue) at a concentration of 1.43µM.
Caveolin 3 - Caveolae Marker was immunoprecipitated using 0.5mg Mouse skeletal muscle whole tissue extract, 5µg of Rabbit polyclonal to Caveolin 3 and 50µl of protein G magnetic beads (+). No antibody was added to the control (-). The antibody was incubated under agitation with Protein G beads for 10min, Mouse skeletal muscle whole tissue extract lysate diluted in RIPA buffer was added to each sample and incubated for a further 10min under agitation. Proteins were eluted by addition of 40µl SDS loading buffer and incubated for 10min at 70oC; 10µl of each sample was separated on a SDS PAGE gel, transferred to a nitrocellulose membrane, blocked with 5% BSA and probed with ab30750. Secondary: Clean blot (HRP conjugate) at 1/1000 dilution. Band: 17kDa: Caveolin 3 - Caveolae Marker.
Valentine CD & Haggie PM Confinement of ß(1)- and ß(2)-adrenergic receptors in the plasma membrane of cardiomyocyte-like H9c2 cells is mediated by selective interactions with PDZ domain and A-kinase anchoring proteins but not caveolae. Mol Biol Cell22:2970-82 (2011).
Read more (PubMed: 21680711) »
Willett M et al. Inhibition of mammalian target of rapamycin (mTOR) signalling in C2C12 myoblasts prevents myogenic differentiation without affecting the hyperphosphorylation of 4E-BP1. Cell Signal21:1504-12 (2009).
Read more (PubMed: 19481146) »