Recombinant Ryanodine Receptor Monoclonal Antibody (AN301983L)

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For research use only.
Verified Samples | Verified Samples in IHC: Human skeletal muscle, Mouse skeletal muscle, Mouse kidney (negative tissue), Rat skeletal muscle, Rat placenta (negative tissue) |
Dilution | IHC 1:500-1:1000 |
Isotype | IgG, κ |
Host | Rabbit |
Reactivity | Human, Rat, Mouse |
Applications | IHC |
Clonality | Monoclonal;Recombinant |
Immunogen | Peptide. This information is proprietary to PTMab. |
Abbre | Ryanodine Receptor |
Synonyms | PPP1R, CCO, KDS, MHS, RYR, MHS1, RYDR, SKRR, RYR-1, PPP1R137, RYR1 |
Swissprot | |
Cellular Localization | Membrane |
Concentration | 1 mg/mL |
Buffer | PBS, 50% glycerol, 0.05% Proclin 300, 0.05% protein protectant. |
Purification Method | Protein A purified |
Research Areas | Neuroscience, Cardiovascular, Cancer, Metabolism |
Clone No. | A703 |
Conjugation | Unconjugated |
Storage | Store at -20°C Valid for 12 months. Avoid freeze / thaw cycles. |
Shipping | Ice bag |
background | Ryanodine receptors (RyRs) are large (>500 kDa), intracellular calcium channels found in the sarcoplasmic/endoplasmic reticulum membrane and are responsible for the release of Ca2+ from intracellular stores in excitable cells, such as muscle and neurons. RyRs exist as three mammalian isoforms (RyR1-3), all of which form homotetramers regulated by phosphorylation and/or direct or indirect interaction with a variety of proteins (L-type calcium channels, PKA, FKBP12/12.6, CaMKII, calmodulin, calsequestrin, junctin, and triadin) and ions (Mg2+ and Ca2+). Regulation of the RyR channel by protein modulators occurs within the large cytoplasmic domain, whereas the carboxy terminal portion of the protein forms the ion-binding and conducting pore. RyR1 and RyR2 are predominantly expressed in skeletal and cardiac muscle, respectively, where they localize exclusively to the sarcoplasmic reticulum (SR) and facilitate calcium-mediated communication between transverse-tubules and sarcoplasmic reticulum. Contraction of skeletal muscle is triggered by release of calcium ions from the SR following depolarization of T-tubules. Research studies have shown that defects in RyR1 are the cause of malignant hyperthermia susceptibility type 1 (MHS1), central core disease of muscle (CCD), multiminicore disease with external ophthalmoplegia, and congenital myopathy with fiber-type disproportion (CFTD), each of which is manifested by defects in muscle function, metabolism, and development. |
Other Clones
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Other Formats
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Unconjugated
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