|Application ||WB, IHC-P, IF, E|
|Other Accession||NP_002463, 153945790|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||Predicted: 213 kDa |
Observed: 220 kDa
|Application Notes||MYH8 antibody can be used for detection of MYH8 by Western blot at 1 - 2 µg/ml. Antibody can also be used for immunohistochemistry starting at 5 µg/mL. For immunofluorescence start at 20 µg/mL.|
|Target/Specificity||MYH8; MYH8 antibody is human, mouse and rat reactive. MYH8 antibody is predicted to not cross-react with other members of the myosin heavy chain family.|
|Reconstitution & Storage||MYH8 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year.|
|Precautions||MYH8 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Cellular Location||Cytoplasm, myofibril. Note=Thick filaments of the myofibrils|
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Provided below are standard protocols that you may find useful for product applications.
Myosins are actin-based motor proteins that function in the generation of mechanical force in eukaryotic cells (1). MYH8 (myosin, heavy chain 8, skeletal muscle, perinatal) is a member of the class II or conventional myosin heavy chains, and functions in skeletal muscle contraction (2,3). This gene is predominantly expressed in fetal skeletal muscle. MYH8 is regulated by phosphorylation via myosin light chain kinase (MLCK) and by intracellular Ca2+ concentrations (3). A mutation in this gene results in trismus-pseudocamptodactyly syndrome (4).
Yu H, Waddell JN, Kuang S, et al. Park7 expression influences myotube size and myosin expression in muscle. PLoS One 2014; 9:e92030.
Feghali R and Leinwand LA. Molecular genetic characterization of a developmentally regulated human perinatal myosin heavy chain. J. Cell Biol. 1989; 108:1791-7.
Jullian EH, Kelly AM, Pompidou AJ, et al. Characterization of a human perinatal myosin heavy-chain transcript. Eur. J. Biochem. 1995; 230:1001-6.
Minzer-Conzetti K, Wu E, Vargervik K, et al. Phenotypic variation in trismus-pseudocamptodactyly syndrome caused by a recurrent MYH8 mutation. Clin. Dysmorphol. 2008; 17:1-4.
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