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|Product Name:||GDF-8||Packing:||Discreet Packing, Or As Request|
|Markets:||Global||Appearance:||White Lyophilized Powder|
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Injectable Growth Hormone Peptides Myostatin Peptide GDF-8 Lyophilized Powder
|Growth Differentiation Factor 8|
Myostatin / GDF-8 is a protein that in humans is encoded by the MSTN gene. It isproduced primarily in skeletal muscle cells, circulates in the blood and acts on muscle tissue. The myostatin propeptide is known to bind and inhibit myostatin in vitro. This interaction is relevant in vivo, with a majority (>70%) of myostatin in serum bound to its propeptide acting as a negative regulator of myostatin. Recombinant human Myostatin Propeptide is a non-glycosylated protein, containing 244 amino acids, with a molecular weight of 27.8 kDa. Our Myostatin 1mg is Tagged. The tags are chains/pile of amino acids/proteins, it is foreign protein that will cause immunization reaction in most cases.
Myostatin / GDF-8 is a member of the TGF beta superfamily of proteins. Human myostatin consists of two identical subunits, each consisting of 109 amino acid residues. Its total molecular weight is 25.0 kDa. The protein is made in an inactive form. For it to be activated, a protease cleaves the NH2-terminal, or "pro-domain" portion of the molecule, resulting in the now-active COOH-terminal dimer
Myostatin (GDF-8) is a member of the transforming growth factor-beta (TGF-beta) superfamily that is highly expressed in skeletal muscle, and myostatin loss-of-function leads to doubling of skeletal muscle mass. Myostatin-deficient mice have been used as a model for studying muscle-bone interactions, and here we review the skeletal phenotype associated with altered myostatin signaling. It is now known that myostatin is a key regulator of mesenchymal stem cell proliferation and differentiation, and mice lacking the myostatin gene show decreased body fat and a generalized increase in bone density and strength.
The increase in bone density is observed in most anatomical regions, including the limbs, spine, and jaw, and myostatin inhibitors have been observed to significantly increase bone formation. Myostatin is also expressed in the early phases of fracture healing, and myostatin deficiency leads to increased fracture callus size and strength. Together, these data suggest that myostatin has direct effects on the proliferation and differentiation of osteoprogenitor cells, and that myostatin antagonists and inhibitors are likely to enhance both muscle mass and bone strength.
1) The gene encoding myostatin was discovered in 1997 by geneticists Se-Jin Lee and Alexandra McPherron who produced a strain of mutant mice that lack the gene. These myostatin "knockout" mice have approximately twice as much muscle as normal mice. These mice were subsequently named "mighty mice".
2) Naturally occurring deficiencies of myostatin have been identified in cattle by Ravi Kambadur, whippets, and humans; in each case the result is a dramatic increase in muscle mass. A mutation in the 3' UTR of the myostatin gene in Texel sheep creates target sites for the microRNAs miR-1 and miR-206. This is likely to cause the muscular phenotype of this breed of sheep.
3) Human myostatin consists of two identical subunits, each consisting of 109 (NCBI database claims human myostatin is 375 residues long) amino acid residues. Its total molecular weight is 25.0 kDa. The protein is inactive until a protease cleaves the NH2-terminal, or "pro-domain" portion of the molecule, resulting in the active COOH-terminal dimer. Myostatin binds to the activin type II receptor, resulting in a recruitment of either coreceptor Alk-3 or Alk-4. This coreceptor then initiates a cell signaling cascade in the muscle, which includes the activation of transcription factors in the SMAD family - SMAD2 and SMAD3. These factors then induce myostatin-specific gene regulation. When applied to myoblasts, myostatin inhibits their differentiation into mature muscle fibers.
Myostatin also inhibits Akt, a kinase that is sufficient to cause muscle hypertrophy, in part through the activation of protein synthesis. However, Akt is not responsible for all of the observed muscle hyperthrophic effects which are mediated by myostatin inhibition Thus myostatin acts in two ways: by inhibiting muscle differentiation, and by inhibiting Akt-induced protein synthesis.
|Description||white lyophilized powder||white lyophilized powder|
|Loss of drying||≤1.0%||0.5%|
|TLC||Only one spot||Only one spot|
|Conclusion||It complies with the USP 32.|
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|CJC1295 without DAC--MOD GRF(1-29)||2mg/vial, 10vials/box|
|PT141 (Bremelanotide)||10mg/vial, 10vials/box|
|MGF (Mechano growthfactor) (IGF- IEC)||2mg/vial, 10vials/box|
|PEG MGF||2mg/vial, 10vials/box|
|Triptorelin/Gnrh Triptoreli||2mg/vial, 10vials/box|
|IGF LR3-1||0.1mg/vial, 10vials/box|
|IGF LR3-1||1mg/vial, 10vials/box|
|IGF IDES||1mg/vial, 10vials/box|
|Follistatin 344||1mg/vial, 10vials/box|
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