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GDF-8 (Myostatin)
- Product description: supply good quality GDF-8 (Myostatin)
PRODUCT INTRODUCTION
GDF-8 (Myostatin) |
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Detailed Product Description |
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Peptide: |
Peptide For Bodybuilding |
Dosage: |
Can Customise As Require |
Recipe: |
Provided For Free To Our Customers |
Powder Source: |
Usp Standard Powder |
Pakage: |
Disguise Package Or As Require |
Price List: |
Welcome Inquiry |
Effect: |
Bodybuilding Fitness |
Shipping Time: |
3-7days |
Min Order: |
10 Vials |
Vial Size: |
3ml |
Labels: |
Please Contact For Detail |
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Myostatin Gdf-8 Peptides Steroids Myostatin Hmp Gdf-8 Peptide For Musclebuilding
Myostatin (also known as growth differentiation factor 8, abbreviated GDF-8) is a myokine, a protein produced and released by myocytes that acts on muscle cells' autocrine function to inhibit myogenesis: muscle cell growth and differentiation. In humans it is encoded by the MSTN gene. Myostatin is a secreted growth differentiation factor that is a member of the TGF beta protein family.
GDF Basic Info.
Gdf-8 Alias: MSTN, Myostatin HMP
Gdf-8 Purity: >98%
Gdf-8 Specification: 1mg
Gdf-8 Storage: 2-8 degree centigrade refrigerator
Gdf-8 Package: 10 Vials/Kit
Gdf-8 Deliver:1 working day for ready goods 3~7 working days to your destination.
Gdf-8 Pacakge:1kit=10vials Alumnium foil+bubble+carton
Gdf-8 Customized:accepted.
Myostatin (GDF-8) Introduction:
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.
Myostatin (GDF-8) is known as a potent inhibitor of muscle growth and development, and myostatin is also expressed early in the fracture healing process. The purpose of this study was to test the hypothesis that a new myostatin inhibitor, a recombinant myostatin propeptide, can enhance the repair and regeneration of both muscle and bone in cases of deep penetrant injury.
GDF-8 / Myostatin Myostatin ----------Structure and mechanism of action:
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.