98% Purity of 1mg / Vial Recombinant Myostatin Gdf 8 Human Myostatin Propeptide

98% Purity Recombinant Myostatin Gdf 8 Human Myostatin Propeptide (HMP)

Quick Details
GDF-8
Basic Info.
Alias: MSTN, Myostatin HMP
Purity: >98%
Specification: 1mg
Package: 10 Vials/Kit
Deliver:1 working day for ready goods 3~7 working days to your destination.



Myostatin (GDF-8) Introduction

Myostatin (GDF-8) is a member of the transforming grow 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.



GDF 8 / 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 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.



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