GDF-8 Muscle Cell Growth Polypeptide 1MG Myostatin

GDF-8 Muscle Cell Growth Polypeptide Myostatin 1MG with High Purity Product Name: GDF-8 Synonyms: GDF-8;MSTN Muscle Hypertrophy;Myostatin Proform human;Monoclonal Anti-MSTN antibody produced in mouse;MSTN;ANTI-MYOSTATIN (GDF8)(N-TERMINAL) antibody produced in rabbit. GDF-8 / Myostatin is a...
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GDF-8 Muscle Cell Growth Polypeptide Myostatin 1MG with High Purity

Product Name: GDF-8
Synonyms: GDF-8;MSTN Muscle Hypertrophy;Myostatin Proform human;Monoclonal Anti-MSTN antibody produced in mouse;MSTN;ANTI-MYOSTATIN (GDF8)(N-TERMINAL) antibody produced in rabbit.

GDF-8 / Myostatin is a secreted protein that is expressed in developing and adult skeletal muscle. It controls myoblast proliferation and is a potent negative regulator of skeletal muscle mass. It is upregulated in mechanically-stressed cardiomyocytes and induces the skeletal muscle wasting which is common in heart failure. The GDF-8 propeptide is cleaved from GDF-8 but remains associated and functions as an inhibitor of mature GDF-8. GDF-8 activity can also be inhibited through its association with Follistatin, FLRG, Decorin, or GASP-1. Active GDF-8 signals through a receptor complex containing Activin RIIB and either Activin RIB/ALK-4 or TGF-beta RI/ALK-5.


What is Gdf-8

Myostatin (also known as growth differentiation factor 8, abbreviated 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.


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