Ultimate Subhuman™
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Follistatin 344 (and 315)
Follistatin, also called activin-binding protein, is found in nearly all tissues of vertebrate animals. Its primary function is to neutralize members of the TGF-β family, which play fundamental roles in everything from growth and development to energy homeostasis and immune system regulation. In particular, follistatin interacts with activin, which plays an important part in cell proliferation and cell death as well as in the immune response as it applies to wound repair.
Follistatin 344 and Follistatin 315 are engineered analogues of naturally occurring follistatin. Both are created by alternative splicing of the follistatin mRNA transcript. Scientific research in non-human primates as well as in mice have indicated that both molecules are capable of improving muscle growth by antagonizing myostatin (a member of the TGF-β family).
The first evidence that follistatin could enhance muscle growth came from studies conducted in mice in 2001. These studies found that myostatin, a known negative regulator of skeletal muscle growth, interacted with activin type II receptors found on muscle cells. Follistatin 344 interacts with these same receptors and is a competitive antagonist to myostatin. By blocking myostatin’s ability to bind to the activin receptors on muscle cells, follistatin 344 can allow for massive increases in muscle mass.
Scientists are speculating on a number of ways that follistatin may be put to clinical use for muscle growth in the future. Research in mice from 2009 has indicated that follistatin might be useful in the disease spinal muscular atrophy (SMA). In SMA, there is a loss of function mutation that causes death of spinal motor neurons. When these nerves die, the muscles that they connect to atrophy as well. Research shows that follistatin not only preserves muscle tissue in mice with SMA, but that it also helps to preserve spinal motor neurons by creating a positive feedback loop. In fact, the mice in the study group lived 30% longer than mice who were not given Follistatin because of enhanced muscle and nerve cell survival.
Follistatin, also called activin-binding protein, is found in nearly all tissues of vertebrate animals. Its primary function is to neutralize members of the TGF-β family, which play fundamental roles in everything from growth and development to energy homeostasis and immune system regulation. In particular, follistatin interacts with activin, which plays an important part in cell proliferation and cell death as well as in the immune response as it applies to wound repair.
Follistatin 344 and Follistatin 315 are engineered analogues of naturally occurring follistatin. Both are created by alternative splicing of the follistatin mRNA transcript. Scientific research in non-human primates as well as in mice have indicated that both molecules are capable of improving muscle growth by antagonizing myostatin (a member of the TGF-β family).
The first evidence that follistatin could enhance muscle growth came from studies conducted in mice in 2001. These studies found that myostatin, a known negative regulator of skeletal muscle growth, interacted with activin type II receptors found on muscle cells. Follistatin 344 interacts with these same receptors and is a competitive antagonist to myostatin. By blocking myostatin’s ability to bind to the activin receptors on muscle cells, follistatin 344 can allow for massive increases in muscle mass.
Scientists are speculating on a number of ways that follistatin may be put to clinical use for muscle growth in the future. Research in mice from 2009 has indicated that follistatin might be useful in the disease spinal muscular atrophy (SMA). In SMA, there is a loss of function mutation that causes death of spinal motor neurons. When these nerves die, the muscles that they connect to atrophy as well. Research shows that follistatin not only preserves muscle tissue in mice with SMA, but that it also helps to preserve spinal motor neurons by creating a positive feedback loop. In fact, the mice in the study group lived 30% longer than mice who were not given Follistatin because of enhanced muscle and nerve cell survival.
