In addition to the propeptide, other binding proteins are capable of regulating
myostatin activity in vitro, including follistatin [19], [21], FLRG [22], and Gasp - 1 [23].
In order to determine whether this effect of follistatin results solely from inhibition of
myostatin activity, I analyzed the effect of this transgene in myostatin - null mice.
As a result, there has been considerable effort directed at developing strategies to modulate
myostatin activity in clinical settings where enhancing muscle growth may be beneficial.
Hence, there is considerable interest in developing agents capable of inhibiting
myostatin activity for both agricultural and human therapeutic applications.
Moreover, loss of
myostatin activity resulting either from postnatal inactivation of the Mstn gene [3], [4] or following administration of various myostatin inhibitors to wild type adult mice [5]--[7] can also lead to significant muscle growth.
To determine whether FLRG can also inhibit
myostatin activity in vivo, I generated a construct in which the FLRG coding sequence was placed downstream of a myosin light chain promoter / enhancer.
To determine whether the FLRG transgene was causing increased muscle growth by blocking
myostatin activity, I examined the effect of combining the FLRG transgene with a loss - of - function mutation in the myostatin gene.
One of these is the follistatin related protein, FLRG, which has been demonstrated to be capable of inhibiting
myostatin activity in vitro.
Not exact matches
Mstn − / − mice carrying a follistatin transgene had about four times the muscle mass of wild type mice, demonstrating the existence of other regulators of muscle mass with similar
activity to
myostatin.
I have presented data showing that FLRG, like follistatin, can promote muscle growth when expressed as a transgene in skeletal muscle and that both of these molecules appear to act by blocking not only
myostatin but also other ligands with similar
activity to
myostatin.
Exercise restores decreased physical
activity levels and increases markers of autophagy and oxidative capacity in
myostatin / activin - blocked mdx mice.
It is the flip - side of
myostatin, as increased follistatin blocks the
activity of
myostatin: either increased follistatin or reduced
myostatin produce similar outcomes in animal studies, with treated individuals demonstrating increased muscle mass.
To test Cas9 / gRNA
activity in goat primary fibroblasts, we designed six gRNAs targeting
myostatin (MSTN), nucleoporin 155 (NUP), prion protein (PrP), and beta - lactoglobulin (BLG), respectively (Figure 1A).
Bodybuilders who use
myostatin blockers experience a dramatic increase in muscle mass in response to weight training and reduced levels of body fat, mainly because of an increased fat breakdown and an increased
activity of the brown body fat, according to a study from Singapore.