Myostatin
Myostatin | ||
---|---|---|
Properties of human protein | ||
Mass / length primary structure | 109 amino acids | |
Secondary to quaternary structure | Homodimer | |
Precursor | (375 aa) | |
Identifier | ||
Gene name | MSTN | |
External IDs | ||
Occurrence | ||
Parent taxon | Vertebrates |
Myostatin is a protein that is produced in the human or animal body. It inhibits muscle growth so that muscles don't grow out of control. Follistatin, on the other hand, has an antagonistic effect by binding to myostatin.
“Gene doping” in the laboratory: The Mstn gene
coding for myostatin was switched off in the right mouse . Myostatin inhibits muscle growth. Due to the lack of myostatin, the muscle mass of the transgenic right mouse is four times higher than that of the wild type (left)
Inactivation of the natural protein function of myostatin leads to excessive muscle growth. In mice, cattle, sheep and dogs of the Whippet breed , individuals are known to develop considerably greater muscle mass than healthy animals due to various mutations in the myostatin gene. For whippets, it was found that dogs with two copies of the mutated gene develop the “bully whippet” phenotype, which is undesirable in breeding . Dogs with only one copy of the mutated gene also developed greater muscle mass than wild-type dogs and achieved significantly higher speeds in competition, but they met the breed standard.
In 2004, a German boy was found to have a mutation in the myostatin gene, which resulted in the formation of a shortened and therefore not fully functional myostatin protein. The boy has been unusually muscular since he was born.
Since then, myostatin has repeatedly been named as a candidate for gene doping in the German-speaking public . However, for gene doping with myostatin, the effect of the natural myostatin protein present in humans would have to be successfully antagonized. So far, this gene therapy approach has only been successful in mice with severe muscle disease and only with moderate success. In contrast, there are conventional therapeutic approaches that have already been successful in animal experiments by directly blocking the natural myostatin effect . It is hoped that this will one day be able to treat muscle degenerative diseases. MYO-029 ( Stamulumab ), an antibody that inhibits natural myostatin, was tested in a clinical study. This did not have any significant success. However, a more targeted inhibitor may give hope for a better effect.
Web links
Individual evidence
- ↑ Homologues at OMA
- ^ A b c Se-Jin Lee: Quadrupling Muscle Mass in Mice by Targeting TGF-ß Signaling Pathways . In: PLoS ONE . tape 2 , no. 8 , August 29, 2007, p. e789 , doi : 10.1371 / journal.pone.0000789 .
- ^ EA Ostrander: Genetics and the Shape of Dogs. In: American Scientist. Volume 95, Number 5, September-October 2007, pp. 406-413, ISSN 0003-0996 . doi: 10.1511 / 2007.67.3724 .
- ↑ DS Mosher et al .: A mutation in the myostatin gene increases muscle mass and enhances racing performance in heterozygous dogs. In: PLoS Genetics. 3, number 5, 2007, e79, doi: 10.1371 / journal.pgen.0030079 . PMID 17530926 .
- ↑ H. Dambeck: Boy prodigy carries muscle gene. In: Spiegel Online. June 24, 2004
- ↑ M. Schuelke, KR Wagner, LE Stolz, C. Hübner, T. Riebel, W. Kömen, T. Braun, JF Tobin, SJ Lee: Myostatin mutation associated with gross muscle hypertrophy in a child. In: The New England Journal of Medicine . Volume 350, Number 26, June 2004, pp. 2682-2688, ISSN 1533-4406 . doi: 10.1056 / NEJMoa040933 . PMID 15215484 .
- ↑ Gene doping - super athletes through biotechnology ( Memento of the original from September 30, 2007 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. (www.3sat.de, last accessed on June 24, 2009).
- ↑ M. Bartoli, J. Poupiot et al. a .: AAV-mediated delivery of a mutated myostatin propeptide ameliorates calpain 3 but not alpha-sarcoglycan deficiency. In: Gene therapy. Volume 14, Number 9, May 2007, pp. 733-740, ISSN 0969-7128 . doi: 10.1038 / sj.gt.3302928 . PMID 17330087 .
- ↑ Clinical study (phase I + II): Study Evaluating MYO-029 in Adult Muscular Dystrophy at Clinicaltrials.gov of the NIH