Anti-Müllerian hormone (AMH), a member of the TGF-β superfamily, is a homodimeric glycoprotein composed of two 55 kDa N-terminal and two 12.5 kDa C-terminal homodimers, non-covalently linked by disulfide bridges.1
Recent studies have shown that the AMH C-terminal homodimer is much less active than the noncovalent complex, but almost all activity can be restored by associating with the N-terminal pro-region, which reforms a complex with the mature C-terminal homodimer. This finding raises the possibility that the AMH noncovalent complex is the active form of protein. It was reported that the cleaved AMH noncovalent complex binds to AMHRII and stimulates intracellular signaling, whereas full-length AMH shows only minimal activity.2
AMH is secreted by the Sertoli cells in males. During embryonic development, AMH is responsible for Müllerian duct regression. AMH continues to be produced by the testes until puberty and then decreases slowly to residual post-puberty values. In females, AMH is produced by the granulosa cells of small growing follicles from the 36th week of gestation onwards until menopause when levels become undetectable. Potential clinical applications of low end anti-müllerian hormone (AMH) have been published in premature ovarian insufficiency, ovarian tumors, menopause and many more.
References:
1. Pepinski, R.B., et al. (1988) J. Biol. Chem., 263, 18961-18964.
2. di Clemente et al. Mol Endocrinol, November 2010, 24 (11): 2193-2206.
3. HHS Publication, 5th ed., 2007. Biosafety in Microbiological and Biomedical Laboratories. Available http://www.cdc.gov/biosafety/publications/bmbl5/BMBL5
4. DHHS (NIOSH) Publication No. 78€“127, August 1976. Current Intelligence Bulletin 13 - Explosive Azide Hazard. Available http:// www.cdc.gov/niosh.
5. Approved Guideline €“ Procedures for the Handling and Processing of Blood Specimens, H18-A3. 2004. Clinical and Laboratory Standards Institute.
6. Kricka L. Interferences in immunoassays €“ still a threat. Clin Chem 2000; 46: 1037€“1038.
