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ProductsMIS/AMH ELISA Test
Company Diagnostic Systems Laboratories, Inc.
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Description Mullerian Inhibiting Substance (MIS), also known as Anti-Mullerian Inhibiting Substance (AMH), is a glycoprotein dimer composed of two 72 kDa monomers linked by disulfide bridges (1). MIS/AMH belongs to the transforming growth factor-? (TGF-?) superfamily which includes TGF-? and the various inhibin and activin glycoproteins (2). All members of this superfamily are dimeric glycoproteins, and all are involved in the regulation of tissue growth and differentiation. The human gene coding for MIS/AMH has been sequenced and isolated, and is located on the short arm of chromosome 19 (3). The structure of a specific receptor for MIS/AMH has also been isolated and characterized (4).

MIS/AMH is produced by the Sertoli cells of the testis in the male, and by ovarian granulosa cells in the female. During embryonic development in males, secretion of MIS/AMH from testicular Sertoli cells is essential for the regression of the Mullerian ducts, and thus the normal development of the male reproductive tract (5). The Mullerian ducts are the primordium for the uterus, Fallopian tubes and upper vagina in the female. In the male, secretion of MIS/AMH by the Sertoli cells commences during embryogenesis and continues throughout life. Levels drop following puberty, decreasing slowly to a relatively low post-puberty value (2). In the female, serum MIS/AMH is undetectable using immunoassay until the onset of puberty. Thereafter, circulating MIS/AMH is maintained at relatively low levels until menopause, at which time MIS/AMH falls again to undetectable levels (as measured by immunoassay).

Potential clinical applications for a specific MIS/AMH assay include: the investigation of ovarian reserve and the perimenopausal transition in women; the detection and management of granulosa cell tumors; the diagnosis of precocious puberty and conversely, its delayed onset in the young; the differential diagnosis of intersex disorders; the diagnosis of cryptoorchidism and anorchidism, and the evaluation of male gonadal function at all ages (2).

  1. Picard JY, Josso N Mol Cell Endocrinol 34: 23-29, 1984.
  2. Teixeira J et al. Endocrine Reviews 22: 657-674, 2001.
  3. Picard JY et al. Proc Natl Acad Sci 83: 5464-5468, 1986.
  4. di Clemente N et al. Mol Endocrinol 8: 1006-1020, 1994.
  5. Picon R Arch Anat Microsc Morphol Exp 58: 1-19, 1969.
  6. Hudson PL et al. J Clin Endocrinol Metab 70: 16-22, 1990.
Info Diagnostic Systems Laboratories, Inc.
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