I will pay for the following article Sex Hormone-Binding Globulin Gene. The work is to be 18 pages with three to five sources, with in-text citations and a reference page. Although the single human SHBG gene is expressed in the testis, human transcripts of this gene are confined to testicular germ cells. This gene encodes an amino-terminally truncated SHBG isoform which accumulates in the acrosome of sperm and subsequently binds to steroids in the same way as plasma SHBG. As a result of its high affinity and selective nature towards sex steroids, the concentration of SHBG in human blood is the major determining factor of the number of free androgens and estrogens in target cells. Additionally, it is possible that SHBG in plasma within the extracellular matrix of particular tissues may affect the biological activities of sex steroids at the target cell level. SHBG can also bind to a number of pharmaceutically manufactured steroids, xenobiotics, and flavonoids. However, such interactions may have far-implicating effects in medicine environmental toxicology. In clinical medicine, these associations are exemplified in areas of hormone-replacement therapy, diagnostic imaging of cancer, and oral contraceptives (Xita & Tsatsoulis, 2010).

In human beings, sex hormone-binding globulin (SHBG) is produced mainly in the liver under the influence of metabolic and hormonal factors. In the circulation, SHBG binds to androgens with high affinity and estrogens with a lower affinity and hence controls their access and action in target tissues. Sex hormone-binding globulin is also produced in other tissues such as the brain, placenta, endometrium, and testis. The proper expression of SHBG by the placenta and fetal liver during growth may be significant in maintaining normal fetal exposures to androgens emanating from both the mother and the fetus itself. Consequently, differences in the levels of SHBG may influence sex steroid bioavailability and cellular effects with resultant clinical ramifications (Hammond & Bocchinfuso, 1995).

Currently, it is known that the synthesis of SHBG is under multifactorial control mechanisms including metabolic, hormonal, and nutritional impacting on SHBG levels. Moreover, genetic predisposition may also contribute to the variation of the levels of SHBG. Not only, therefore, are environmental factors critical in SHBG level variation but also genetic factors come into play. Given the clinical importance of the SHBG gene, numerous studies have evaluated the potential link between polymorphisms of the SHBG gene and serum SHBG levels that can be related to the pathogenesis of several clinical conditions. As such, polymorphisms within the coding sequence and potentially within the regulatory sequence of the SHBG gene which modulate production and metabolism of the protein is useful in the genetic underpinning of its activity in humans (Xita, Tsatsoulis, Chatzikyriakidou & Georgiou, 2003).