Disease relevance of Shbg

• Shbg is thus a candidate for Hd, comprising autopodium (hand and foot) reduction and male sterility resulting from spermatogenesis impairment [1].
• It is known that sex hormone-binding globulin (SHBG), which binds both testosterone and estradiol in human serum, is markedly elevated in cirrhosis [2].
• Rabbit sex hormone binding globulin: primary structure, tissue expression, and structure/function analyses by expression in Escherichia coli [3].
• Thirty postmenopausal women (11 omnivores, 10 vegetarians and 9 apparently healthy women with surgically removed breast cancer) were investigated with regard to the association of their urinary excretion of estrogens, lignans and isoflavonoids (all diphenols) with plasma sex hormone binding globulin (SHBG) [4].
• SHBG, SHBG plus estradiol (SHBG-E), and SHBG-E plus oxytocin all significantly increased female sexual receptivity over vehicle or estradiol plus oxytocin infused controls, as measured by lordosis quotients and receptivity scores, at 40, and 90 min after their infusions into the medial preoptic area [5].

High impact information on Shbg

• Rat androgen-binding protein: evidence for identical subunits and amino acid sequence homology with human sex hormone-binding globulin [6].
• Hepatocytes are the major source of sex hormone-binding globulin (SHBG), a glycoprotein that transports sex steroids in the blood and regulates their access to target tissues [7].
• Mutagenesis of essential functional residues of rat androgen-binding protein/sex hormone-binding globulin [8].
• These proteins, which are secreted by the testis (ABP) and liver [sex hormone-binding globulin (SHBG)], are encoded by the same gene [9].
• To investigate the role of oligosaccharides in ABP/sex hormone-binding globulin subunit structure, secretion, and steroid binding, mutant rat ABP proteins were constructed that eliminated one or both of the two potential sites of asparagine (Asn)-linked glycosylation [10].

Chemical compound and disease context of Shbg

• It thus appears that urinary loss of protein-bound (sex hormone binding globulin-bound) testosterone in the nephrotic syndrome leads to increased basal secretion of luteinizing hormone, presumably as a result of increased luteinizing releasing hormone secretion [11].

Biological context of Shbg

• Both Northern blot and DNA sequence analysis confirmed the results of the RT-PCR for SHBG [12].
• In PCOD patients mean alpha-subunit, free androgen index [FAI; testosterone x 100/sex hormone-binding globulin (SHBG)], androstenedione, estrone, and estradiol (E2) were significantly elevated compared to levels in the early follicular phase of control cycles and non-PCOD patients [13].
• The rabbit sex hormone-binding globulin gene: structural organization and characterization of its 5-flanking region [14].
• Like the human and rat shbg promoter sequences, the rbshbg proximal promoter lacks a typical TATA box [14].
• Overexpression of androgen-binding protein/sex hormone-binding globulin in male transgenic mice: tissue distribution and phenotypic disorders [15].

Anatomical context of Shbg

• SELDI-TOF MS analysis demonstrated that in vivo estradiol treatments resulted in dramatically decreased levels of SHBG in the hypothalamus and that a reduction in SHBG mRNA by estradiol treatment also resulted in a reduction in SHBG protein levels [12].
• We also used surface-enhanced laser desorption ionization time of flight (SELDI-TOF) mass spectrometry (MS) to analyze the effects of estradiol in ovariectomized rats on SHBG levels in the MPOA-MH as well as the neurohypophysis [12].
• This change in ERalpha, ERbeta, and SHBG expression did not occur in the hippocampus [12].
• Hepatocyte nuclear factor-4 controls transcription from a TATA-less human sex hormone-binding globulin gene promoter [7].
• The data indicate that albumin-bound testosterone, albumin-bound estradiol, and sex hormone-binding globulin-bound estradiol are all exchangeable in salivary gland capillaries [16].

Associations of Shbg with chemical compounds

• That in vivo estradiol treatments had the same inhibitory effects on mRNA levels for SHBG and both ERs suggests similar translational control mechanisms for all three steroid-binding proteins in the brain [12].
• The results are compatible with the influx of albumin-bound E2 into all three tissues and the influx of sex hormone-binding globulin-bound E2 into the liver [17].
• Fasting serum concentrations of 17-hydroxyprogesterone (17-OHP), androstenedione, testosterone, estrone, estradiol, and sex hormone-binding globulin were determined as possible endocrine correlates of LH isotypes [18].
• Subsequently, tubules were perfused with ACF or ACF containing physiological concentrations of sex hormone-binding globulin (SHBG; an androgen-binding protein [ABP] homolog), 5 alpha-dihydrotestosterone (DHT), or SHBG+DHT.(ABSTRACT TRUNCATED AT 250 WORDS)[19]
• The present studies assess the effects of human sex hormone-binding globulin (SHBG) on the conversion of [3H]testosterone (T) into dihydrotestosterone (DHT) in rat ventral prostate gland in vivo using a constant aortic infusion technique [20].

Other interactions of Shbg

• Sex hormone binding globulin (SHBG) is produced in brain where it is often co-localized with oxytocin [21].
• The nonradioactive steroid binds with high affinity and specificity to the androgen receptor and binds poorly, if at all, to other steroid receptors and plasma sex hormone binding globulin [22].

Analytical, diagnostic and therapeutic context of Shbg

• However, RT-PCR analysis revealed a significantly higher level of the Shbg transcript in hypodactylous rats compared to SHR controls [1].
• Moreover, linkage mapping of Hd revealed that an intragenic marker for Shbg, D10Wox12, was non-recombinant with Hd [1].
• We conclude that the presence of 4% HSA in the perfusion medium increases the biologic activity of estradiol and estrone on the isolated rat liver, and this increase is inhibited in the presence of sex hormone-binding globulin [23].
• Isoelectric focusing in gel slabs allows rapid separation (1.5 hr) of receptors from other non-receptor proteins that bind steroid hormones, such as transcortin and sex hormone-binding globulin [24].
• IN SITU hybridization showed increased SHBG mRNA signal during late pregnancy [25].

References