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Gene Review

Serpina6  -  serine (or cysteine) peptidase inhibitor,...

Mus musculus

Synonyms: AI265318, AV104445, CBG, Cbg, Corticosteroid-binding globulin, ...
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Disease relevance of Serpina6

  • Quantitative trait-loci analysis of TNF-induced induction of IL-6 and of hypothermia also points to the importance of this locus (P < 0.0002 and P = 0.017, respectively), more particularly the Cbg and Spi2 loci, in the resistance to TNF [1].
  • Rather, the mice exhibited increased activity of the pituitary axis of hormonal control, normal levels of gluconeogenetic enzymes, and fatigue, as well as an aggravated response to septic shock, indicating an inability to appropriately respond to the excess free corticosterone in the absence of CBG [2].
  • The time-dependent spontaneous reversal of dex-induced hyperglycemia correlated with re-expression of CBG mRNA transcripts and reduced levels of EST transcripts and enzyme activity [3].
  • Overall, the data accumulated in this study point to Cbg gene as a key regulator of cortisol levels and obesity susceptibility [4].
  • In contrast, serum CBG levels progressively decreased in adult female mice during five days of treatment with 0.5 microgram dexamethasone/g body weight per day [5].

High impact information on Serpina6


Biological context of Serpina6

  • The amount of CBG mRNA in these cells increased transiently to a maximum on days 15-16 of gestation and was negligible by day 19 [6].
  • However, CBG mRNA was not detected in the placenta at any gestational age [6].
  • Glucocorticoids influence fetal development, and their actions are regulated by plasma corticosteroid-binding globulin (CBG) [6].
  • Therefore, CBG present in the placenta is most likely of maternal origin and may influence the activities of steroid hormones that control placental development and/or function [6].
  • The mouse Cbg gene structure has been deduced from two non-overlapping DNA fragments of a lambda EMBL-3 genomic library, as well as PCR amplification of the approx. 2 kb of genomic DNA that lies between them [7].

Anatomical context of Serpina6

  • In the fetus, CBG mRNA was first detectable in the hepatocytes on day 11 of gestation [6].
  • Immunoreactive CBG was detected in the tubular cells of the developing fetal kidney as early as day 13, but CBG mRNA was never found in the fetal kidney, suggesting that the protein is probably sequestered from fetal blood directly or via the glomerular filtrate [6].
  • Upon sacrifice, brains, thymus, adrenals and blood were harvested, the last for corticosteroid binding globulin (CBG) [8].
  • Expression of these mutants in the MDCK cell line indicated that the Lys201-->Glu substitution accounts for the abnormal steroid-binding affinity of CBG in RIIIS/J mice [7].
  • The CBG within the proximal convoluted tubules was located in secretory granules close to the luminal surface of the epithelial cells, suggesting that it is secreted into the tubular lumen [9].

Associations of Serpina6 with chemical compounds

  • The results presented here suggest that temporal and spatial changes in the localization of CBG and its mRNA in the fetus may influence the effects of steroid hormones on developing tissues [6].
  • Corticosteroid-binding globulin (CBG) is a member of the serine proteinase inhibitor superfamily and is responsible for the plasma transport of glucocorticoids [7].
  • Intron-specific oligodeoxyribonucleotide primers were also used to PCR-amplify Cbg coding regions from several mouse strains [7].
  • In addition to the dexamethasone-binding activity, a binding substance identical to corticosteroid-binding globulin (CBG) was identified in the cytosol fraction of mammary glands [10].
  • The results demonstrate that the uptake of corticosterone, which binds to transcortin, was reduced by addition of serum while uptake of triamcinolone acetonide, which is not bound by transcortin, was unaffected [11].

Physical interactions of Serpina6


Other interactions of Serpina6


Analytical, diagnostic and therapeutic context of Serpina6


  1. Identification of a locus on distal mouse chromosome 12 that controls resistance to tumor necrosis factor-induced lethal shock. Libert, C., Wielockx, B., Hammond, G.L., Brouckaert, P., Fiers, W., Elliott, R.W. Genomics (1999) [Pubmed]
  2. Hyporesponsiveness to glucocorticoids in mice genetically deficient for the corticosteroid binding globulin. Petersen, H.H., Andreassen, T.K., Breiderhoff, T., Bräsen, J.H., Schulz, H., Gross, V., Gröne, H.J., Nykjaer, A., Willnow, T.E. Mol. Cell. Biol. (2006) [Pubmed]
  3. Dexamethasone-induced hyperglycemia in obese Avy/a (viable yellow) female mice entails preferential induction of a hepatic estrogen sulfotransferase. Gill, A.M., Leiter, E.H., Powell, J.G., Chapman, H.D., Yen, T.T. Diabetes (1994) [Pubmed]
  4. Corticosteroid binding globulin: a new target for cortisol-driven obesity. Ousova, O., Guyonnet-Duperat, V., Iannuccelli, N., Bidanel, J.P., Milan, D., Genêt, C., Llamas, B., Yerle, M., Gellin, J., Chardon, P., Emptoz-Bonneton, A., Pugeat, M., Mormède, P., Moisan, M.P. Mol. Endocrinol. (2004) [Pubmed]
  5. Glucocorticoids induce corticosteroid-binding globulin biosynthesis by immature mouse liver and kidney. Zhao, X.F., Scrocchi, L.A., Hammond, G.L. J. Steroid Biochem. Mol. Biol. (1997) [Pubmed]
  6. Spatial and temporal distribution of corticosteroid-binding globulin and its messenger ribonucleic acid in embryonic and fetal mice. Scrocchi, L.A., Orava, M., Smith, C.L., Han, V.K., Hammond, G.L. Endocrinology (1993) [Pubmed]
  7. Structure and chromosomal location of the gene encoding mouse corticosteroid-binding globulin: strain differences in coding sequence and steroid-binding activity. Orava, M., Zhao, X.F., Leiter, E., Hammond, G.L. Gene (1994) [Pubmed]
  8. Contribution of sex and genetics to neuroendocrine adaptation to stress in mice. Jones, B.C., Sarrieau, A., Reed, C.L., Azar, M.R., Mormède, P. Psychoneuroendocrinology (1998) [Pubmed]
  9. Corticosteroid-binding globulin biosynthesis in the mouse liver and kidney during postnatal development. Scrocchi, L.A., Hearn, S.A., Han, V.K., Hammond, G.L. Endocrinology (1993) [Pubmed]
  10. Interaction of steroids with dexamethasone-binding receptor and corticosteroid-binding globulin in the mammary gland of the mouse in relation to lactation. Lindenbaum, M., Chatterton, R.T. Endocrinology (1981) [Pubmed]
  11. Conditions affecting AtT-20 cell glucocorticoid uptake. Svec, F., Harrison, R.W. Steroids (1981) [Pubmed]
  12. Transcortin and vitamin D-binding protein levels in mouse serum. Faict, D., De Moor, P., Bouillon, R., Heyns, W., Heiniger, H.J., Corrow, D., Lesaffre, E. J. Endocrinol. (1986) [Pubmed]
  13. The glucocorticoid receptor is essential for maintaining basal and dexamethasone-induced repression of the murine corticosteroid-binding globulin gene. Cole, T.J., Harris, H.J., Hoong, I., Solomon, N., Smith, R., Krozowski, Z., Fullerton, M.J. Mol. Cell. Endocrinol. (1999) [Pubmed]
  14. alpha-Fetoprotein and transcortin behave as acute phase reactants in the maternal and fetal compartments of the inflammatory pregnant mouse. Vranckx, R., Savu, L., Maya, M., Nunez, E.A. Endocrinology (1987) [Pubmed]
  15. An enzyme-linked immunosorbent assay for corticosteroid-binding globulin using monoclonal and polyclonal antibodies: decline in CBG following synthetic ACTH. Lewis, J.G., Lewis, M.G., Elder, P.A. Clin. Chim. Acta (2003) [Pubmed]
  16. A simple method for the purification of murine corticosteroid binding globulin: characterization of a monomer. Nyberg, L., Jones, I. J. Steroid Biochem. (1988) [Pubmed]
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