Anti-AHSG polyclonal antibody [Biotin]

Alpha2-HS glycoprotein (AHSG) is a human serum glycoprotein synthesized by liver cells. It is a natural inhibitor of the insulin receptor tyrosine kinase activity. We produced this protein in insect cells by using a recombinant baculovirus expressing the whole coding sequence of the protein. By analyzing AHSG on isoelectric focusing and on sodium dodecyl sulfate (SDS) gels, followed by immunoblot, AHSG produced in insect cells was found to be phosphorylated and to possess the connecting peptide between the A and the B chains. The same features were found in the protein produced by Hep3B, a human liver cell line that synthesizes AHSG. By contrast, no phosphorylation could be detected in AHSG present in normal human plasma, and the connecting peptide was clipped. As the protein produced in insect cells is active on insulin receptors, in contrast to the plasma protein, our results suggest that the biological activity of the protein may be associated with its single chain form together with its phosphorylation.

Background: Vascular calcification ( VC) and accelerated atherosclerosis are major causes of cardiovascular ( CV) morbidity and mortality in haemodialysis ( HD) patients. Inhibitory proteins are associated with reduced VC and may play a key role in preventing CV in chronic kidney disease ( CKD) patients. Fetuin-A, also known as alpha(2)-Heremans-Schmid glycoprotein ( AHSG), is a circulating plasma protein with inhibitory effects on VC that has been associated with inflammation and CV mortality in HD patients. In the present study, we investigated the associations between serum fetuin-A levels and its gene ( AHSG) polymorphisms in an Italian HD population. Methods: Ninety-six patients on stable chronic HD treatment and 57 healthy controls were genotyped for the common polymorphisms on the AHSG ( T256S). In addition, serum fetuin-A levels were tested. Results: In this study, serum fetuin-A levels were lower in HD patients (0.35 +/- 0.11 g/l) compared with healthy controls (0.62 +/- 0.31 g/l, p < 0.05). In both HD patients and the control group, the distribution of the AHSG gene did not show significant association between low serum fetuin-A levels and the Ser/Ser genotype, known to be associated with a higher CV mortality risk in the HD population. Moreover, the distribution of AHSG gene polymorphisms in HD patients and in healthy controls was similar. Conclusions: In contrast with previous reports, this study suggests that CKD patients on HD treatment have a similar polymorphism distribution of the AHSG gene compared with the normal population and that the reduction in serum fetuin-A levels in Italian HD patients is not associated with an alteration in the distribution of AHSG T256S polymorphisms. Copyright (C) 2007 S. Karger AG, Basel.