EC Number |
Application |
Reference |
---|
3.4.21.106 | biotechnology |
the aim of this study is to establish a cell line that directly secrets rFVIIa into cell culture medium: Factor VII and hepsin cDNAs are isolated from HepG2 cell line and cloned into pcDNA3-1 vector. The constructs are co-trasfected to CHO cell line. A cell line that permanently expresses recombinant factor VII (rFVII) and hepsin is established. FVIIa protein is secreted to medium of CHO cells co-transfected with pcNDA3-1-FVII and pcNDA3-1-hepsin. A three- to fourfold decrease in clotting time is observed when human FVII-depleted plasma is used in combination with human thromboplastin in the presence of rFVII, confirming the biological activity of rFVII. A cell line is established expressing FVIIa using genetic engineering methods |
701403 |
3.4.21.106 | medicine |
alpha-methylacyl-CoA racemase and hepsin are unable to diagnose prostate cancer with better true positive and false negative rates than prostate-specific antigen. There are no correlations between alpha-methylacyl-CoA racemase levels, hepsin levels, tumor stage of benign prostate hyperplasia and prostate cancer, and Gleason score |
753876 |
3.4.21.106 | medicine |
association of five of eleven single nucleotide polymorphisms on the hepsin gene HPN with susceptibility to prostate cancer among men of European descent. Association of one of the single nucleotide polymorphisms with Gleason score, which suggests a role of HPN in tumor aggressiveness |
687027 |
3.4.21.106 | medicine |
direct cleavage of Laminin-332 may be one mechanism by which hepsin promotes prostate tumor progression and metastasis, possibly by up-regulating prostate cancer cell motility |
698824 |
3.4.21.106 | medicine |
expression of the non-transmembrane isoform in vivo does not exert any apparent inhibitory effect on cell growth |
672315 |
3.4.21.106 | medicine |
germline genetic variation of HPN does not seem to contribute to risk of prostate cancer or prognosis |
710461 |
3.4.21.106 | medicine |
hepsin expression in tumours is dysregulated and may influence tumorigenesis through inappropiate activation and/or regulation of hepatocyte growth factor receptor functions |
671835 |
3.4.21.106 | medicine |
hepsin has a potential therapeutic effect that inhibits through upregulation of p53-dependent apoptosis and caspase-3, -6, and -7 activations. Hepsin may be useful in ovarian cancer treatment |
674067 |
3.4.21.106 | medicine |
hepsin is a potent activator of pro-hepatocyte growth factor, thus contributing to tumor progression |
673609 |
3.4.21.106 | medicine |
hepsin is not necessary for embryonic development of mice and postnatal survival and is dispensable for normal hemostasis and liver function |
686903 |