Gene Expression, Regulation and Cell Surface Presentation of the Kininogens

摘要: Publisher Summary This chapter discusses the key areas for future investigation in a vibrant and evolving field of vascular biology. Although first recognized 21 years ago as defect associated with very prolonged activated partial thromboplastin time (APTT), genetic deficiency high-molecular-weight kininogen (HMWK) is not bleeding. These features have been both benefit discomfort to investigators this field. Recognition HMWK greatly facilitated by prolongation APTT, although homozygous HMWK-deficient patient rare. Alternatively, APTT has contributed masking physiological importance an antithrombin its role ordering assembly activation plasma kallikrein (KLK)-dependent fibrinolytic pathway on biologic membranes. activities are paradoxical any screening test The weight current evidence indicates that kininogens, especially HMWK, antithrombins profibrinolytic proteins. gene expression regulation protein chemistry function kininogens relation their structures, characterization biological membranes emphasizes based upon functions. low-molecular-weight (LMWK) assemble cell membranes, allowing bradykinin (BK) be liberated protected environment, wherein potent, bioactive peptide can activate receptors influence