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Human Molecular Genetics|April 30, 2003
Functional polymorphisms in the paternally expressed XLalphas and its cofactor ALEX decrease their mutual interaction and enhance receptor-mediated cAMP formationKathleen Freson, Jaak Jaeken, Monique Van Helvoirt, et al.Blood|September 13, 2003
Deletion of alanine 2201 in the FVIII C2 domain results in mild hemophilia A by impairing FVIII binding to VWF and phospholipids and destroys a major FVIII antigenic determinant involved in inhibitor developmentRoseline d'Oiron, Jean-Maurice Lavergne, Renaud Lavend'homme, et al.The Journal of Clinical Investigation|April 7, 2004
The pituitary adenylate cyclase-activating polypeptide is a physiological inhibitor of platelet activationKathleen Freson, Hitoshi Hashimoto, Chantal Thys, et al.Blood|October 24, 2002
CD4+ T-cell clones specific for wild-type factor VIII: a molecular mechanism responsible for a higher incidence of inhibitor formation in mild/moderate hemophilia AMarc Jacquemin, Valérie Vantomme, Cécile Buhot, et al.Journal of Hypertension|December 5, 2006
-391 C to G substitution in the regulator of G-protein signalling-2 promoter increases susceptibility to the metabolic syndrome in white European men: consistency between molecular and epidemiological studiesKathleen Freson, Katarzyna Stolarz, Raymond Aerts, et al.Blood|January 11, 2003
Overexpression of the platelet P2X1 ion channel in transgenic mice generates a novel prothrombotic phenotypeCécile Oury, Marijke J E Kuijpers, Emese Toth-Zsamboki, et al.Pageof 3