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      Deletion of murine kininogen gene 1 (mKng1) causes loss of plasma kininogen and delays thrombosis.

      Blood
      Amino Acid Sequence, Animals, Base Sequence, Bradykinin, blood, Gene Deletion, Genetic Vectors, genetics, Homozygote, Kininogens, chemistry, deficiency, metabolism, Mice, Mice, Knockout, Molecular Sequence Data, Plasma, RNA, Messenger, Sequence Alignment, Thrombosis, Time Factors

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          Abstract

          High-molecular-weight kininogen (HK) plays an important role in the assembly of the plasma kallikrein-kinin system. While the human genome contains a single copy of the kininogen gene, 3 copies exist in the rat (1 encoding K-kininogen and 2 encoding T-kininogen). Here, we confirm that the mouse genome contains 2 homologous kininogen genes, mKng1 and mKng2, and demonstrate that these genes are expressed in a tissue-specific manner. To determine the roles of these genes in murine development and physiology, we disrupted mKng1, which is expressed primarily in the liver. mKng1(-/-) mice were viable, but lacked plasma HK and low-molecular-weight kininogen (LK), as well as DeltamHK-D5, a novel kininogen isoform that lacks kininogen domain 5. Moreover, despite normal tail vein bleeding times, mKng1(-/-) mice displayed a significantly prolonged time to carotid artery occlusion following Rose Bengal administration and laser-induced arterial injury. These results suggest that a single gene, mKng1, is responsible for production of plasma kininogen, and that plasma HK contributes to induced arterial thrombosis in mice.

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