The mutation Ser511Asn leads to N-glycosylation and increases the cleavage of high molecular weight kininogen in rats genetically susceptible to inflammation.

doi:10.1182/blood-2003-02-0661

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The mutation Ser511Asn leads to N-glycosylation and increases the cleavage of high molecular weight kininogen in rats genetically susceptible to inflammation.

Blood - 15 Oct 2003

Isordia-Salas Irma, Pixley Robin A, Parekh Hemant, Kunapuli Satya P, Li Fengling, Stadnicki Anthony, Lin Yingzhang, Sartor R Balfour, Colman Robert W

Abstract excerpt

Crohn disease is immunologically mediated and characterized by intestinal and systemic chronic inflammation. In a rat model, injection of peptidoglycan-polysaccharide complexes into the intestinal wall induced chronic inflammation in Lewis but neither Fischer nor Buffalo rats, indicating a differential genetic susceptibility. Proteolysis of plasma high molecular weight kininogen (HK) yielding bradykinin and...

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The mutation Ser511Asn leads to N-glycosylation and increases the cleavage of high molecular weight kininogen in rats genetically susceptible to inflammation.

Abstract excerpt

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