Assay of factor XII in human plasma using prekallikrein or the chromogenic peptide S-2222 as substrates - significance of the functional state of plasma kallikrein

Hoem, Nils; Johannesen, Steinar; Briseid, Kjell

doi:10.1016/0049-3848(89)90227-2

Cited by 10 publications

(2 citation statements)

References 15 publications

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“…The evaluation of the influence of immobilized PAS on blood coagulation was made in according to the method of interaction between the test materials and coagulation factor XII (FXII). The FXII activation measurements were performed by chromogenic peptide substrate assay with the tetrapeptide Bz-lle-Glu-Gly-Arg p-nitrophenylanilide (S-2222) [37][38][39]. Plasma samples were obtained after centrifugation of citrated whole human blood (one volume of 100 mm sodium citrate dihydrate solution to nine volumes of blood) at 3000 g (201C, 15 min).…”

Section: Factor XII Assaymentioning

confidence: 99%

Immobilization of a nonsteroidal antiinflammatory drug onto commercial segmented polyurethane surface to improve haemocompatibility properties

2002

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Section: Factor XII Assaymentioning

confidence: 99%

Immobilization of a nonsteroidal antiinflammatory drug onto commercial segmented polyurethane surface to improve haemocompatibility properties

2002

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“…The autoactivation of FXII on a negatively charged surface, FXII activation induced by kallikrein cleavage and the proteolysis of prekallikrein and FXI by FXIIa are indispensable for the clotting activity of FXII. We developed three methods with which to measure the three distinct functions of FXII using the modified chromogenic substrate assay described by Hoem et al (19).…”

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confidence: 99%

Factor XII Osaka: Abnormal factor XII with partially defective prekallikrein cleavage activity

Iijima

Arakawa²,

Sugahara³

et al. 2011

Thromb Haemost

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A healthy Japanese male had reduced factor XII (FXII) activity (35%) in contrast to normal antigen levels (81%). The F12 of this proband had a 9775G to C mutation in exon 10 and an 11276G to A mutation in exon 13 that resulted in two amino acid substitutions of Ala324Pro (GCG→CCG) in the proline-rich connecting region and Gly531Glu (GGG→GAG) near the active Ser544 in the catalytic domain. His father had the nucleotide 46T/T and a heterozygous 9775G/C mutation. The FXII activity (32%) and antigen level (38%) of the father were about half that of normal individuals with 46T/T, suggesting a heterozygous cross reacting material (CRM)-negative deficiency. His mother had a 46C/T and heterozygous 11276G/A mutation, and 80% FXII activity was incompatible with the corresponding antigen level (125%), suggesting a heterozygous CRM-positive deficiency. The substitution of Ala324Pro probably caused the CRM-negative mutation and the Gly531Glu caused the CRM-positive mutation. We developed three methods based on chromogenic substrates to assay the distinct functions of FXII, namely its autoactivation on a negatively charged surface, activation by kallikrein cleavage and the prekallikrein cleavage activity of FXIIa. The ratios of autoactivated FXIIa/FXII antigen (0.80-1.10) and of kallikrein-induced FXIIa/FXII antigen (0.86-1.00) in plasma from the proband were within normal ranges, whereas those of FXIIa-induced kallikrein/FXII antigen were reduced to 0.41-0.45. In conclusion, the 9775G to C and 11276G to A mutations of F12 led to a CRM-negative and -positive FXII deficiency, and the F12 with 11276A produced a dysfunctional type of FXII with a partial defect (0.41-0.45) in prekallikrein cleavage activity.

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Functional correlation between kallikrein and factor XII activated in human plasma

Briseid

Hoem

Johannesen

et al. 1990

Thrombosis Research

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Assay of factor XII in human plasma using prekallikrein or the chromogenic peptide S-2222 as substrates - significance of the functional state of plasma kallikrein

Cited by 10 publications

References 15 publications

Immobilization of a nonsteroidal antiinflammatory drug onto commercial segmented polyurethane surface to improve haemocompatibility properties

Immobilization of a nonsteroidal antiinflammatory drug onto commercial segmented polyurethane surface to improve haemocompatibility properties

Factor XII Osaka: Abnormal factor XII with partially defective prekallikrein cleavage activity

Functional correlation between kallikrein and factor XII activated in human plasma

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