Fig. 5.
Fig. 5. Cross-linking of fibrin in normal and FXIII-deficient plasma clotted by thrombin and CaCl2 shown on 7.5% SDS-PAGE. Lane 1, Mr marker proteins; lane 2, fibrinogen standard; lane 3, control plasma; lane 4, patient II-3; lane 5, patient II-1; lane 6, control plasma + iodoacetamide acid (IAA); lane 7, patient II-3 + IAA; and lane 8, patient II-1 + IAA. Cross-linking pattern in the control plasma shows disappearance of γ- and α-chains and formation of γ-γ dimers and α polymers. Cross-linking pattern in the patients; plasma shows diminution of the γ-chains and formation of γ-γ dimers and possibly even some α polymers at the top of the stacking gel, indicating the presence of true FXIII activity. The process is inhibited by treatment with transglutaminase inhibitor iodoacetamide acid.

Cross-linking of fibrin in normal and FXIII-deficient plasma clotted by thrombin and CaCl2 shown on 7.5% SDS-PAGE. Lane 1, Mr marker proteins; lane 2, fibrinogen standard; lane 3, control plasma; lane 4, patient II-3; lane 5, patient II-1; lane 6, control plasma + iodoacetamide acid (IAA); lane 7, patient II-3 + IAA; and lane 8, patient II-1 + IAA. Cross-linking pattern in the control plasma shows disappearance of γ- and α-chains and formation of γ-γ dimers and α polymers. Cross-linking pattern in the patients; plasma shows diminution of the γ-chains and formation of γ-γ dimers and possibly even some α polymers at the top of the stacking gel, indicating the presence of true FXIII activity. The process is inhibited by treatment with transglutaminase inhibitor iodoacetamide acid.

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