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11. |
Monoclonal antibody directed to a fibrinogen Aα #529–539 epitope inhibits α‐chain crosslinking by transglutaminases |
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Blood Coagulation and Fibrinolysis,
Volume 7,
Issue 1,
1996,
Page 85-92
O. Mitkevich,
J. Sobel,
J. Shainoff,
T. Vlasik,
G. Kalantarov,
I. Trakht,
Z. Streltsova,
G. Samokhin,
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摘要:
A monoclonal antibody (5A2) recognizing a segment near the C-terminus of the fibrin(ogen) Aα-chain (Aα #529–539) was found to inhibit α-chain crosslinking catalyzed by coagulation factor XIII and by tissue-transglutaminase. The rapid γ-chain cross-linking by factor XIIIawas not affected by the antibody. Results obtained from direct binding and competitive immunoassay established that the antigenic determinant recognized by 5A2 was included within the CNBr fragment referred to as CNBr X (Aα #518–584), and that it survived trypsin digestion but was destroyed by treatment with Staph V-8 protease or chymotrypsin. Reverse-phase (C-18) high performance liquid chromatography (HPLC) was employed to obtain a CNBr X tryptic fingerprint, which was subsequently characterized by compositional and NH2-terminal analysis. Assay of the HPLC column effluent revealed a single peak of 5A2 immunoreactivity that coincided with elution of the eleven-residue tryptic peptide, Aα #529–539. When this isolated peptide and its parent CNBr fragment were employed as solution phase competitors in the 5A2 immunoassay, the relative cross-reactivities (18.3%, peptide: fragment) indicated that a significant proportion of the 5A2 epitope was preserved within the small peptide. This is a region that is released from fibrinogen early in its degradation by plasmin. Thus, the antibody can be used as a probe for intact fibrin(ogen) and C-terminal (A)α-chain fragments, in addition to assessing roles of the Aα-chain C-terminus in cross-linking.
ISSN:0957-5235
出版商:OVID
年代:1996
数据来源: OVID
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12. |
Factor VII G331Da variant molecule involving replacement of a residue in the substrate‐binding region of the catalytic domain |
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Blood Coagulation and Fibrinolysis,
Volume 7,
Issue 1,
1996,
Page 93-96
D-Q. Zheng,
M. Shurafa,
H. James,
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PDF (278KB)
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摘要:
An individual identified as having a dysfunctional factor VII was studied to seek underlying genetic defects. A heterozygous mutation in the factor VII gene exon 8 was identified as substitution of A for G at nucleotide position 10,909 [Gly331(GGC) to Asp (GAC)]. An abolishedMspI restriction site was used to confirm heterozygosity for the defect. The mutation occurs within the substrate-binding pocket at a locus on the surface of the factor VII molecule containing a protein-protein interactive site for substrates, providing an explanation for the observed dysfunctional procoagulant activity.
ISSN:0957-5235
出版商:OVID
年代:1996
数据来源: OVID
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13. |
Idiopathic chronic DIC controlled with low‐molecular‐weight heparin |
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Blood Coagulation and Fibrinolysis,
Volume 7,
Issue 1,
1996,
Page 97-98
G. Majumdar,
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摘要:
Chronic disseminated intravascular coagulation (DIC) is a rare coagulation problem usually associated with malignant diseases. The present report concerns a patient with chronic immune thrombocytopenic purpura (ITP) who developed chronic DIC which responded to low-molecular-weight heparin (LMWH) therapy.
ISSN:0957-5235
出版商:OVID
年代:1996
数据来源: OVID
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14. |
Molecular Basis of Thrombosis and Hemostasis |
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Blood Coagulation and Fibrinolysis,
Volume 7,
Issue 1,
1996,
Page 99-99
John Francis,
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PDF (39KB)
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ISSN:0957-5235
出版商:OVID
年代:1996
数据来源: OVID
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