Epitope Mapping Immunoassay Analysis of the Interaction between -Amyloid and Fibrinogen
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Giau, Vo Van | - |
dc.contributor.author | An, Seong Soo A. | - |
dc.date.available | 2020-02-27T04:41:42Z | - |
dc.date.created | 2020-02-05 | - |
dc.date.issued | 2019-02-01 | - |
dc.identifier.issn | 1422-0067 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/1862 | - |
dc.description.abstract | The vast majority of patients with Alzheimer's disease (AD) suffer from impaired cerebral circulation. Substantial evidence indicates that fibrinogen (Fbg) and fibrin clot formation play an important role in this circulatory dysfunction in AD. Fbg interacts with -amyloid (1-42) (A), forming plasmin-resistant abnormal blood clots, and increased fibrin deposition has been discovered in the brains of AD patients and mouse models. In this study, biochemical approaches and the epitope mapping immunoassay were employed to characterize binding epitopes within the Fbg and complementary epitopes in A. We discovered the A5-25 peptide as the most critical region for the interaction, which can be inhibited by specific monoclonal and polyclonal antibodies against the central region of A. A binding to Fbg may block plasmin-mediated fibrin cleavage at this site, resulting in the generation of increased levels of plasmin-resistant fibrin degradation fragments. Our study elucidates the A-Fbg interaction that may involve the mechanism by which A-Fbg binding delays fibrinolysis by plasmin, providing valuable information in the development of therapeutic approaches for AD. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | MDPI | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.subject | ALZHEIMERS-DISEASE | - |
dc.subject | COGNITIVE DECLINE | - |
dc.subject | COMPLEX-FORMATION | - |
dc.subject | BINDING-SITES | - |
dc.subject | THROMBOSIS | - |
dc.subject | ADHESION | - |
dc.subject | PROTEIN | - |
dc.title | Epitope Mapping Immunoassay Analysis of the Interaction between -Amyloid and Fibrinogen | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000462412500040 | - |
dc.identifier.doi | 10.3390/ijms20030496 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.20, no.3 | - |
dc.identifier.scopusid | 2-s2.0-85060520033 | - |
dc.citation.title | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.citation.volume | 20 | - |
dc.citation.number | 3 | - |
dc.contributor.affiliatedAuthor | Giau, Vo Van | - |
dc.contributor.affiliatedAuthor | An, Seong Soo A. | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Alzheimer&apos | - |
dc.subject.keywordAuthor | s disease | - |
dc.subject.keywordAuthor | amyloid- | - |
dc.subject.keywordAuthor | epitope mapping | - |
dc.subject.keywordAuthor | ligand | - |
dc.subject.keywordAuthor | fibrinogen | - |
dc.subject.keywordPlus | ALZHEIMERS-DISEASE | - |
dc.subject.keywordPlus | COGNITIVE DECLINE | - |
dc.subject.keywordPlus | COMPLEX-FORMATION | - |
dc.subject.keywordPlus | BINDING-SITES | - |
dc.subject.keywordPlus | THROMBOSIS | - |
dc.subject.keywordPlus | ADHESION | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Chemistry | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Multidisciplinary | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
1342, Seongnam-daero, Sujeong-gu, Seongnam-si, Gyeonggi-do, Republic of Korea(13120)031-750-5114
COPYRIGHT 2020 Gachon University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.