Dopamine D2 Receptor-mediated Epidermal Growth Factor Receptor Transactivation through a Disintegrin and Metalloprotease Regulates Dopaminergic Neuron Development via Extracellular Signal-related Kinase Activation
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Yoon, Sehyoun | - |
dc.contributor.author | Baik, Ja-Hyun | - |
dc.date.accessioned | 2021-09-05T20:19:46Z | - |
dc.date.available | 2021-09-05T20:19:46Z | - |
dc.date.created | 2021-06-15 | - |
dc.date.issued | 2013-10-04 | - |
dc.identifier.issn | 0021-9258 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/101894 | - |
dc.description.abstract | Dopamine D2 receptor (D2R)-mediated extracellular signal-regulated kinase (ERK) activation plays an important role in the development of dopaminergic mesencephalic neurons. Here, we demonstrate that D2R induces the shedding of heparin-binding epidermal growth factor (EGF) through the activation of a disintegrin and metalloprotease (ADAM) 10 or 17, leading to EGF receptor transactivation, downstream ERK activation, and ultimately an increase in the number of dopaminergic neurons and their neurite length in primary mesencephalic cultures from wild-type mice. These outcomes, however, were not observed in cultures from D2R knock-out mice. Our findings show that D2R-mediated ERK activation regulates mesencephalic dopaminergic neuron development via EGF receptor transactivation through ADAM10/17. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC | - |
dc.subject | PARKINSONS-DISEASE | - |
dc.subject | EGF RECEPTOR | - |
dc.subject | HB-EGF | - |
dc.subject | SURVIVAL | - |
dc.subject | EXPRESSION | - |
dc.subject | GENERATION | - |
dc.subject | ADAM10 | - |
dc.subject | NURR1 | - |
dc.title | Dopamine D2 Receptor-mediated Epidermal Growth Factor Receptor Transactivation through a Disintegrin and Metalloprotease Regulates Dopaminergic Neuron Development via Extracellular Signal-related Kinase Activation | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Baik, Ja-Hyun | - |
dc.identifier.doi | 10.1074/jbc.M113.461202 | - |
dc.identifier.scopusid | 2-s2.0-84885168622 | - |
dc.identifier.wosid | 000330298800002 | - |
dc.identifier.bibliographicCitation | JOURNAL OF BIOLOGICAL CHEMISTRY, v.288, no.40, pp.28435 - 28446 | - |
dc.relation.isPartOf | JOURNAL OF BIOLOGICAL CHEMISTRY | - |
dc.citation.title | JOURNAL OF BIOLOGICAL CHEMISTRY | - |
dc.citation.volume | 288 | - |
dc.citation.number | 40 | - |
dc.citation.startPage | 28435 | - |
dc.citation.endPage | 28446 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.subject.keywordPlus | PARKINSONS-DISEASE | - |
dc.subject.keywordPlus | EGF RECEPTOR | - |
dc.subject.keywordPlus | HB-EGF | - |
dc.subject.keywordPlus | SURVIVAL | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | GENERATION | - |
dc.subject.keywordPlus | ADAM10 | - |
dc.subject.keywordPlus | NURR1 | - |
dc.subject.keywordAuthor | ADAM | - |
dc.subject.keywordAuthor | ADAMTS | - |
dc.subject.keywordAuthor | Dopamine Receptors | - |
dc.subject.keywordAuthor | Epidermal Growth Factor Receptor (EGFR) | - |
dc.subject.keywordAuthor | ERK | - |
dc.subject.keywordAuthor | Signal Transduction | - |
dc.subject.keywordAuthor | Dopaminergic Neuron Development | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
(02841) 서울특별시 성북구 안암로 14502-3290-1114
COPYRIGHT © 2021 Korea 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.