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CB1R에 의한 췌장 베타 새포의 사멸과 증식 조절
| DC Field | Value | Language |
|---|---|---|
| dc.contributor.advisor | 김욱 | - |
| dc.contributor.author | Kim, Jihye | - |
| dc.date.accessioned | 2018-11-08T08:21:59Z | - |
| dc.date.available | 2018-11-08T08:21:59Z | - |
| dc.date.issued | 2015-08 | - |
| dc.identifier.other | 20334 | - |
| dc.identifier.uri | https://dspace.ajou.ac.kr/handle/2018.oak/13162 | - |
| dc.description | 학위논문(석사)--아주대학교 일반대학원 :분자과학기술학과,2015. 8 | - |
| dc.description.tableofcontents | Ⅰ. INTRODUCTION Ⅱ. MATERIALS and METHODS Ⅲ. RESULTS 1. Activation of CB1R with WIN55,212-2 induces β cell death and cell cycle arrest at G1 phase. 2. WIN55,212-2 leads to decreased levels of Bcl-2 and Cyclin D2 in pancreatic β cells. 3. CB1R blockade increases levels of Cyclin D2 and Bcl-2 in pancreatic β cells of STZ-treated and db/db mice. Ⅳ. DISCUSSION Ⅴ. REFERENCE Ⅵ. ABSTRACT IN KOREAN(국문초록) | - |
| dc.language.iso | eng | - |
| dc.publisher | The Graduate School, Ajou University | - |
| dc.rights | 아주대학교 논문은 저작권에 의해 보호받습니다. | - |
| dc.title | CB1R에 의한 췌장 베타 새포의 사멸과 증식 조절 | - |
| dc.title.alternative | Regulation of Apoptosis and Proliferation by Cannabinoids in Pancreatic Beta Cells: Involvement of Bcl-2 and Cyclin D2 | - |
| dc.type | Thesis | - |
| dc.contributor.affiliation | 아주대학교 일반대학원 | - |
| dc.contributor.alternativeName | Jihye Kim | - |
| dc.contributor.department | 일반대학원 분자과학기술학과 | - |
| dc.date.awarded | 2015. 8 | - |
| dc.description.degree | Master | - |
| dc.identifier.localId | 705411 | - |
| dc.identifier.url | http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000020334 | - |
| dc.subject.keyword | pancreatic beta-cell | - |
| dc.subject.keyword | cannabinoid receptor | - |
| dc.subject.keyword | diabetes | - |
| dc.description.alternativeAbstract | Recent reports have shown that cannabinoid 1 receptors (CB1Rs) are expressed in pancreatic β cells, where they induce cell death by directly inhibiting activation of insulin receptor. Here I report that anti-apoptotic protein Bcl-2 and cell cycle regulator Cyclin D2 are involved in cannabinoid-induced β-cell death and growth arrest. Treatment of MIN6 and βTC6 cells with a synthetic CB1R agonist WIN55,212-2 leads to decrease in the expression of Bcl-2 and Cyclin D2, in turn inducing an arrest of the cell cycle in the G0/G1 phase and caspase-3-dependent apoptosis. Consistently, genetic deletion and pharmacological blockade of CB1Rs leads to increased β-cell survival and proliferation after injury due to increased levels of Bcl-2 and Cyclin D2. These findings provide evidence for involvement of Bcl-2 and Cyclin D2 in the regulation of β-cell survival and growth and will serve as a basis for developing new therapeutic interventions to enhance β-cell function and growth in diabetes. | - |
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- Graduate School of Ajou University > Department of Molecular Science and Technology > 3. Theses(Master)
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