보고서 정보
주관연구기관 |
서울대학교 산학협력단 |
연구책임자 |
정용근
|
참여연구자 |
최의주
,
박철승
|
보고서유형 | 2단계보고서 |
발행국가 | 대한민국 |
언어 |
한국어
|
발행년월 | 2009-05 |
과제시작연도 |
2008 |
주관부처 |
교육과학기술부 |
사업 관리 기관 |
한국과학재단 Korea Science and Engineering Foundtion |
등록번호 |
TRKO200900074390 |
과제고유번호 |
1345085994 |
사업명 |
뇌기능활용 및 뇌질환치료기술개발사업 |
DB 구축일자 |
2015-01-08
|
키워드 |
뇌질환.세포기반 유전자 발굴.이온채널.세포사멸.Neurodisease.cell-based assay.gene isolation.CIIA.ion channel.cell death.
|
초록
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$\cdot$ 치매 병 유발인자 (ADRGs) 8개 발굴 및 기능연구: Ab receptor, memory조절(AIMP, 특허), E2-25K (J. Cell Biol.), AIMP와 ADRG10 KO mice 제조, 분석을 통한 새로운 AD drug target 제시 및 제어제 발굴
$\cdot$ HD 조절 인자(HDRGs) 9개 발굴 및 기능연구
$\cdot$ Batten disease: CLN3 기전규명 (Hum Mol Genetics), 조절 제어제 발굴<
$\cdot$ 치매 병 유발인자 (ADRGs) 8개 발굴 및 기능연구: Ab receptor, memory조절(AIMP, 특허), E2-25K (J. Cell Biol.), AIMP와 ADRG10 KO mice 제조, 분석을 통한 새로운 AD drug target 제시 및 제어제 발굴
$\cdot$ HD 조절 인자(HDRGs) 9개 발굴 및 기능연구
$\cdot$ Batten disease: CLN3 기전규명 (Hum Mol Genetics), 조절 제어제 발굴
$\cdot$ Cell death 분자기전 연구: (AK2, Nat Cell Biol), Ab toxicity receptor 연구(AIMP-논문 준비 중), Ischemic/hypoxic cell death 연구(APIP, Oncogene)(ARC, J. Biol. Chem), CRBN (허혈신경세포 사멸), CIIA (허혈성 뇌신경세포독성)
$\cdot$ $BK_{Ca}$ 채널의 '결합단백체' 확보, Myelin basic protein과 calmodulin 결합규명
$\cdot$ CIIA transgenic mice 제조 (국내 특허 출원).
$\cdot$ CIIA가 ALS 신경독성을 억제 (국내 특허 출원). CIIA의 타겟인자 발굴 (manuscript submitted), MST1 neuroinflammation에 관여(논문 투고중)
Abstract
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This project is was designed to better understand molecular mechanism of neuronal disease by isolating new genes and characterizing their functions in vivo, postulating new drug targets. We performed cell-based assay together with bioinformatics and isolated new modulators which may function in cell
This project is was designed to better understand molecular mechanism of neuronal disease by isolating new genes and characterizing their functions in vivo, postulating new drug targets. We performed cell-based assay together with bioinformatics and isolated new modulators which may function in cell death and human diseases, such as Alzheimer's disease, ischemic damage, and Huntington disease. We characterized the role of AK2 in cell death (Nat Cell Biol 2007), ARC in ischemic cell death (J. Biol. Chem 2008), APIP in ischemic cell death (Oncogene 2007), role of E2-25K in amyloid toxicity (J. Cell Biol. 2008), role of CLN3 in Batten disease (Hum Mol Genetics 2007), role of Scamps in Huntington diserase (J. Biol Chem. 2009), and role of CIIA in brain ischemic cell death (manuscript in preparation, 2009). In addition, we also isolated new modulatory genes for neuronal diseases, such as Alzheimer disease-associated genes (ADRGs), Huntington-disease-associated genes (HDRGs) using cell-based assays and are characterizing their functions. Especially, the role of AIMP in the amyloid toxicity was characterized in vitro and in vivo and is postulated as a possible drug target. (patent in progress in USA and europe, 2007, 2008). Also, role of CRBN in cellular function and role of potassium channel in ionic transmission was characterized in detail by via its binding proteins and are under characterization by generating transgenic mice model. In addition, we showed that CIIA regulates ischemic death of neuronal cells by regulating JNK-p38 pathway Further, CIIA transgenic mice was generated and is analyzed ta better understand CIIA-mediated signal transduction. These results elucidate these genes and proteins as possible new modulators of brain function and its associated diseases.
목차 Contents
- 제 1 장 연구개발과제의 개요 ...8
- 제 2 장 국내외 기술개발 현황 ...13
- 제 3 장 연구개발수행 내용 및 결과 ...29
- 제 4 장 목표달성도 및 관련분야에의 기여도 ...47
- 제 5 장 연구개발결과의 활용계획 ...49
- 제 6 장 연구개발과정에서 수집한 해외과학기술정보 ...50
- 제 7 장 참고문헌 ...52
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