APEX-1 (인간 apyrimidinic / apurinic 효소)은 염기성 사이트 및 DNA단일 가닥 결손으로 손상된 DNA을 복구 할 수 있는 다기능 단백질이다. 또한 APEX-1은 많은 전사 인자들의 redox-modifying factor (산화 환원...
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https://www.riss.kr/link?id=A101744828
2013
English
470
KCI등재
학술저널
1183-1191(9쪽)
0
0
상세조회0
다운로드국문 초록 (Abstract)
APEX-1 (인간 apyrimidinic / apurinic 효소)은 염기성 사이트 및 DNA단일 가닥 결손으로 손상된 DNA을 복구 할 수 있는 다기능 단백질이다. 또한 APEX-1은 많은 전사 인자들의 redox-modifying factor (산화 환원...
APEX-1 (인간 apyrimidinic / apurinic 효소)은 염기성 사이트 및 DNA단일 가닥 결손으로 손상된 DNA을 복구 할 수 있는 다기능 단백질이다. 또한 APEX-1은 많은 전사 인자들의 redox-modifying factor (산화 환원 수정 요소)로서의 역할을 한다고 알려져 있다. 이런 APEX-1의 전사 타겟을 동정하는 것은 APEX-1의 다양한 세포 내 작용 메커니즘을 이해하는데 필수적이다. 따라서 이 논문에서는 먼저 Expression array analysis를 통해 glial cell-derived neurotropic factor receptor α1 (GFRα1)을 동정하였다. GFRα1은 glial cell-derived neurotropic factor (GDNF) family 수용체이며 APEX-1에 의해 발현이 증가된다. APEX-1이 과발현된 세포에서 GDNF처리에 의해GDNF/ GFRα1 시그널 타겟인 c-Src가 Tyr418잔기에서 인산화 됨을 관찰하였다. 또한 APEX-1이 과발현된 세포에 GDNF처리하면, 세포증식이 증가함을 보았다. 반면, APEX-1 발현을 siRNA을 이용하여 감소시키면 GFR α1 발현과 GDNF에 의한 c-Src 인산화 및 세포증식이 감소함을 확인하였다. 이상의 결과는 APEX-1은 GDNF/GFRα1 시그널을 통해 세포 생존과 증식을 조절함을 증명하였다. 따라서 본 연구를 통해 APEX-1의 세포 증식을 조절하는 새로운 기전을 규명하였다.
다국어 초록 (Multilingual Abstract)
Human apurinic/apyrimidinic endonuclease (APEX-1) is a multifunctional protein that is capable of repairing abasic sites and single-strand breaks in damaged DNA. In addition, it serves as a redox-modifying factor for a number of transcription factors....
Human apurinic/apyrimidinic endonuclease (APEX-1) is a multifunctional protein that is capable of repairing abasic sites and single-strand breaks in damaged DNA. In addition, it serves as a redox-modifying factor for a number of transcription factors. Identifying the transcriptional targets of APEX-1 is essential for understanding how it affects various cellular outcomes. Expression array analysis was used to identify glial cell-derived neurotropic factor receptor α1 (GFRα1), which is an encoding receptor for the glial cell-derived neurotropic factor (GDNF) family, the expression of which is induced by APEX-1. A target of GDNF/GFRα signaling, c-Src (Tyr418) was strongly phosphorylated by GNDF in the APEX-1 expressing cells. Moreover, GDNF initiated cell proliferation, measured by counting the number of cells, in the APEX-1 expressing cells. Importantly, the down-regulation of APEX-1 by siRNA caused a marked reduction in the GFRα1 expression level, and it reduced the ability of GDNF to phosphorylate c-Src (Tyr418) and stimulate cell proliferation. These results demonstrate an association between APEX-1 and GDNF/GFRα signaling and suggest a potential molecular mechanism for the involvement of APEX-1 in cell survival and proliferation.
목차 (Table of Contents)
참고문헌 (Reference)
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2 Xu, Y., "The apurinic/apyrimidinic endonuclease(APE/ref-1)DNA repair enzyme is elevated in premalignant and malignant cervical cancer" 17 : 3713-3719, 1997
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1 Xanthoudakis, S., "The redox/DNA repair protein, Ref-1, is essential for early embryonic development in mice" 93 : 8919-8923, 1996
2 Xu, Y., "The apurinic/apyrimidinic endonuclease(APE/ref-1)DNA repair enzyme is elevated in premalignant and malignant cervical cancer" 17 : 3713-3719, 1997
3 Airaksinen, M. S., "The GDNF family : signalling, biological functions and therapeutic value" 3 : 383-394, 2002
4 Moore, M. W., "Renal and neuronal abnormalities in mice lacking GDNF" 382 : 76-79, 1996
5 Sanchez, M. P., "Renal agenesis and the absence of enteric neurons in mice lacking GDNF" 382 : 70-73, 1996
6 Meng, X., "Regulation of cell fate decision of undifferentiated spermatogonia by GDNF" 287 : 1489-1493, 2000
7 Xanthoudakis, S., "Identification and characterization of Ref-1, a nuclear protein that facilitates AP-1 DNA-binding activity" 11 : 653-665, 1992
8 Evans, A. R., "Going APE over ref-1" 461 : 83-108, 2000
9 Cacalano, G., "GFRalpha1 is an essential receptor component for GDNF in the developing nervous system and kidney" 21 : 53-62, 1998
10 Jing, S., "GDNF-induced activation of the ret protein tyrosine kinase is mediated by GDNFR-alpha, a novel receptor for GDNF" 85 : 1113-1124, 1996
11 Popsueva, A., "GDNF promotes tubulogenesis of GFRalpha1-expressing MDCK cells by Src-mediated phosphorylation of Met receptor tyrosine kinase" 161 : 119-129, 2003
12 Airaksinen, M. S., "GDNF family neurotrophic factor signaling: four masters, one servant?" 13 : 313-325, 1999
13 Lin, L. F., "GDNF : a glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons" 260 : 1130-1132, 1993
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16 Wilson, T. M., "Differential expression of the apurinic / apyrimidinic endonuclease(APE/ref-1)multifunctional DNA base excision repair gene during fetal development and in adult rat brain and testis" 362 : 237-248, 1996
17 Pichel, J. G., "Defects in enteric innervation and kidney development in mice lacking GDNF" 382 : 73-76, 1996
18 Bobola, M. S., "Apurinic/apyrimidinic endonuclease activity is elevated in human adult gliomas" 7 : 3510-3518, 2001
19 Grosch, S., "Apurinic endonuclease(Ref-1)is induced in mammalian cells by oxidative stress and involved in clastogenic adaptation" 58 : 4410-4416, 1998
20 Moore, D. H., "Alterations in the expression of the DNA repair/redox enzyme APE/ref-1 in epithelial ovarian cancers" 6 : 602-609, 2000
21 Veit, C., "Activation of phosphatidylinositol, 3-kinase and extracellular signal-regulated kinase is required for glial cell line-derived neurotrophic factor-induced migration and invasion of pancreatic carcinoma cells" 64 : 5291-5300, 2004
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24 Klein, R. D., "A GPI-linked protein that interacts with Ret to form a candidate neurturin receptor" 387 : 717-721, 1997
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학술지 이력
연월일 | 이력구분 | 이력상세 | 등재구분 |
---|---|---|---|
2027 | 평가예정 | 재인증평가 신청대상 (재인증) | |
2021-01-01 | 평가 | 등재학술지 유지 (재인증) | |
2018-01-01 | 평가 | 등재학술지 유지 (등재유지) | |
2015-01-01 | 평가 | 등재학술지 유지 (등재유지) | |
2011-08-03 | 학술지명변경 | 외국어명 : Korean Journal of Life Science -> Journal of Life Science | |
2011-01-01 | 평가 | 등재학술지 유지 (등재유지) | |
2009-01-01 | 평가 | 등재학술지 유지 (등재유지) | |
2007-01-01 | 평가 | 등재학술지 유지 (등재유지) | |
2004-01-01 | 평가 | 등재학술지 선정 (등재후보2차) | |
2003-01-01 | 평가 | 등재후보 1차 PASS (등재후보1차) | |
2001-07-01 | 평가 | 등재후보학술지 선정 (신규평가) |
학술지 인용정보
기준연도 | WOS-KCI 통합IF(2년) | KCIF(2년) | KCIF(3년) |
---|---|---|---|
2016 | 0.37 | 0.37 | 0.42 |
KCIF(4년) | KCIF(5년) | 중심성지수(3년) | 즉시성지수 |
0.43 | 0.43 | 0.774 | 0.09 |