메뉴 건너뛰기
.. 내서재 .. 알림
소속 기관/학교 인증
인증하면 논문, 학술자료 등을  무료로 열람할 수 있어요.
한국대학교, 누리자동차, 시립도서관 등 나의 기관을 확인해보세요
(국내 대학 90% 이상 구독 중)
로그인 회원가입 고객센터 ENG
주제분류

추천
검색
질문

논문 기본 정보

자료유형
학술대회자료
저자정보
저널정보
한국실험동물학회 한국실험동물학회 학술발표대회 논문집 2005년 한국실험동물학회 춘계학술대회
발행연도
2005.6
수록면
265 - 276 (12page)

이용수

표지
📌
연구주제
📖
연구배경
🔬
연구방법
🏆
연구결과
AI에게 요청하기
추천
검색
질문

초록· 키워드

오류제보하기
The AP-1 (activator protein 1) protein is the bZip group of DNA binding transcription factors belonging to protooncogenes. The AP-1 is composed of Jun family members (c-Jun, JunB and JunD) and Fos family members (c-Fos, FosB, Fra-1 and Fra-2). Jun proteins form both homodimers and heterodimers with Fos proteins, whereas Fos proteins do not form homodimers and require heterodimerization to bind DNA. The AP-1 regulates a wide range of cellular processes, including cell proliferation, survival, differentiation and death. However, despite increasing knowledge regarding the physiological functions of AP-1, the roles of AP-1 in the early development of vertebrate were hardly elucidated. Through our previous investigations, the involvement of AP-1 in mesoderm induction as a major downstream mediator of FGF signaling and AP-1 (Jun-Jun homodimer) involvement in BMP-4 signaling have been demonstrated.
While further investigating the roles of AP-1 in the early development of vertebrate using Xenopus animal cap explants, it was found that AP-1(c-Jun and c-Fos) might mediate activin signaling which is well known as dorsal mesoderm and neural inducer in early Xenopus development. Ectopic overexpression of two components of AP-1 (c-jun and c-fos together, but not alone) induced several markers that could be induced only by activin or smad2/3 (activin signal mediators), but not by any concentration of FGF treatment in the animal cap explants culture. AP-1 transcription activity was regulated by dose-dependent manner of activin treatment. Ectopic overexpression of AP-1 activated the promoter activities of several activin responsive genes. Also the inhibition of AP-1 activity using morpholino c-juns blocked morphological change, gene expression and AP-1 Luciferase activity increased by activin. Additionally, co-injection of c-jun mRNA rescued the morpholino c-juns effects for activin. Smad-mediated-function in downstream of activin signaling was also turned out to be mediated by AP-1. These results suggest that hederodimeric c-Jun and c-Fos may have roles in activin signaling for the regulation of dorsal mesoderm and neural formation.
On the other hand, another heterodimeric component of AP-1 (JunD and c-Fos) had opposite effect to the heterodimeric AP-1 of c-Jun and c-Fos during Xenopus development. Ectopic overexpression of the heterodimeric components of AP-1 (junD and c-fos together, but not alone) induced several ventral markers and ventral blood island markers (hematopoietic transcription factors and globin) that could be induced usually by BMP-4 signaling, a critical ventralizing factor and inducers of hematopoietic stem cell. Also ectopic overexpression of junD and c-fos activated the promoter activities of ventral mesoderm and primitive hematopoietic markers. Further investigation of co-injection with junD/c-fos and BMP-4 mRNAs suggest that heterodimeric JunD and c-Fos have synergic effect with BMP-4 for hematopoiesis. Moreover it was found that BMP-4 was necessary for blood formation induced by heterodimeric JunD and c-Fos. Taken together, the results suggest that heterodimeric c-Jun and c-Fos may be required for dorsal mesoderm formation and neurogenesis as a downstream of activin signaling, and heterodimeric JunD and c-Fos may have an important role in blood formation, in synergy with BMP-4, during Xenopus development. Taken together, the results indicate that AP-1 may have important roles by formation of different complexes of AP-1 components and may be involved in the developmentally critical signalings during the early development of vertebrate embryos.

목차

등록된 정보가 없습니다.

참고문헌 (0)

참고문헌 신청

함께 읽어보면 좋을 논문

논문 유사도에 따라 DBpia 가 추천하는 논문입니다. 함께 보면 좋을 연관 논문을 확인해보세요!

이 논문의 저자 정보

최근 본 자료

전체보기

댓글(0)

0

UCI(KEPA) : I410-ECN-0101-2009-510-016368370