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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2005.1
- 수록면
- 488 - 491 (4page)
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초록· 키워드
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NF-Y transcription factor binds to CCAAT boxes on promoters of cell cycle regulatory genes such as cdc2, cyclin B, cdc25C, and cyclin A. We previously reported that the DNA binding activity of NF-Y is regulated by p53-p21-cdk2 pathway. CBF/HSP70 was originally identified as a transcription factor binding to the CCAAT box on the hsp70 promoter and mediates transcription repression of hsp70 pro- moter by p53. Recently it was demonstrated that CBF/HSP70 interacts and cooperates with NF-Y. In this study, we found that p53 represses the trans- cription of CBF/HSP70. Since transactivation ability of NF-Y is regulated in a cell cycle-dependent maner, we examined the transcription of CBF/HSP70 during the cell cycle. After synchronization of a human bladder carcinoma cell lacking functional p53 at early S phase, we infect the cells with adenovirus encoding p53. Cels infected with control virus progressed to S and G2 after release from the arrest. In contrast, cells expressing p53 enter S and G2 phases, but arrest at G2/M. The expression of CBF/HSP70 was induced at S/G2 phase in cells infected with a control virus, but kept to be repressed in cells expressing p53. Thus, these results suggest that p53 suppresses the expression of cell cycle regulatory genes though inhibiting both CCAAT binding factors, CBF/HSP70 and NF-Y.
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참고문헌 (12)
참고문헌 신청
/ / Cdk2-dependent phosphorylationof the NF-Y transcription factor and its involvement in thep53-p21 signaling pathway
/ / Constitutive activation of cyclin B1-associated cdc2 kinaseoverrides p53-mediated G2-M arrest 60 : 542 ~ 5
/ / EJ cells were synchronized at G1-S boundary and infected with a recombinantadenovirus that encodes p53 After release from the growth arrest cells were harvested at the i
/ / NF-Ymediates the transcriptional inhibition of the cyclin B1 and cdc25C promoters upon induced G2 arrest : 5570 ~ 6
/ 1995 / implications for cancer : 3 ~ 15
/ / Constitutive activation of cyclin B1-associated cdc2 kinaseoverrides p53-mediated G2-M arrest 60 : 542 ~ 5
/ / EJ cells were synchronized at G1-S boundary and infected with a recombinantadenovirus that encodes p53 After release from the growth arrest cells were harvested at the i
/ / NF-Ymediates the transcriptional inhibition of the cyclin B1 and cdc25C promoters upon induced G2 arrest : 5570 ~ 6
/ 1995 / implications for cancer : 3 ~ 15
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