Transcriptional repression of the eukaryotic initiation factor 4E gene by wild type p53.
Transcriptional repression of the eukaryotic initiation factor 4E gene by wild type p53.
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野生型 p53 对真核起始因子 4E 基因的转录抑制。
DOI：
10.1016/j.bbrc.2005.08.026
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Zhou,Muxiang
中科院分区：
文献类型：
--
作者：
Zhu,Ningxi;Gu,Lubing;Findley,HarryW;Zhou,Muxiang
The eukaryotic initiation factor 4E (eIF4E) plays important roles in transformation and cancer progression. It is frequently overexpressed in malignant cells, one mechanism of which is through transcriptional activation by c-myc. Here, we report that high level of eIF4E expression and its tumorigenicity could be alternatively associated with defects of p53, since we found that induction of wt-p53 repressed eIF4E expression. Gene transfection of p53 inhibited eIF4E promoter activity, while inactivation of p53 either by mutation or by over-expression of MDM2 resulted in stimulation of eIF4E promoter activity. We demonstrated that p53-repression of eIF4E was regulated by c-myc. The wt-p53 can physically bind to c-myc, which inhibited binding of c-myc to eIF4E promoter and c-myc-stimulated promoter activity. These results suggest that the expression of eIF4E is reciprocally regulated by p53 and c-myc, and loss of p53-mediated control over c-myc-dependent transactivation of eIF4E may represent a novel mechanism for eIF4E-mediated neoplastic transformation and cancer progression.
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影响因子：
11.4
作者：
ZHANG, W;GUO, XY;DEISSEROTH, AB
通讯作者：
DEISSEROTH, AB
影响因子：
9
作者：
Li, BDL;McDonald, JC;De Benedetti, A
通讯作者：
De Benedetti, A
影响因子：
11.2
作者：
Xiao-ying Yin;L. Grove;N. Datta;K. Katula;M. Long;M. Long;E. Prochownik;E. Prochownik
通讯作者：
Xiao-ying Yin;L. Grove;N. Datta;K. Katula;M. Long;M. Long;E. Prochownik;E. Prochownik
影响因子：
11.2
作者：
Cherie-Ann O. Nathan;Kenneth W. Sanders;F. Abreo;Raja Nassar;Jonathan Glass
通讯作者：
Cherie-Ann O. Nathan;Kenneth W. Sanders;F. Abreo;Raja Nassar;Jonathan Glass
DOI：
10.1073/pnas.88.22.9979
发表时间：
1991-11-01
影响因子：
11.1
作者：
GINSBERG, D;MECHTA, F;OREN, M
通讯作者：
OREN, M