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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Jacob, Harrys K. C. Beijersbergen, Roderick L. Bernards, Rene Lechuga, Carmen G. Huang, Sidong García-medina, Raquel Drosten, Matthias Sum, Eleanor Y. M. Simón-carrasco, Lucía Barbacid, Mariano |
| Description | Author Affiliation: Drosten M ( Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas, 28029 Madrid, Spain); Sum EY ( Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas, 28029 Madrid, Spain); Lechuga CG ( Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas, 28029 Madrid, Spain); Simón-Carrasco L ( Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas, 28029 Madrid, Spain); Jacob HK ( Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas, 28029 Madrid, Spain); García-Medina R ( Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas, 28029 Madrid, Spain); Huang S ( Division of Molecular Carcinogenesis and Center for Biomedical Genetics, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.); Beijersbergen RL ( Division of Molecular Carcinogenesis and Center for Biomedical Genetics, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.); Bernards R ( Division of Molecular Carcinogenesis and Center for Biomedical Genetics, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.); Barbacid M ( Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas, 28029 Madrid, Spain); |
| Abstract | The Ras family of small GTPases constitutes a central node in the transmission of mitogenic stimuli to the cell cycle machinery. The ultimate receptor of these mitogenic signals is the retinoblastoma (Rb) family of pocket proteins, whose inactivation is a required step to license cell proliferation. However, little is known regarding the molecular events that connect Ras signaling with the cell cycle. Here, we provide genetic evidence to illustrate that the p53/p21 Cdk-interacting protein 1 (Cip1)/Rb axis is an essential component of the Ras signaling pathway. Indeed, knockdown of p53, p21Cip1, or Rb restores proliferative properties in cells arrested by ablation of the three Ras loci, H-, N- and K-Ras. Ras signaling selectively inactivates p53-mediated induction of p21Cip1 expression by inhibiting acetylation of specific lysine residues in the p53 DNA binding domain. Proliferation of cells lacking both Ras proteins and p53 can be prevented by reexpression of the human p53 ortholog, provided that it retains an active DNA binding domain and an intact lysine residue at position 164. These results unveil a previously unidentified role for p53 in preventing cell proliferation under unfavorable mitogenic conditions. Moreover, we provide evidence that cells lacking Ras and p53 proteins owe their proliferative properties to the unexpected retroactivation of the Raf/Mek/Erk cascade by a Ras-independent mechanism. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 42 |
| Volume Number | 111 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2014-10-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Cell Proliferation MAP Kinase Signaling System Tumor Suppressor Protein P53 Metabolism Ras Proteins Alleles Amino Acid Sequence Animals Cell Cycle Cyclin-Dependent Kinase Inhibitor P21 Extracellular Signal-Regulated MAP Kinases Genes, Ras Lysine Chemistry Mice Microscopy, Fluorescence Mitogen-Activated Protein Kinase Kinases Molecular Sequence Data Neoplasms Sequence Homology, Amino Acid Raf Kinases Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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