Interaction of c-Abl and p73α and their collaboration to induce apoptosis
@article{Agami1999InteractionOC, title={Interaction of c-Abl and p73α and their collaboration to induce apoptosis}, author={R. Agami and G. Blandino and M. Oren and Y. Shaul}, journal={Nature}, year={1999}, volume={399}, pages={809-813} }
c-Abl, a non-receptor tyrosine kinase, is activated by agents that damage DNA. This activation results in either arrest of the cell cycle in phase G1 or apoptotic cell death, both of which are dependent on the kinase activity of c-Abl. p73, a member of the p53 family of tumour-suppressor proteins,, can also induce apoptosis. Here we show that the apoptotic activity of p73α requires the presence of functional, kinase-competent c-Abl. Furthermore, p73 and c-Abl can associate with each other, and… CONTINUE READING
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- 2003
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- 2007
- 69
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- Journal of Biological Chemistry
- 2004
- 73
- PDF
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References
SHOWING 1-10 OF 21 REFERENCES
c-Abl Neutralizes the Inhibitory Effect of Mdm2 on p53*
- Biology, Medicine
- The Journal of Biological Chemistry
- 1999
- 110
- PDF
Identification of a novel p53 functional domain that is necessary for efficient growth suppression.
- Biology, Medicine
- Proceedings of the National Academy of Sciences of the United States of America
- 1996
- 480
- PDF
The polyproline region of p53 is required to activate apoptosis but not growth arrest
- Biology, Medicine
- Oncogene
- 1997
- 328
- PDF
Determination of cell fate by c-Abl activation in the response to DNA damage
- Biology, Medicine
- Oncogene
- 1998
- 173
- PDF
Abi-2, a novel SH3-containing protein interacts with the c-Abl tyrosine kinase and modulates c-Abl transforming activity.
- Biology, Medicine
- Genes & development
- 1995
- 275
- PDF
The potential tumor suppressor p73 differentially regulates cellular p53 target genes.
- Biology, Medicine
- Cancer research
- 1998
- 354
- PDF
Abl-interactor-1, a novel SH3 protein binding to the carboxy-terminal portion of the Abl protein, suppresses v-abl transforming activity.
- Biology, Medicine
- Genes & development
- 1995
- 248
- PDF