p53-mediated apoptosis requires inositol hexakisphosphate kinase-2

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Inositol pyrophosphates have been implicated in numerous biological processes. Inositol hexakisphosphate kinase-2 (IP6K2), which generates the inositol pyrophosphate, diphosphoinositol pentakisphosphate (IP7), influences apoptotic cell death. The tumor suppressor p53 responds to genotoxic stress by engaging a transcriptional program leading to cell-cycle arrest or apoptosis. We demonstrate that IP6K2 is required for p53-mediated apoptosis and modulates the outcome of the p53 response. Gene disruption of IP6K2 in colorectal cancer cells selectively impairs p53-mediated apoptosis, instead favoring cell-cycle arrest. IP6K2 acts by binding directly to p53 and decreasing expression of proarrest gene targets such as the cyclin-dependent kinase inhibitor p21.
Publisher
NATL ACAD SCIENCES
Issue Date
2010-12
Language
English
Article Type
Article
Keywords

OVARIAN-CARCINOMA CELLS; HUMAN CANCER-CELLS; ANTICANCER AGENTS; TELOMERE LENGTH; GENE DELETION; DNA-DAMAGE; P53; PYROPHOSPHATES; PUMA; FAMILY

Citation

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, v.107, no.49, pp.20947 - 20951

ISSN
0027-8424
DOI
10.1073/pnas.1015671107
URI
http://hdl.handle.net/10203/99290
Appears in Collection
BS-Journal Papers(저널논문)
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