Activation of p53 protein function in response to cellular irradiation
Activation of p53 protein function in response to cellular irradiation
p53 protein is a key regulatory component of a stress-inducible cell-cycle checkpoint pathway in mammalian cells, which can promote either cell-growth arrest or apoptosis, depending on the type of cell and damaging agent utilized. Environmental insults that can activate the p53 pathway are quite distinct, and include ionizing and nonionizing radiation (1–5), antimetabolites which inhibit ribonucleotide biosynthesis (6), inhibitors of spindle formation (7), microtubule-affecting drugs (8), factors inducing differentiation (9), signaling pathways activated in transformed cells during anchorage-independent growth (10), heat shock (11), and hypoxia (12).
1064-3745
591-598
Blaydes, J.P.
e957f999-fd91-4f77-ad62-5b4ef069b15b
Sparks, A.
4f709f59-96e2-4ead-b1e5-79fc9eb28b80
Hupp, T.R.
da952289-a4c5-4280-8f9f-e4a28cc141a5
1999
Blaydes, J.P.
e957f999-fd91-4f77-ad62-5b4ef069b15b
Sparks, A.
4f709f59-96e2-4ead-b1e5-79fc9eb28b80
Hupp, T.R.
da952289-a4c5-4280-8f9f-e4a28cc141a5
Blaydes, J.P., Sparks, A. and Hupp, T.R.
(1999)
Activation of p53 protein function in response to cellular irradiation.
In,
Henderson, Daryl S.
(ed.)
DNA Repair Protocols. Eukaryotic Systems.
(Methods in Molecular Biology, 113)
New York, US.
Humana Press, .
(doi:10.1385/1592596754).
Record type:
Book Section
Abstract
p53 protein is a key regulatory component of a stress-inducible cell-cycle checkpoint pathway in mammalian cells, which can promote either cell-growth arrest or apoptosis, depending on the type of cell and damaging agent utilized. Environmental insults that can activate the p53 pathway are quite distinct, and include ionizing and nonionizing radiation (1–5), antimetabolites which inhibit ribonucleotide biosynthesis (6), inhibitors of spindle formation (7), microtubule-affecting drugs (8), factors inducing differentiation (9), signaling pathways activated in transformed cells during anchorage-independent growth (10), heat shock (11), and hypoxia (12).
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Published date: 1999
Identifiers
Local EPrints ID: 150567
URI: http://eprints.soton.ac.uk/id/eprint/150567
ISBN: 1064-3745
PURE UUID: 132c5d8e-5e0e-45f1-bac0-e01889434c26
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Date deposited: 20 Jul 2010 13:50
Last modified: 14 Mar 2024 02:45
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Contributors
Author:
A. Sparks
Author:
T.R. Hupp
Editor:
Daryl S. Henderson
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