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Transforming growth factor-beta1 mediates cellular response to DNA damage in situ

Ewan, Kenneth, Henshall-Powell, R. L., Ravani, S. A., Tang, Y., Akhurst, R., Wakefield, L. and Barcellos-Hoff, M. H. 2002. Transforming growth factor-beta1 mediates cellular response to DNA damage in situ. Cancer Research 62 (20) , pp. 5627-5631.

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Transforming growth factor (TGF)-beta1 is rapidly activated after ionizing radiation, but its specific role in cellular responses to DNA damage is not known. Here we use Tgfbeta1 knockout mice to show that radiation-induced apoptotic response is TGF-beta1 dependent in the mammary epithelium, and that both apoptosis and inhibition of proliferation in response to DNA damage decrease as a function of TGF-beta1 gene dose in embryonic epithelial tissues. Because apoptosis in these tissues has been shown previously to be p53 dependent, we then examined p53 protein activation. TGF-beta1 depletion, by either gene knockout or by using TGF-beta neutralizing antibodies, resulted in decreased p53 Ser-18 phosphorylation in irradiated mammary gland. These data indicate that TGF-beta1 is essential for rapid p53-mediated cellular responses that mediate cell fate decisions in situ.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
Publisher: American Association for Cancer Research
ISSN: 0008-5472
Last Modified: 04 Jun 2017 06:53

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