p53-degradation by HPV-16 E6 preferentially affects the removal of cyclobutane pyrimidine dimers from non-transcribed strand and sensitizes mammary epithelial cells to UV-irradiation (Q73567230)

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scientific article published on 01 March 2000

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English	p53-degradation by HPV-16 E6 preferentially affects the removal of cyclobutane pyrimidine dimers from non-transcribed strand and sensitizes mammary epithelial cells to UV-irradiation	scientific article published on 01 March 2000

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5 November 2019

p53-degradation by HPV-16 E6 preferentially affects the removal of cyclobutane pyrimidine dimers from non-transcribed strand and sensitizes mammary epithelial cells to UV-irradiation (English)

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5 November 2019

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M A El-Mahdy

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F M Hamada

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M A Wani

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Q Zhu

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A A Wani

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1 March 2000

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Mutation Research

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459

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135-145

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Role of DNA excision repair gene defects in the etiology of cancer.

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DNA excision repair

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Expression of wild-type p53 is required for efficient global genomic nucleotide excision repair in UV-irradiated human fibroblasts

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Li-Fraumeni syndrome fibroblasts homozygous for p53 mutations are deficient in global DNA repair but exhibit normal transcription-coupled repair and enhanced UV resistance

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Modulation of (+/-)-anti-BPDE mediated p53 accumulation by inhibitors of protein kinase C and poly(ADP-ribose) polymerase

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Immortalization of distinct human mammary epithelial cell types by human papilloma virus 16 E6 or E7.

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Identifiers

10.1016/S0921-8777(99)00066-X

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