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本文引用的文献
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Xeroderma pigmentosum group C protein complex is the initiator of global genome nucleotide excision repair.
Mol Cell. 1998 Aug;2(2):223-32. doi: 10.1016/s1097-2765(00)80132-x.
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p48 Activates a UV-damaged-DNA binding factor and is defective in xeroderma pigmentosum group E cells that lack binding activity.
Mol Cell Biol. 1998 Jul;18(7):4391-9. doi: 10.1128/MCB.18.7.4391.
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Excision-repair patch lengths are similar for transcription-coupled repair and global genome repair in UV-irradiated human cells.
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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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A model for p53-induced apoptosis.
Nature. 1997 Sep 18;389(6648):300-5. doi: 10.1038/38525.
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Down-regulation of actin genes precedes microfilament network disruption and actin cleavage during p53-mediated apoptosis.
J Cell Sci. 1997 Feb;110 ( Pt 4):489-95. doi: 10.1242/jcs.110.4.489.
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Mammalian nucleotide excision repair and syndromes.
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p53, the cellular gatekeeper for growth and division.
Cell. 1997 Feb 7;88(3):323-31. doi: 10.1016/s0092-8674(00)81871-1.
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DNA-dependent protein kinase is not required for accumulation of p53 or cell cycle arrest after DNA damage.
Cancer Res. 1997 Jan 1;57(1):68-74.
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