p53 modulation of TFIIH–associated nucleotide excision repair activity

X. W. Wang; H. Yeh; L. Schaeffer; R. Roy; V. Moncollin; J. M. Egly; Z. Wang; E. C. Friedberg; M. K. Evans; B. G. Taffe; V. A. Bohr; G. Weeda; J. H J Hoeijmakers; K. Forrester; C. C. Harris

doi:10.1038/ng0695-188

p53 modulation of TFIIH–associated nucleotide excision repair activity

X. W. Wang, H. Yeh, L. Schaeffer, R. Roy, V. Moncollin, J. M. Egly, Z. Wang, E. C. Friedberg, M. K. Evans, B. G. Taffe, V. A. Bohr, G. Weeda, J. H J Hoeijmakers, K. Forrester, C. C. Harris

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517 Scopus citations

Abstract

p53 has pleiotropic functions including control of genomic plasticity and integrity. Here we report that p53 can bind to several transcription factor IIH–associated factors, including transcription–repair factors, XPD (Rad3) and XPB, as well as CSB involved in strand–specific DNA repair, via its C–terminal domain. We also found that wild–type, but not Arg273His mutant p53 inhibits XPD (Rad3) and XPB DNA helicase activities. Moreover, repair of UV–induced dimers is slower in Li–Fraumeni syndrome cells (heterozygote p53 mutant) than in normal human cells. Our findings indicate that p53 may play a direct role in modulating nucleotide excision repair pathways.

Original language	English (US)
Pages (from-to)	188-195
Number of pages	8
Journal	Nature genetics
Volume	10
Issue number	2
DOIs	https://doi.org/10.1038/ng0695-188
State	Published - Jun 1995

ASJC Scopus subject areas

Genetics

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title = "p53 modulation of TFIIH–associated nucleotide excision repair activity",

abstract = "p53 has pleiotropic functions including control of genomic plasticity and integrity. Here we report that p53 can bind to several transcription factor IIH–associated factors, including transcription–repair factors, XPD (Rad3) and XPB, as well as CSB involved in strand–specific DNA repair, via its C–terminal domain. We also found that wild–type, but not Arg273His mutant p53 inhibits XPD (Rad3) and XPB DNA helicase activities. Moreover, repair of UV–induced dimers is slower in Li–Fraumeni syndrome cells (heterozygote p53 mutant) than in normal human cells. Our findings indicate that p53 may play a direct role in modulating nucleotide excision repair pathways.",

author = "Wang, {X. W.} and H. Yeh and L. Schaeffer and R. Roy and V. Moncollin and Egly, {J. M.} and Z. Wang and Friedberg, {E. C.} and Evans, {M. K.} and Taffe, {B. G.} and Bohr, {V. A.} and G. Weeda and Hoeijmakers, {J. H J} and K. Forrester and Harris, {C. C.}",

year = "1995",

month = jun,

doi = "10.1038/ng0695-188",

language = "English (US)",

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T1 - p53 modulation of TFIIH–associated nucleotide excision repair activity

AU - Wang, X. W.

AU - Yeh, H.

AU - Schaeffer, L.

AU - Roy, R.

AU - Moncollin, V.

AU - Egly, J. M.

AU - Wang, Z.

AU - Friedberg, E. C.

AU - Evans, M. K.

AU - Taffe, B. G.

AU - Bohr, V. A.

AU - Weeda, G.

AU - Hoeijmakers, J. H J

AU - Forrester, K.

AU - Harris, C. C.

PY - 1995/6

Y1 - 1995/6

N2 - p53 has pleiotropic functions including control of genomic plasticity and integrity. Here we report that p53 can bind to several transcription factor IIH–associated factors, including transcription–repair factors, XPD (Rad3) and XPB, as well as CSB involved in strand–specific DNA repair, via its C–terminal domain. We also found that wild–type, but not Arg273His mutant p53 inhibits XPD (Rad3) and XPB DNA helicase activities. Moreover, repair of UV–induced dimers is slower in Li–Fraumeni syndrome cells (heterozygote p53 mutant) than in normal human cells. Our findings indicate that p53 may play a direct role in modulating nucleotide excision repair pathways.

AB - p53 has pleiotropic functions including control of genomic plasticity and integrity. Here we report that p53 can bind to several transcription factor IIH–associated factors, including transcription–repair factors, XPD (Rad3) and XPB, as well as CSB involved in strand–specific DNA repair, via its C–terminal domain. We also found that wild–type, but not Arg273His mutant p53 inhibits XPD (Rad3) and XPB DNA helicase activities. Moreover, repair of UV–induced dimers is slower in Li–Fraumeni syndrome cells (heterozygote p53 mutant) than in normal human cells. Our findings indicate that p53 may play a direct role in modulating nucleotide excision repair pathways.

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JO - Nature genetics

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ER -

p53 modulation of TFIIH–associated nucleotide excision repair activity

Abstract

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