A nucleotide excision repair master-switch: p53 regulated coordinate induction of global genomic repair genes

Sally A. Amundson, Andrew David Patterson, K. T. Do, A. J. Fornace

Research output: Contribution to journalArticle

78 Citations (Scopus)

Abstract

The tumor suppressor gene p53 is mutated in many human cancers. One of its major roles is as a transcription factor, and its many effector genes control key cellular processes including cell cycle checkpoints and apoptosis. An important role in DNA repair is also emerging for both p53 itself and some of its effector genes. The products of two p53-regulated genes, GADD45a and DDB2, are now known to participate in the global genomic repair (GGR) sub-pathway of nucleotide excision repair (NER). We recently reported the induction of a third GGR gene, XPC, following exposure of normal human peripheral blood lymphocytes to ?-rays. We now show that XPC is induced in a variety of human cell lines in response to both ionizing and ultra-violet (UV) radiation and alkylating agents, and that this induction requires wild-type p53.

Original languageEnglish (US)
Pages (from-to)145-149
Number of pages5
JournalCancer Biology and Therapy
Volume1
Issue number2
DOIs
StatePublished - Jan 1 2002

Fingerprint

DNA Repair
Genes
Alkylating Agents
p53 Genes
Cell Cycle Checkpoints
Tumor Suppressor Genes
Transcription Factors
Lymphocytes
Radiation
Apoptosis
Cell Line
Neoplasms

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Oncology
  • Pharmacology
  • Cancer Research

Cite this

@article{c4fe4ad9aa55414099f4b13722f8168b,
title = "A nucleotide excision repair master-switch: p53 regulated coordinate induction of global genomic repair genes",
abstract = "The tumor suppressor gene p53 is mutated in many human cancers. One of its major roles is as a transcription factor, and its many effector genes control key cellular processes including cell cycle checkpoints and apoptosis. An important role in DNA repair is also emerging for both p53 itself and some of its effector genes. The products of two p53-regulated genes, GADD45a and DDB2, are now known to participate in the global genomic repair (GGR) sub-pathway of nucleotide excision repair (NER). We recently reported the induction of a third GGR gene, XPC, following exposure of normal human peripheral blood lymphocytes to ?-rays. We now show that XPC is induced in a variety of human cell lines in response to both ionizing and ultra-violet (UV) radiation and alkylating agents, and that this induction requires wild-type p53.",
author = "Amundson, {Sally A.} and Patterson, {Andrew David} and Do, {K. T.} and Fornace, {A. J.}",
year = "2002",
month = "1",
day = "1",
doi = "10.4161/cbt.59",
language = "English (US)",
volume = "1",
pages = "145--149",
journal = "Cancer Biology and Therapy",
issn = "1538-4047",
publisher = "Landes Bioscience",
number = "2",

}

A nucleotide excision repair master-switch : p53 regulated coordinate induction of global genomic repair genes. / Amundson, Sally A.; Patterson, Andrew David; Do, K. T.; Fornace, A. J.

In: Cancer Biology and Therapy, Vol. 1, No. 2, 01.01.2002, p. 145-149.

Research output: Contribution to journalArticle

TY - JOUR

T1 - A nucleotide excision repair master-switch

T2 - p53 regulated coordinate induction of global genomic repair genes

AU - Amundson, Sally A.

AU - Patterson, Andrew David

AU - Do, K. T.

AU - Fornace, A. J.

PY - 2002/1/1

Y1 - 2002/1/1

N2 - The tumor suppressor gene p53 is mutated in many human cancers. One of its major roles is as a transcription factor, and its many effector genes control key cellular processes including cell cycle checkpoints and apoptosis. An important role in DNA repair is also emerging for both p53 itself and some of its effector genes. The products of two p53-regulated genes, GADD45a and DDB2, are now known to participate in the global genomic repair (GGR) sub-pathway of nucleotide excision repair (NER). We recently reported the induction of a third GGR gene, XPC, following exposure of normal human peripheral blood lymphocytes to ?-rays. We now show that XPC is induced in a variety of human cell lines in response to both ionizing and ultra-violet (UV) radiation and alkylating agents, and that this induction requires wild-type p53.

AB - The tumor suppressor gene p53 is mutated in many human cancers. One of its major roles is as a transcription factor, and its many effector genes control key cellular processes including cell cycle checkpoints and apoptosis. An important role in DNA repair is also emerging for both p53 itself and some of its effector genes. The products of two p53-regulated genes, GADD45a and DDB2, are now known to participate in the global genomic repair (GGR) sub-pathway of nucleotide excision repair (NER). We recently reported the induction of a third GGR gene, XPC, following exposure of normal human peripheral blood lymphocytes to ?-rays. We now show that XPC is induced in a variety of human cell lines in response to both ionizing and ultra-violet (UV) radiation and alkylating agents, and that this induction requires wild-type p53.

UR - http://www.scopus.com/inward/record.url?scp=0036490207&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036490207&partnerID=8YFLogxK

U2 - 10.4161/cbt.59

DO - 10.4161/cbt.59

M3 - Article

C2 - 12170774

AN - SCOPUS:0036490207

VL - 1

SP - 145

EP - 149

JO - Cancer Biology and Therapy

JF - Cancer Biology and Therapy

SN - 1538-4047

IS - 2

ER -