Williams, Ashley B. and Schumacher, Bjoern (2016). p53 in the DNA-Damage-Repair Process. Cold Spring Harb. Perspect. Med., 6 (5). COLD SPRING HARBOR: COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT. ISSN 2157-1422

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Abstract

The cells in the human body are continuously challenged by a variety of genotoxic attacks. Erroneous repair of the DNA can lead to mutations and chromosomal aberrations that can alter the functions of tumor suppressor genes or oncogenes, thus causing cancer development. As a central tumor suppressor, p53 guards the genome by orchestrating a variety of DNA-damage-response (DDR) mechanisms. Already early in metazoan evolution, p53 started controlling the apoptotic demise of genomically compromised cells. p53 plays a prominent role as a facilitator of DNA repair by halting the cell cycle to allow time for the repair machineries to restore genome stability. In addition, p53 took on diverse roles to also directly impact the activity of various DNA-repair systems. It thus appears as if p53 is multitasking in providing protection from cancer development by maintaining genome stability.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Williams, Ashley B.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Schumacher, BjoernUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-277544
DOI: 10.1101/cshperspect.a026070
Journal or Publication Title: Cold Spring Harb. Perspect. Med.
Volume: 6
Number: 5
Date: 2016
Publisher: COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
Place of Publication: COLD SPRING HARBOR
ISSN: 2157-1422
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
NUCLEOTIDE EXCISION-REPAIR; STRAND BREAK REPAIR; WILD-TYPE P53; GLOBAL GENOMIC REPAIR; TUMOR-SUPPRESSOR P53; HOMOLOGOUS RECOMBINATION; MISMATCH REPAIR; CAENORHABDITIS-ELEGANS; HOLLIDAY JUNCTIONS; MUTANT P53Multiple languages
Medicine, Research & ExperimentalMultiple languages
Refereed: Yes
URI: http://kups.ub.uni-koeln.de/id/eprint/27754

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