Ou, Hui-Ling and Schumacher, Bjoe (2018). DNA damage responses and p53 in the aging process. Blood, 131 (5). S. 488 - 496. WASHINGTON: AMER SOC HEMATOLOGY. ISSN 1528-0020

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Abstract

The genome is constantly attacked by genotoxic insults. DNA damage has long been established as a cause of cancer development through its mutagenic consequences. Conversely, radiation therapy and chemotherapy induce DNA damage to drive cells into apoptosis or senescence as outcomes of the DNA damage response (DDR). More recently, DNA damage has been recognized as a causal factor for the aging process. The role of DNA damage in aging and age-related diseases is illustrated by numerous congenital progeroid syndromes that are caused by mutations in genome maintenance pathways. During the past 2 decades, understanding how DDR drives cancer development and contributes to the aging process has progressed rapidly. It turns out that the DDR factor p53 takes center stage during tumor development and also plays an important role in the aging process. Studies in metazoan models ranging from Caenorhabditis elegans to mammals have revealed cell-autonomous and systemic DDR mechanisms that orchestrate adaptive responses that augment maintenance of the aging organism amid gradually accumulating DNA damage.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Ou, Hui-LingUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Schumacher, BjoeUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-197825
DOI: 10.1182/blood-2017-07-746396
Journal or Publication Title: Blood
Volume: 131
Number: 5
Page Range: S. 488 - 496
Date: 2018
Publisher: AMER SOC HEMATOLOGY
Place of Publication: WASHINGTON
ISSN: 1528-0020
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
HEMATOPOIETIC STEM-CELLS; NUCLEOTIDE EXCISION-REPAIR; CAUSES EARLY-ONSET; TUMOR-SUPPRESSOR; XERODERMA-PIGMENTOSUM; SENESCENT CELLS; FANCONI-ANEMIA; LIFE-SPAN; COCKAYNE-SYNDROME; OXIDATIVE STRESSMultiple languages
HematologyMultiple languages
Refereed: Yes
URI: http://kups.ub.uni-koeln.de/id/eprint/19782

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