Results 61 to 70 of about 64,997 (303)
Base Excision Repair Gene Polymorphisms and Wilms Tumor Susceptibility
EBioMedicine, 2018 Base excision repair (BER) is the main mechanism to repair endogenous DNA lesions caused by reactive oxygen species. BER deficiency is linked with cancer susceptibility and premature aging.
Jinhong Zhu +6 more
doaj +1 more source
Structural basis for APE1 processing DNA damage in the nucleosome
Nature Communications, 2022 AP endonuclease 1 (APE1) processes genomic AP sites during base excision repair. Here, the authors determine the structural mechanism used by APE1 to process nucleosomal AP sites, providing new insight into DNA repair in chromatin.
Tyler M. Weaver +5 more
doaj +1 more source
Base Excision Repair Variants in Cancer [PDF]
, 2017 Base excision repair (BER) is a key genome maintenance pathway that removes endogenously damaged DNA bases that arise in cells at very high levels on a daily basis. Failure to remove these damaged DNA bases leads to increased levels of mutagenesis and chromosomal instability, which have the potential to drive carcinogenesis.
Carolyn G, Marsden +3 more
openaire +2 more sources
Mammalian Base Excision Repair: the Forgotten Archangel [PDF]
Nucleic Acids Research, 2013 Base excision repair (BER) is a frontline repair system that is responsible for maintaining genome integrity and thus preventing premature aging, cancer and many other human diseases by repairing thousands of DNA lesions and strand breaks continuously caused by endogenous and exogenous mutagens.
Dianov, Grigory L, Hübscher, Ulrich
openaire +5 more sources
, 2010 Xeroderma pigmentosum factor D (XPD) is a 5'-3' superfamily 2 helicase and the founding member of a family of DNA helicases with iron-sulphur cluster domains.
Rouillon, Christophe +3 more
core +1 more source
Gut microbiome and aging—A dynamic interplay of microbes, metabolites, and the immune system
FEBS Letters, EarlyView.Age‐dependent shifts in microbial communities engender shifts in microbial metabolite profiles. These in turn drive shifts in barrier surface permeability of the gut and brain and induce immune activation. When paired with preexisting age‐related chronic inflammation this increases the risk of neuroinflammation and neurodegenerative diseases.
Aaron Mehl, Eran Blacher
wiley +1 more source
Exploiting DNA repair defects in triple negative breast cancer to improve cell killing
Therapeutic Advances in Medical Oncology, 2020 Background: The lack of molecular targets for triple negative breast cancer (TNBC) has limited treatment options and reduced survivorship. Identifying new molecular targets may help improve patient survival and decrease recurrence and metastasis.
Kevin J. Lee +5 more
doaj +1 more source
Hyperosmotic stress induces PARP1‐mediated HPF1‐dependent mono(ADP‐ribosyl)ation
FEBS Letters, EarlyView.Sorbitol‐induced hyperosmotic stress rapidly induces reversible mono(ADP‐ribosyl)ation (MARylation) on PARP1 without the signs of genotoxic signaling. We show that PARP1 autoMARylation is HPF1 dependent and forms hydroxylamine‐resistant O‐glycosidic linkages.
Anna Georgina Kopasz +11 more
wiley +1 more source
MicrobiologyOpen, 2018 The absence of base excision repair (BER) proteins involved in processing ROS‐promoted genetic insults activates a DNA damage scanning (DisA)‐dependent checkpoint event in outgrowing Bacillus subtilis spores.
Luz I. Valenzuela‐García +4 more
doaj +1 more source
FEBS Letters, EarlyView.Embryo‐like structures (stembryos) are an innovative tool, but they are hindered by experimental variability and limited developmental potential. DNA methylation is crucial for mammalian development, but its status in stembryo models is poorly characterized.
Sara Canil +4 more
wiley +1 more source