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• W1922232495 startingPage "2337" @default.
• W1922232495 abstract "We tested the hypothesis that biotinylation of K12 in histone H4 plays a role in the cellular response to double-strand breaks (DSB) of DNA in human cells. DSB were caused by treating choriocarcinoma JAr cells with etoposide. Biotinylation of K12 in histone H4 decreased by 50% as early as 10–20 min after initiation of treatment with etoposide. Biotinylation returned to initial levels 30–40 min after the addition of etoposide to the medium. Temporal patterns of K12-biotinylation were similar for human lymphoma cells. Phosphorylation of S14 of histone H2B and poly(ADP-ribosylation) of glutamate residues on histone H2A are known markers of DSB in DNA; these modifications increased 10–40 min after alterations in K12-biotinylation occurred. Decreased biotinylation of K12 of histone H4 was specific for DSB but was not detectable in response to single-strand breaks or the formation of thymine dimers. Biotin-deficient choriocarcinoma cells exhibited a 40% decrease in rates of survival in response to etoposide compared with biotin-sufficient controls. These studies suggest that the lack of biotinylation of K12 in histone H4 is an early signaling event in response to DSB." @default.
• W1922232495 created "2016-06-24" @default.
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• W1922232495 creator A5044003397 @default.
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• W1922232495 date "2005-10-01" @default.
• W1922232495 modified "2023-10-16" @default.
• W1922232495 title "Biotinylation of K12 in Histone H4 Decreases in Response to DNA Double-Strand Breaks in Human JAr Choriocarcinoma Cells," @default.
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• W1922232495 doi "https://doi.org/10.1093/jn/135.10.2337" @default.
• W1922232495 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1262666" @default.
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