HDAC1 has a role in double strand break repair by regulating γH2AX signalling
Marqueta-Gracia, J.; Bejarano-Franco, M.; Spaag, S.; Silva, S.; Aguilera, A.; Gomez-Gonzalez, B.
Show abstract
Genome integrity is challenged by DNA damage. DNA double-strand breaks are the most harmful DNA lesions as they block DNA replication and transcription leading to chromosome reorganisations or cell death if not properly repaired. In addition, increasing evidence points to chromatin as a relevant modulator of the efficiency of repair in eukaryotes. Here, we show that inhibition or depletion of human histone deacetylase 1 (HDAC1) regulates DSB repair by controlling the phosphorylation of H2AX, an early step of the DNA damage response. Thus, DSB repair is regulated by a crosstalk between histone acetylation and phosphorylation. Our study provides evidence that histone acetylation regulates DSB signalling supporting that histone deacetylase inhibitors could enhance genotoxic treatment of cancer.
Matching journals
The top 1 journal accounts for 50% of the predicted probability mass.
Similar papers in this journal
- Phosphorylation Status Of MUS81 Is A Modifier Of Olaparib Sensitivity In BRCA2-Deficient Cells 98%
- Tetrameric INTS6-SOSS1 complex facilitates DNA:RNA hybrid autoregulation at double-strand breaks 97%
- Recovery of protein synthesis to measure transcription-coupled DNA repair in living cells and tissues 97%
Similar papers in this journal
- The CIP2A-TOPBP1 complex safeguards chromosomal stability during mitosis 96%
- The RING Finger E3 Ligase RNF25 Protects DNA Replication Forks Independently of its Canonical Roles in Ubiquitin Signaling 96%
- Nucleolar reorganization after cellular stress is orchestrated by SMN shuttling between nuclear compartments 95%
Similar papers in this journal
- RAD18 opposes transcription-associated genome instability through FANCD2 recruitment 97%
- JMJD6 participates in the maintenance of ribosomal DNA integrity in response to DNA damage 96%
- Hrq1/RECQL4 regulation is critical for preventing aberrant recombination during DNA intrastrand crosslink repair and is upregulated in breast cancer. 96%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.