Publication: Spontaneous DNA-RNA hybrids: differential impacts throughout the cell cycle.
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Date
2020-02-16
Authors
Gómez-González, Belén
Barroso, Sonia
Herrera-Moyano, Emilia
Aguilera, Andrés
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Abstract
A large body of research supports that transcription plays a major role among the many sources of replicative stress contributing to genome instability. It is therefore not surprising that the DNA damage response has a role in the prevention of transcription-induced threatening events such as the formation of DNA-RNA hybrids, as we have recently found through an siRNA screening. Three major DDR pathways were defined to participate in the protection against DNA-RNA hybrids: ATM/CHK2, ATR/CHK1 and Postreplication Repair (PRR). Based on these observations, we envision different scenarios of DNA-RNA hybridization and their consequent DNA damage.
Description
MeSH Terms
Animals
Ataxia Telangiectasia Mutated Proteins
Base Pairing
Cell Cycle
Checkpoint Kinase 1
DNA Damage
DNA Repair
DNA Replication
DNA, Single-Stranded
Humans
RNA
Ataxia Telangiectasia Mutated Proteins
Base Pairing
Cell Cycle
Checkpoint Kinase 1
DNA Damage
DNA Repair
DNA Replication
DNA, Single-Stranded
Humans
RNA
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Keywords
DNA damage response, DNA-RNA hybrids, genetic instability, postreplication repair, replicative stress