The repair of DNA lesions that occur endogenously or in response to diverse genotoxic stresses is indispensable for genome integrity. DNA lesions activate checkpoint pathways that regulate specific DNA-repair mechanisms in the different phases of the cell cycle. Checkpoint-arrested cells resume cell-cycle progression once damage has been repaired, whereas cells with unrepairable DNA lesions undergo permanent cell-cycle arrest or apoptosis. Recent studies have provided insights into the mechanisms that contribute to DNA repair in specific cell-cycle phases and have highlighted the mechanisms that ensure cell-cycle progression or arrest in normal and cancerous cells
In order to maintain genetic integrity, cells are equipped with cell cycle checkpoints that detect D...
In order to maintain genetic integrity, cells are equipped with cell cycle checkpoints that detect D...
Failure of cells to process toxic double-strand breaks (DSBs) constitutes a major intrinsic source o...
In response to genotoxic stress, which can be caused by environmental or endogenous genotoxic insult...
In response to genomic insults cells trigger a signal transduction pathway, known as DNA damage chec...
Cell cycle checkpoint activation and DNA repair pathways govern genomic stability after genotoxic st...
DNA damage caused by many factors may lead to missense mutation, deletion or illegal recombination. ...
The maintenance of genome integrity is important for normal cellular functions, organism development...
The cellular response to DNA damage is vital for the cell�s ability to maintain genomic integrity. C...
damage checkpoints were initially identified as controls that regulate cell cycle progression after ...
Cell cycle checkpoints activated by DNA double-strand breaks (DSBs) are essential for the maintenanc...
Abstract DNA is labile and constantly subject to damage. In addition to external mutagens, DNA is c...
Checkpoint proteins were initially identified because their loss of function resulted in defects in ...
Cycling cells must ensure homeostasis of the genetic information during repeated chromosome replicat...
Cycling cells must ensure homeostasis of the genetic information during repeated chromosome replicat...
In order to maintain genetic integrity, cells are equipped with cell cycle checkpoints that detect D...
In order to maintain genetic integrity, cells are equipped with cell cycle checkpoints that detect D...
Failure of cells to process toxic double-strand breaks (DSBs) constitutes a major intrinsic source o...
In response to genotoxic stress, which can be caused by environmental or endogenous genotoxic insult...
In response to genomic insults cells trigger a signal transduction pathway, known as DNA damage chec...
Cell cycle checkpoint activation and DNA repair pathways govern genomic stability after genotoxic st...
DNA damage caused by many factors may lead to missense mutation, deletion or illegal recombination. ...
The maintenance of genome integrity is important for normal cellular functions, organism development...
The cellular response to DNA damage is vital for the cell�s ability to maintain genomic integrity. C...
damage checkpoints were initially identified as controls that regulate cell cycle progression after ...
Cell cycle checkpoints activated by DNA double-strand breaks (DSBs) are essential for the maintenanc...
Abstract DNA is labile and constantly subject to damage. In addition to external mutagens, DNA is c...
Checkpoint proteins were initially identified because their loss of function resulted in defects in ...
Cycling cells must ensure homeostasis of the genetic information during repeated chromosome replicat...
Cycling cells must ensure homeostasis of the genetic information during repeated chromosome replicat...
In order to maintain genetic integrity, cells are equipped with cell cycle checkpoints that detect D...
In order to maintain genetic integrity, cells are equipped with cell cycle checkpoints that detect D...
Failure of cells to process toxic double-strand breaks (DSBs) constitutes a major intrinsic source o...