Correction to: DNA mismatch repair in the context of chromatin
An amendment to this paper has been published and can be accessed via the original article.
An amendment to this paper has been published and can be accessed via the original article.
Limited mitochondria outer membrane permeability (MOMP) is a novel biological process where mammalian cells initiate the intrinsic apoptosis pathway with increased mitochondrial permeability but survive. One o...
As an important player in DNA damage response, BRCA1 maintains genomic stability and suppresses tumorigenesis by promoting DNA double-strand break (DSB) repair through homologous recombination (HR). Since the ...
Telomeric DNA are TTAGGG tandem repeats, which are susceptible for oxidative DNA damage and hotspot regions for formation of DNA secondary structures such as t-loop, D-loop, G-quadruplexes (G4), and R-loop. In...
Fanconi anemia (FA) is a recessive genetic disorder caused by biallelic mutations in at least one of 22 FA genes. Beyond its pathological presentation of bone marrow failure and congenital abnormalities, FA is...
Nucleosome assembly during DNA replication is tightly coupled to ongoing DNA synthesis. This process, termed DNA replication-coupled (RC) nucleosome assembly, is essential for chromatin replication and has a g...
Poly(ADP-ribose) polymerase (PARP) inhibitors represent one of the successful novel approaches to targeted cancer treatment. Indeed, the US Food and Drug Administration (FDA) has recently approved PARP inhibit...
To escape replicative senescence, cancer cells have to overcome telomere attrition during DNA replication. Most of cancers rely on telomerase to extend and maintain telomeres, but 4–11% of cancers use a homolo...
Common fragile sites (CFSs) are large chromosomal regions that exhibit breakage on metaphase chromosomes upon replication stress. They become preferentially unstable at the early stage of cancer development an...
Both environmental and endogenous factors induce various forms of DNA damage. DNA double strand break (DSB) is the most deleterious DNA lesion. The swift initiation of a complexed network of interconnected pat...
DNA mismatch repair (MMR) maintains replication fidelity by correcting mispaired nucleotides incorporated by DNA polymerases. Defects in MMR lead to cancers characterized by microsatellite instability. Recentl...
Histone marks control many cellular processes including DNA damage repair. This review will focus primarily on the active histone mark H3K36me3 in the regulation of DNA damage repair and the maintenance of gen...
DNA damage, especially DNA double strand breaks (DSBs) and replication stress, activates a complex post-translational network termed DNA damage response (DDR). Our review focuses on three PI3-kinase related pr...
Poly(ADP-ribosyl)ation (PARylation) mediated by poly ADP-ribose polymerases (PARPs) plays a key role in DNA damage repair. Suppression of PARylation by PARP inhibitors impairs DNA damage repair and induces apo...
When a protein is covalently and irreversibly bound to DNA (i.e., a DNA–protein cross-link [DPC]), it may obstruct any DNA-based transaction, such as transcription and replication. DPC formation is very common...