Endonuclease G initiates DNA rearrangements at the MLL breakpoint cluster upon replication stress.
about
Leukemogenic rearrangements at the mixed lineage leukemia gene (MLL)-multiple rather than a single mechanismEndonuclease G preferentially cleaves 5-hydroxymethylcytosine-modified DNA creating a substrate for recombinationReplication stress in MLL-rearrangementsNF-κB-dependent DNA damage-signaling differentially regulates DNA double-strand break repair mechanisms in immature and mature human hematopoietic cells.Executioner caspases and CAD are essential for mutagenesis induced by TRAIL or vincristine.Quercetin alters the DNA damage response in human hematopoietic stem and progenitor cells via TopoII- and PI3K-dependent mechanisms synergizing in leukemogenic rearrangements.Base excision repair proteins couple activation-induced cytidine deaminase and endonuclease G during replication stress-induced MLL destabilization.Phenotypic Analysis of ATM Protein Kinase in DNA Double-Strand Break Formation and Repair.Endonuclease G promotes mitochondrial genome cleavage and replication.Cardiomyocyte hypertrophy induced by Endonuclease G deficiency requires reactive oxygen radicals accumulation and is inhibitable by the micropeptide humanin.
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P2860
Endonuclease G initiates DNA rearrangements at the MLL breakpoint cluster upon replication stress.
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Endonuclease G initiates DNA r ...... uster upon replication stress.
@en
Endonuclease G initiates DNA r ...... uster upon replication stress.
@nl
type
label
Endonuclease G initiates DNA r ...... uster upon replication stress.
@en
Endonuclease G initiates DNA r ...... uster upon replication stress.
@nl
prefLabel
Endonuclease G initiates DNA r ...... uster upon replication stress.
@en
Endonuclease G initiates DNA r ...... uster upon replication stress.
@nl
P2093
P2860
P356
P1433
P1476
Endonuclease G initiates DNA r ...... uster upon replication stress.
@en
P2093
P2860
P2888
P304
P356
10.1038/ONC.2014.268
P407
P577
2014-08-18T00:00:00Z