Molecular Mechanism of the Recruitment of NBS1/hMRE11/hRAD50 Complex to DNA Double-strand Breaks: NBS1 Binds to γ-H2AX through FHA/BRCT Domain
Open Access
- 1 January 2004
- journal article
- review article
- Published by Oxford University Press (OUP) in Journal of Radiation Research
- Vol. 45 (4), 473-478
- https://doi.org/10.1269/jrr.45.473
Abstract
DNA double-strand breaks represent the most potentially serious damage to a genome, and hence, many repair proteins are recruited to DNA damage sitesKeywords
This publication has 37 references indexed in Scilit:
- Homologous recombination-mediated double-strand break repairDNA Repair, 2004
- The cellular response to DNA double-strand breaks: defining the sensors and mediatorsTrends in Cell Biology, 2003
- ATM-related Tel1 associates with double-strand breaks through an Xrs2-dependent mechanismGenes & Development, 2003
- Nibrin Forkhead-associated Domain and Breast Cancer C-terminal Domain Are Both Required for Nuclear Focus Formation and PhosphorylationPublished by Elsevier ,2003
- Histone H2AX phosphorylation is dispensable for the initial recognition of DNA breaksNature Cell Biology, 2003
- DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociationNature, 2003
- Nijmegen breakage syndrome gene, NBS1, and molecular links to factors for genome stabilityOncogene, 2002
- Nbs1 is essential for DNA repair by homologous recombination in higher vertebrate cellsNature, 2002
- NBS1 Localizes to γ-H2AX Foci through Interaction with the FHA/BRCT DomainCurrent Biology, 2002
- Chk2 Activation Dependence on Nbs1 after DNA DamageMolecular and Cellular Biology, 2001