11 research outputs found
Imaging Local Deposition of Newly Synthesized Histones in UVC-Damaged Chromatin
No full textInternational audienc
The HP1–p150/CAF-1 interaction is required for pericentric heterochromatin replication and S-phase progression in mouse cells
No full textPilot RNAi screening using mammalian cell-based system identifies novel putative silencing factors including Kat5/Tip60
No full textTurnover of histones and histone variants in postnatal rat brain: effects of alcohol exposure
No full textThe CAF-1 and Hir Histone Chaperones Associate with Sites of Meiotic Double-Strand Breaks in Budding Yeast
No full textATR Suppresses Endogenous DNA Damage and Allows Completion of Homologous Recombination Repair
No full textASF1 is required to load histones on the HIRA complex in preparation of paternal chromatin assembly at fertilization
No full textEfficient Differentiation of Steroidogenic and Germ-Like Cells from Epigenetically-Related iPSCs Derived from Ovarian Granulosa Cells
No full textUnderstanding nucleotide excision repair and its roles in cancer and ageing
No full textNucleotide excision repair (NER) eliminates various structurally unrelated DNA lesions by a multiwise 'cut and patch'-type reaction. The global genome NER (GG-NER) subpathway prevents mutagenesis by probing the genome for helix-distorting lesions, whereas transcription-coupled NER (TC-NER) removes transcription-blocking lesions to permit unperturbed gene expression, thereby preventing cell death. Consequently, defects in GG-NER result in cancer predisposition, whereas defects in TC-NER cause a variety of diseases ranging from ultraviolet radiation-sensitive syndrome to severe premature ageing conditions such as Cockayne syndrome. Recent studies have uncovered new aspects of DNA-damage detection by NER, how NER is regulated by extensive post-translational modifications, and the dynamic chromatin interactions that control its efficiency. Based on these findings, a mechanistic model is proposed that explains the complex genotype-phenotype correlations of transcription-coupled repair disorders
