DNA helicases Sgs1 and BLM promote DNA double-strand break resection

A key cellular response to DNA double-strand breaks (DSBs) is 5'-to-3' DSB resection by nucleases to generate regions of ssDNA that then trigger cell cycle checkpoint signaling and DSB repair by homologous recombination (HR). Here, we reveal that in the absence of exonuclease Exo1 activity...

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Veröffentlicht in:	Genes & development 2008-10, Vol.22 (20), p.2767-2772
Hauptverfasser:	Gravel, Serge, Chapman, J Ross, Magill, Christine, Jackson, Stephen P
Format:	Artikel
Sprache:	eng
Schlagworte:	Bloom Syndrome - metabolism Bone Neoplasms - genetics Bone Neoplasms - metabolism Bone Neoplasms - pathology DNA Breaks, Double-Stranded DNA Helicases - antagonists & inhibitors DNA Helicases - genetics DNA Helicases - metabolism DNA Repair - drug effects Exodeoxyribonucleases - metabolism Humans Microscopy, Fluorescence Mutation - genetics Osteosarcoma - genetics Osteosarcoma - metabolism Osteosarcoma - pathology Plasmids Recombination, Genetic RecQ Helicases - antagonists & inhibitors RecQ Helicases - genetics RecQ Helicases - metabolism Research Communication RNA, Small Interfering - pharmacology Saccharomyces cerevisiae Saccharomyces cerevisiae - genetics Saccharomyces cerevisiae - growth & development Saccharomyces cerevisiae - metabolism Saccharomyces cerevisiae Proteins - antagonists & inhibitors Saccharomyces cerevisiae Proteins - genetics Saccharomyces cerevisiae Proteins - metabolism Transfection Tumor Cells, Cultured
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