Cdk1 uncouples CtIP-dependent resection and Rad51 filament formation during M-phase double-strand break repair. [electronic resource]
Producer: 20120124Description: 705-20 p. digitalISSN:- 1540-8140
- Animals
- Antigens, Nuclear -- metabolism
- Ataxia Telangiectasia Mutated Proteins
- CDC2 Protein Kinase -- antagonists & inhibitors
- Cell Cycle Proteins -- metabolism
- Cell Division -- physiology
- Cell Nucleus -- metabolism
- Cell-Free System
- Checkpoint Kinase 1
- Chromatin -- metabolism
- Cyclin-Dependent Kinase 2 -- antagonists & inhibitors
- DNA Breaks, Double-Stranded
- DNA Helicases -- metabolism
- DNA Repair -- physiology
- DNA, Single-Stranded -- metabolism
- DNA-Binding Proteins -- metabolism
- Endonucleases -- metabolism
- HeLa Cells
- Histones -- metabolism
- Humans
- Ku Autoantigen
- MRE11 Homologue Protein
- Meiosis -- physiology
- Mitosis -- physiology
- Nuclear Envelope -- physiology
- Ovum
- Phosphorylation -- drug effects
- Protein Binding -- drug effects
- Protein Kinase Inhibitors -- pharmacology
- Protein Kinases -- metabolism
- Protein Serine-Threonine Kinases -- metabolism
- Rad51 Recombinase -- metabolism
- RecQ Helicases -- metabolism
- Replication Protein A -- metabolism
- S Phase -- physiology
- Tumor Suppressor Proteins -- metabolism
- Werner Syndrome Helicase
- Xenopus Proteins -- antagonists & inhibitors
- Xenopus laevis
No physical items for this record
Publication Type: Journal Article; Research Support, N.I.H., Extramural
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