Initiation of genetic recombination and recombination-dependent replication.
By S. Kowalczykowski. TIBS -Trends in Biochemical Sciences. Regular ed, 2000
707 citations recorded by the source corpus.
Subfields: Genetics, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/8a26b547d2adfee3499140b22bd945df236bc6f7
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In Genetics
In Molecular Biology
- Gregory J. Hannon
- Scott M. Hammond
- Amy A. Caudy
- Ian D. Hickson
- R. Scully
- D. Slade
- M. Radman
- D. Livingston
Citations in the corpus
- Post-transcriptional gene silencing by double-stranded RNA (2001, background): “So it seems likely that the RISC enzyme contains some mechanism to search the cellular transcriptome for its specific substrates, similar to the ability of RECA family proteins to search genomic DNA for homologous sequence”
- Acetylation of histone H4 by Esa1 is required for DNA double-strand break repair (2002, background): “An intriguing possibility is the poorly understood role of the recombination-mediated restart of stalled replication forks, which is well documented in bacterial cell”
- Oxidative Stress Resistance in Deinococcus radiodurans (2011, background): “replication fork restart in UV-damaged cells (322, 333).”
- Chromosomal stability and the DNA double-stranded break connection (2001, neutral): “Repair of the DSB and the restart of replication are assisted by H”
- In search of the tumour-suppressor functions of BRCA1 and BRCA2 (2000, background): “Indeed, work in prokaryotes indicates that replication arrest is a common event during DNA synthesis and that recombination functions are required for replication restart, genome integrity maintenance, and cell viability (reviewed in ref”
- RecQ helicases: caretakers of the genome (2003, background): “There are several potential strategies for restoring replication following fork demise, and the choice of which to use probably depends on the type of lesion and the template strand that is damaged (for recent reviews, see Ref”
- Homologous Recombination by the RecBCD and RecF Pathways. (2005, background): “When synthesis of a DNA strand is blocked by a non-coding lesion (for example, an abasic site or an intra-strand crosslink, such as a thymine dimer), continued replication of the flawless strand beyond the lesion produces a single-strand DNA gap (Figure 1c) (42, 54).”