Sister chromatid gene conversion is a prominent double‐strand break repair pathway in mammalian cells

By Roger D. Johnson, M. Jasin. EMBO Journal, 2000

626 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/329e6ed48346a677eead4c8f2effe207618c6ac6

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. Alan Ashworth
2. M. Moynahan
3. K. Gudmundsdottir
4. R. Abraham
5. Holger Puchta
6. M. Jasin
7. B. Kaina
8. W. Roos

In Molecular Biology

1. Alan Ashworth
2. Thomas Helleday
3. M. Jasin
4. M. Moynahan
5. B. Kaina
6. W. Roos
7. K. Gudmundsdottir
8. R. Abraham

Citations in the corpus

• Meiotic Recombination: The Essence of Heredity. (2015, neutral): “1) (Kadyk and Hartwell 1992; Johnson and Jasin 2000; Bzymek et al. 2010; Lao and Hunter 2010; Humphryes and Hochwagen 2014; Brown and Bishop 2015).”
• Pathways of DNA Double-Strand Break Repair during the Mammalian Cell Cycle (2003, neutral): “conversion and not reciprocal exchange (25).”
• The Bloom's syndrome helicase suppresses crossing over during homologous recombination (2003, background): “In vivo , these pathways are highly regulated, with the formation of crossovers being promoted during meiosis but suppressed during mitosi”
• PARP is activated at stalled forks to mediate Mre11‐dependent replication restart and recombination (2009, background): “In contrast, recombination induced by the restriction endonu- clease I-SceI produces a two-ended DSB, which is repaired by synthesis-dependent-strand annealing and results in gene conversion (Johnson and Jasin, 2000; Saleh-Gohari et al, 2005).”
• Crossover/noncrossover differentiation, synaptonemal complex formation, and regulatory surveillance at the leptotene/zygotene transition of meiosis. (2004, neutral): “(Johnson and Jasin, 2000).”
• Homologous recombination and human health: the roles of BRCA1, BRCA2 and associated proteins (2015, neutral): “1) (Rouet et al. 1994; Liang et al. 1998; Johnson and Jasin 2000).”
• DNA double-strand break repair: from mechanistic understanding to cancer treatment. (2007, background): “Importantly, when resolution products are analyzed following introduction of a site-specific double-strand break, crossover products are rarely observed [33].”
• Mitotic homologous recombination maintains genomic stability and suppresses tumorigenesis (2010, positive): “Generally, HR between repeats on the same chromosome is efficient in both rodent and human cells, and can be as efficient as NHE”
• The repair of double-strand breaks in plants: mechanisms and consequences for genome evolution. (2004, background): “Sister chromatids can be used as a template in the G 2 stage of the cell cycle, and this pathway works efficiently in mammals (Johnson and Jasin, 2000), however, due to experimental limitations it has not been possible to address this question in plant cells in connection with DSB induction until…”
• BRCA2 is required for homology-directed repair of chromosomal breaks. (2001, background): “The profound defect inal., 1999; Johnson and Jasin, 2000), which leads us to HDR of chromosome breaks in BRCA2 mutant cells con-propose that BRCA2 has a general role in sister chromafirms a caretaker function for BRCA2 in protecting geno-tid recombination in proliferating cells.”
• Mechanisms of human DNA repair: an update. (2003, background): “NHEJ occurs mainly in G0/G1, whereas HR occurs during the late S and G2 phases (Johnson and Jasin, 2000; Takata et al., 1998).”
• The roles of BRCA1 and BRCA2 and associated proteins in the maintenance of genomic stability (2006, background): “Furthermore, crossover events are suppressed in mammalian cells as these can result in genome alterations (Johnson and Jasin, 2000).”
• Chromosomal stability and the DNA double-stranded break connection (2001, background): “HR is most efficient in the S and G2 phases of the cell cycle because of the availability of sister chromatids as repair template”
• Cell cycle checkpoint signaling through the ATM and ATR kinases. (2001, background): “Fortunately, DNA damage detected during S phase is apt to be repaired precisely via homologous recombination mechanisms involving sister chromatids (Johnson and Jasin 2000).”