Biochemical mechanism of DSB end resection and its regulation.
New Haven, United States. In Dna Repair (amst), Aug 2015
Topics addressed will include how resection initiates via the introduction of an endonucleolytic incision close to the break end, the molecular mechanism of the conserved MRE11 complex in conjunction with Sae2/CtIP within such a model, the role of BRCA1 and 53BP1 in regulating resection initiation in mammalian cells, the influence of chromatin in the resection process, and potential roles of novel factors.
Genome-wide scan for selection signatures in six cattle breeds in South Africa.
South Africa. In Genet Sel Evol, 2014
In addition, a number of candidate genes associated with the nervous system (WNT5B, FMOD, PRELP, and ATP2B), immune response (CYM, CDC6, and CDK10), production (MTPN, IGFBP4, TGFB1, and AJAP1) and reproductive performance (ADIPOR2, OVOS2, and RBBP8) were also detected as being under selection.
53BP1 regulates DSB repair using Rif1 to control 5' end resection.
New York City, United States. In Science, 2013
Rif1 inhibits resection involving CtIP, BLM, and Exo1; limits accumulation of BRCA1/BARD1 complexes at sites of DNA damage; and defines one of the mechanisms by which 53BP1 causes chromosomal abnormalities in Brca1-deficient cells.
The yeast Fun30 and human SMARCAD1 chromatin remodellers promote DNA end resection.
Leiden, Netherlands. In Nature, 2012
In yeast, the Mre11-Rad50-Xrs2 complex (Xrs2 is known as NBN or NBS1 in humans) and Sae2 (known as RBBP8 or CTIP in humans) initiate end resection, whereas long-range resection depends on the exonuclease Exo1, or the helicase-topoisomerase complex Sgs1-Top3-Rmi1 together with the endonuclease Dna2 (refs 1-6).
CtIP Mutations Cause Seckel and Jawad Syndromes.
Århus, Denmark. In Plos Genet, 2011
the SCKL2 mutation creates an alternative splicing site leading to both the normal and aberrant CtIP proteins coexisting in the cells of patients and carriers