Research Topics
Genomes and Genes
Species | Agata SmogorzewskaSummaryAffiliation: The Rockefeller University Country: USA Publications
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Detail Information
Publications
A genetic screen identifies FAN1, a Fanconi anemia-associated nuclease necessary for DNA interstrand crosslink repairAgata Smogorzewska
Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, and Brigham and Women s Hospital, Boston, MA 02115, USA
Mol Cell 39:36-47. 2010..We propose that FAN1 is a repair nuclease that is recruited to sites of crosslink damage in part through binding the ubiquitinated ID complex through its UBZ domain...
ATM and ATR substrate analysis reveals extensive protein networks responsive to DNA damageShuhei Matsuoka
Department of Genetics and Center for Genetics and Genomics, Brigham and Women s Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA
Science 316:1160-6. 2007..This database paints a much broader landscape for the DDR than was previously appreciated and opens new avenues of investigation into the responses to DNA damage in mammals...
Mammalian BTBD12/SLX4 assembles a Holliday junction resolvase and is required for DNA repairJennifer M Svendsen
Department of Pathology, Harvard Medical School, Boston, MA 02115, USA
Cell 138:63-77. 2009..Thus, SLX4 assembles a modular toolkit for repair of specific types of DNA lesions and is critical for cellular responses to replication fork failure...
Abraxas and RAP80 form a BRCA1 protein complex required for the DNA damage responseBin Wang
Department of Genetics, Center for Genetics and Genomics, Brigham and Women s Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA
Science 316:1194-8. 2007..The RAP80-Abraxas complex may help recruit BRCA1 to DNA damage sites in part through recognition of ubiquitinated proteins...
A genome-wide homologous recombination screen identifies the RNA-binding protein RBMX as a component of the DNA-damage responseBritt Adamson
Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, Division of Genetics, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
Nat Cell Biol 14:318-28. 2012..Our screen also revealed that off-target depletion of RAD51 is a common source of RNAi false positives, raising a cautionary note for siRNA screens and RNAi-based studies of HR...
Cancer proliferation gene discovery through functional genomicsMichael R Schlabach
Howard Hughes Medical Institute and Department of Genetics, Center for Genetics and Genomics, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Science 319:620-4. 2008..Such efforts are complementary to the Cancer Genome Atlas and provide an alternative functional view of cancer cells...
The Fanconi anemia pathway promotes replication-dependent DNA interstrand cross-link repairPuck Knipscheer
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA
Science 326:1698-701. 2009..Reversal of these defects requires ubiquitylated FANCI-FANCD2. Our results show that multiple steps of the essential S-phase ICL repair mechanism fail when the Fanconi anemia pathway is compromised...
Polybromo-associated BRG1-associated factor components BRD7 and BAF180 are critical regulators of p53 required for induction of replicative senescenceAnna E Burrows
The Howard Hughes Medical Institute and Department of Genetics, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 107:14280-5. 2010..BRD7 is a deletion target in human cancer, suggesting that loss of BRD7 may provide an additional mechanism to antagonize p53 function in cancer cells...
Identification of the FANCI protein, a monoubiquitinated FANCD2 paralog required for DNA repairAgata Smogorzewska
Department of Genetics, Howard Hughes Medical Institute, Center for Genetics and Genomics, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Cell 129:289-301. 2007..Mutation in FANCI is responsible for loss of a functional FA pathway in a patient with Fanconi anemia complementation group I...
