Research Topics
Genomes and Genes | Agata SmogorzewskaSummaryAffiliation: Massachusetts General Hospital Country: USA Publications
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Detail Information
Publications
Regulation of telomerase by telomeric proteinsAgata Smogorzewska
The Rockefeller University, New York, New York 10021, USA
Annu Rev Biochem 73:177-208. 2004..Here we discuss the details of telomerase and its regulation by the telomere...
Homologous recombination generates T-loop-sized deletions at human telomeresRichard C Wang
Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA
Cell 119:355-68. 2004..These findings show that t-loop deletion by HR influences the integrity and dynamics of mammalian telomeres...
Different telomere damage signaling pathways in human and mouse cellsAgata Smogorzewska
Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, NY 10021, USA
EMBO J 21:4338-48. 2002..These findings reveal a fundamental difference in telomere damage signaling in human and mouse cells that bears on the use of mouse models for the telomere tumor suppressor pathway...
DNA ligase IV-dependent NHEJ of deprotected mammalian telomeres in G1 and G2Agata Smogorzewska
Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA
Curr Biol 12:1635-44. 2002..However, the molecular nature of these fusions and the mechanism by which they occur have not been elucidated...
DNA damage foci at dysfunctional telomeresHiroyuki Takai
Laboratory for Cell Biology and Genetics, The Rockefeller University, New York, NY 10021, USA
Curr Biol 13:1549-56. 2003..Furthermore, induction of TIFs through TRF2 inhibition provides an opportunity to study the DNA damage response within the context of well-defined, physically marked lesions...
Ubiquitylation and the Fanconi anemia pathwayElizabeth Garner
Laboratory of Genome Maintenance, The Rockefeller University, New York, NY 10065, USA
FEBS Lett 585:2853-60. 2011..Importantly, ubiquitylation provides the foundations for cross-talk between repair pathways, which in concert with the FA pathway, resolve interstrand crosslink damage and maintain genomic stability...
Senescence induced by altered telomere state, not telomere lossJan Karlseder
Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA
Science 295:2446-9. 2002..Thus, replicative senescence is induced by a change in the protected status of shortened telomeres rather than by a complete loss of telomeric DNA...
Structure of the FANCI-FANCD2 complex: insights into the Fanconi anemia DNA repair pathwayWoo Joo
Structural Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
Science 333:312-6. 2011....
Mutations of the SLX4 gene in Fanconi anemiaYonghwan Kim
Laboratory of Genome Maintenance, The Rockefeller University, New York, New York, USA
Nat Genet 43:142-6. 2011....
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...
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...
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...
