SCAI promotes DNA double-strand break repair in distinct chromosomal contexts

[1]  B. Reina-San-Martin,et al.  Temporal and Spatial Uncoupling of DNA Double Strand Break Repair Pathways within Mammalian Heterochromatin. , 2016, Molecular cell.

[2]  N. Mailand,et al.  Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers , 2016, Nature Reviews Molecular Cell Biology.

[3]  José A. Dianes,et al.  2016 update of the PRIDE database and its related tools , 2016, Nucleic Acids Res..

[4]  N. Hunter.  Meiotic Recombination: The Essence of Heredity. , 2015, Cold Spring Harbor perspectives in biology.

[5]  Jürgen Cox,et al.  Proteomics reveals dynamic assembly of repair complexes during bypass of DNA cross-links , 2015, Science.

[6]  H. van Attikum,et al.  Opposing ISWI- and CHD-class chromatin remodeling activities orchestrate heterochromatic DNA repair , 2014, The Journal of cell biology.

[7]  Jiri Bartek,et al.  TRIP12 and UBR5 Suppress Spreading of Chromatin Ubiquitylation at Damaged Chromosomes , 2014, Cell.

[8]  J. Rouse,et al.  Improved Genome Editing in Human Cell Lines Using the CRISPR Method , 2014, PloS one.

[9]  E. Soutoglou,et al.  Double strand break (DSB) repair in heterochromatin and heterochromatin proteins in DSB repair. , 2014, DNA repair.

[10]  Marco Y. Hein,et al.  Accurate Proteome-wide Label-free Quantification by Delayed Normalization and Maximal Peptide Ratio Extraction, Termed MaxLFQ * , 2014, Molecular & Cellular Proteomics.

[11]  Jeannie T. Lee,et al.  BRCA1 establishes DNA damage signaling and pericentric heterochromatin of the X chromosome in male meiosis , 2014, The Journal of cell biology.

[12]  N. Mailand,et al.  ATR Prohibits Replication Catastrophe by Preventing Global Exhaustion of RPA , 2013, Cell.

[13]  N. Mailand,et al.  ATR Prohibits Replication Catastrophe by Preventing Global Exhaustion of RPA , 2013, Cell.

[14]  A. Shibata,et al.  Opposing roles for 53BP1 during homologous recombination , 2013, Nucleic acids research.

[15]  A. Nussenzweig,et al.  End-joining, translocations and cancer , 2013, Nature Reviews Cancer.

[16]  F. Alt,et al.  53BP1 Mediates Productive and Mutagenic DNA Repair through Distinct Phosphoprotein Interactions , 2013, Cell.

[17]  N. Mailand,et al.  The Deubiquitylating Enzyme USP44 Counteracts the DNA Double-strand Break Response Mediated by the RNF8 and RNF168 Ubiquitin Ligases* , 2013, Journal of Biological Chemistry.

[18]  Adam P. Rosebrock,et al.  A cell cycle-dependent regulatory circuit composed of 53BP1-RIF1 and BRCA1-CtIP controls DNA repair pathway choice. , 2013, Molecular cell.

[19]  Facundo D. Batista,et al.  RIF1 Is Essential for 53BP1-Dependent Nonhomologous End Joining and Suppression of DNA Double-Strand Break Resection , 2013, Molecular cell.

[20]  Michel C. Nussenzweig,et al.  Rif1 Prevents Resection of DNA Breaks and Promotes Immunoglobulin Class Switching , 2013, Science.

[21]  S. B. Buonomo,et al.  53BP1 Regulates DSB Repair Using Rif1 to Control 5′ End Resection , 2013, Science.

[22]  Matthias Mann,et al.  A map of general and specialized chromatin readers in mouse tissues generated by label-free interaction proteomics. , 2013, Molecular cell.

[23]  B. Neumann,et al.  TRIP12 and UBR5 Suppress Spreading of Chromatin Ubiquitylation at Damaged Chromosomes , 2012, Cell.

[24]  A. Nussenzweig,et al.  Loss of ATM kinase activity leads to embryonic lethality in mice , 2012, The Journal of cell biology.

[25]  Julian Lange,et al.  Homeostatic control of recombination is implemented progressively in mouse meiosis , 2012, Nature Cell Biology.

[26]  Jeremy M. Stark,et al.  I-SceI-based assays to examine distinct repair outcomes of mammalian chromosomal double strand breaks. , 2012, Methods in molecular biology.

[27]  J. Bartek,et al.  More than just a focus: The chromatin response to DNA damage and its role in genome integrity maintenance , 2011, Nature Cell Biology.

[28]  P. Jeggo,et al.  KAP-1 phosphorylation regulates CHD3 nucleosome remodeling during the DNA double-strand break response , 2011, Nature Structural &Molecular Biology.

[29]  M. Nussenzweig,et al.  Regulation of DNA end joining, resection, and immunoglobulin class switch recombination by 53BP1. , 2011, Molecular cell.

[30]  N. Mailand,et al.  Assembly and function of DNA double-strand break repair foci in mammalian cells. , 2010, DNA repair.

[31]  S. Elledge,et al.  The DNA damage response: making it safe to play with knives. , 2010, Molecular cell.

[32]  Andrei Seluanov,et al.  Analysis of DNA double-strand break (DSB) repair in mammalian cells. , 2010, Journal of visualized experiments : JoVE.

[33]  K. Zhao,et al.  PTIP Promotes Chromatin Changes Critical for Immunoglobulin Class Switch Recombination , 2010, Science.

[34]  A. Hyman,et al.  Quantitative proteomics combined with BAC TransgeneOmics reveals in vivo protein interactions , 2010, The Journal of cell biology.

[35]  Jeremy M. Stark,et al.  53BP1 Inhibits Homologous Recombination in Brca1-Deficient Cells by Blocking Resection of DNA Breaks , 2010, Cell.

[36]  A. Shibata,et al.  53BP1-dependent robust localized KAP-1 phosphorylation is essential for heterochromatic DNA double-strand break repair , 2010, Nature Cell Biology.

[37]  J. Bartek,et al.  The DNA-damage response in human biology and disease , 2009, Nature.

[38]  Jianming Xu,et al.  Regulation of myocardin-related transcriptional coactivators through cofactor interactions in differentiation and cancer , 2009, Cell cycle.

[39]  S. Jackson,et al.  The DNA-damage response: new molecular insights and new approaches to cancer therapy. , 2009, Biochemical Society transactions.

[40]  E. Kremmer,et al.  SCAI acts as a suppressor of cancer cell invasion through the transcriptional control of β1-integrin , 2009, Nature Cell Biology.

[41]  P. Jeggo,et al.  ATM signaling facilitates repair of DNA double-strand breaks associated with heterochromatin. , 2008, Molecular cell.

[42]  M. Tilby,et al.  γH2AX Foci Form Preferentially in Euchromatin after Ionising-Radiation , 2007, PloS one.

[43]  M. Nussenzweig,et al.  ATM Prevents the Persistence and Propagation of Chromosome Breaks in Lymphocytes , 2007, Cell.

[44]  Jiri Bartek,et al.  Spatial organization of the mammalian genome surveillance machinery in response to DNA strand breaks , 2006, The Journal of cell biology.

[45]  Thomas Helleday,et al.  Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase , 2005, Nature.

[46]  Alan Ashworth,et al.  Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy , 2005, Nature.

[47]  Jiri Bartek,et al.  Cell-cycle checkpoints and cancer , 2004, Nature.

[48]  M. Nussenzweig,et al.  53BP1 is required for class switch recombination , 2004, The Journal of cell biology.

[49]  P. Cohen,et al.  Mismatch repair proteins, meiosis, and mice: understanding the complexities of mammalian meiosis. , 2004, Experimental cell research.

[50]  F. Alt,et al.  53BP1 links DNA damage-response pathways to immunoglobulin heavy chain class-switch recombination , 2004, Nature Immunology.

[51]  Junjie Chen,et al.  p53 Binding Protein 53BP1 Is Required for DNA Damage Responses and Tumor Suppression in Mice , 2003, Molecular and Cellular Biology.

[52]  C. E. Ford,et al.  AN AIR-DRYING METHOD FOR MEIOTIC PREPARATIONS FROM MAMMALIAN TESTES. , 1964, Cytogenetics.