53BP1 Is Limiting for NHEJ Repair in ATM-deficient Model Systems That Are Subjected to Oncogenic Stress or Radiation
暂无分享,去创建一个
S. Desiderio | S. Franco | D. Huso | T. Reynolds | J. Chou | M. Prakash | Ivana Rybanska-Spaeder | Tameca Jefferson | Jeremy Chou
[1] S. Franco,et al. PARP1 and DNA-PKcs synergize to suppress p53 mutation and telomere fusions during T-lineage lymphomagenesis , 2013, Oncogene.
[2] Lin Feng,et al. RIF1 Counteracts BRCA1-mediated End Resection during DNA Repair* , 2013, The Journal of Biological Chemistry.
[3] 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.
[4] 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.
[5] M. Nussenzweig,et al. 53BP1 alters the landscape of DNA rearrangements and suppresses AID-induced B cell lymphoma. , 2013, Molecules and Cells.
[6] Michel C. Nussenzweig,et al. Rif1 Prevents Resection of DNA Breaks and Promotes Immunoglobulin Class Switching , 2013, Science.
[7] S. B. Buonomo,et al. 53BP1 Regulates DSB Repair Using Rif1 to Control 5′ End Resection , 2013, Science.
[8] M. Nussenzweig,et al. RPA accumulation during class switch recombination represents 5'-3' DNA-end resection during the S-G2/M phase of the cell cycle. , 2013, Cell reports.
[9] M. Dyer,et al. Biallelic ATM inactivation significantly reduces survival in patients treated on the United Kingdom Leukemia Research Fund Chronic Lymphocytic Leukemia 4 trial. , 2012, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[10] C. Shao,et al. 53BP1 functions as a tumor suppressor in breast cancer via the inhibition of NF-κB through miR-146a. , 2012, Carcinogenesis.
[11] N. Schultz,et al. 53BP1 is a haploinsufficient tumor suppressor and protects cells from radiation response in glioma. , 2012, Cancer research.
[12] S. Ganesan,et al. Low p53 binding protein 1 (53BP1) expression is associated with increased local recurrence in breast cancer patients treated with breast-conserving surgery and radiotherapy. , 2012, International journal of radiation oncology, biology, physics.
[13] T. de Lange,et al. Removal of Shelterin Reveals the Telomere End-Protection Problem , 2012, Science.
[14] David Pellman,et al. Causes and consequences of aneuploidy in cancer , 2012, Nature Reviews Genetics.
[15] L. Symington,et al. Double-strand break end resection and repair pathway choice. , 2011, Annual review of genetics.
[16] Angela T. Noon,et al. 53BP1-mediated DNA double strand break repair: insert bad pun here. , 2011, DNA Repair.
[17] M. Nussenzweig,et al. Regulation of DNA end joining, resection, and immunoglobulin class switch recombination by 53BP1. , 2011, Molecular cell.
[18] S. Desiderio,et al. Coupling of V(D)J recombination to the cell cycle suppresses genomic instability and lymphoid tumorigenesis. , 2011, Immunity.
[19] M. Dyer,et al. The PARP inhibitor olaparib induces significant killing of ATM-deficient lymphoid tumor cells in vitro and in vivo. , 2010, Blood.
[20] D. Durocher,et al. The ubiquitous role of ubiquitin in the DNA damage response , 2010, DNA Repair.
[21] Jeremy M. Stark,et al. ATM Limits Incorrect End Utilization during Non-Homologous End Joining of Multiple Chromosome Breaks , 2010, PLoS genetics.
[22] Michael M. Murphy,et al. ATM-deficient thymic lymphoma is associated with aberrant tcrd rearrangement and gene amplification , 2010, The Journal of experimental medicine.
[23] D. Adams,et al. 53BP1 loss rescues BRCA1 deficiency and is associated with triple-negative and BRCA-mutated breast cancers , 2010, Nature Structural &Molecular Biology.
[24] Jeremy M. Stark,et al. 53BP1 Inhibits Homologous Recombination in Brca1-Deficient Cells by Blocking Resection of DNA Breaks , 2010, Cell.
[25] M. Nussenzweig,et al. 53BP1 regulates DNA resection and the choice between classical and alternative end joining during class switch recombination , 2010, The Journal of experimental medicine.
[26] S. Franco,et al. Differential Requirement for H2AX and 53BP1 in Organismal Development and Genome Maintenance in the Absence of Poly(ADP)ribosyl Polymerase 1 , 2010, Molecular and Cellular Biology.
[27] P. Jeggo,et al. 53BP1 promotes ATM activity through direct interactions with the MRN complex , 2010, The EMBO journal.
[28] A. Shibata,et al. 53BP1-dependent robust localized KAP-1 phosphorylation is essential for heterochromatic DNA double-strand break repair , 2010, Nature Cell Biology.
[29] J. Bartek,et al. The DNA-damage response in human biology and disease , 2009, Nature.
[30] F. Alt,et al. Essential role for DNA-PKcs in DNA double-strand break repair and apoptosis in ATM-deficient lymphocytes. , 2009, Molecular cell.
[31] D. Spector,et al. 53BP1 promotes non-homologous end joining of telomeres by increasing chromatin mobility , 2008, Nature.
[32] M. Nussenzweig,et al. 53BP1 facilitates long-range DNA end-joining during V(D)J recombination , 2008, Nature.
[33] M. Lavin,et al. Ataxia-telangiectasia: from a rare disorder to a paradigm for cell signalling and cancer , 2008, Nature Reviews Molecular Cell Biology.
[34] C. Bassing,et al. Aberrant V(D)J Recombination in Ataxia Telangiectasia Mutated-Deficient Lymphocytes Is Dependent on Nonhomologous DNA End Joining1 , 2008, The Journal of Immunology.
[35] Michael M. Murphy,et al. DNA-PKcs and Artemis function in the end-joining phase of immunoglobulin heavy chain class switch recombination , 2008, The Journal of experimental medicine.
[36] Jiri Bartek,et al. An Oncogene-Induced DNA Damage Model for Cancer Development , 2008, Science.
[37] T. Golub,et al. Integrative analysis reveals 53BP1 copy loss and decreased expression in a subset of human diffuse large B-cell lymphomas , 2008, Oncogene.
[38] J Wade Harper,et al. The DNA damage response: ten years after. , 2007, Molecular cell.
[39] M. Nussenzweig,et al. ATM Prevents the Persistence and Propagation of Chromosome Breaks in Lymphocytes , 2007, Cell.
[40] B. A. Ballif,et al. ATM and ATR Substrate Analysis Reveals Extensive Protein Networks Responsive to DNA Damage , 2007, Science.
[41] Fraser McBlane,et al. Recombinase, chromosomal translocations and lymphoid neoplasia: targeting mistakes and repair failures. , 2006, DNA repair.
[42] T. Pandita,et al. ATM stabilizes DNA double-strand-break complexes during V(D)J recombination , 2006, Nature.
[43] Michael M. Murphy,et al. H2AX prevents DNA breaks from progressing to chromosome breaks and translocations. , 2006, Molecular cell.
[44] Junjie Chen,et al. p53 Binding Protein 53BP1 Is Required for DNA Damage Responses and Tumor Suppression in Mice , 2003, Molecular and Cellular Biology.
[45] T. Ried,et al. Abnormal rearrangement within the α/δ T-cell receptor locus in lymphomas from Atm-deficient mice , 2000 .
[46] F. Alt,et al. Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[47] Shridar Ganesan,et al. Loss of 53BP1 causes PARP inhibitor resistance in Brca1-mutated mouse mammary tumors. , 2013, Cancer discovery.
[48] Jiri Bartek,et al. ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks , 2006, Nature Cell Biology.
[49] T. Ried,et al. Abnormal rearrangement within the alpha/delta T-cell receptor locus in lymphomas from Atm-deficient mice. , 2000, Blood.