Modeling Damage Complexity-Dependent Non-Homologous End-Joining Repair Pathway
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Mendeley | Further Information

{"title"=>"Modeling damage complexity-dependent non-homologous end-joining repair pathway", "type"=>"journal", "authors"=>[{"first_name"=>"Yongfeng", "last_name"=>"Li", "scopus_author_id"=>"35262096900"}, {"first_name"=>"Pamela", "last_name"=>"Reynolds", "scopus_author_id"=>"57196956014"}, {"first_name"=>"Peter", "last_name"=>"O'Neill", "scopus_author_id"=>"7201735460"}, {"first_name"=>"Francis A.", "last_name"=>"Cucinotta", "scopus_author_id"=>"7005205351"}], "year"=>2014, "source"=>"PLoS ONE", "identifiers"=>{"issn"=>"19326203", "pui"=>"372537575", "pmid"=>"24520318", "doi"=>"10.1371/journal.pone.0085816", "sgr"=>"84895540434", "scopus"=>"2-s2.0-84895540434"}, "id"=>"08c84e14-db47-3bab-8f21-51a6875595c1", "abstract"=>"Non-homologous end joining (NHEJ) is the dominant DNA double strand break (DSB) repair pathway and involves several repair proteins such as Ku, DNA-PKcs, and XRCC4. It has been experimentally shown that the choice of NHEJ proteins is determined by the complexity of DSB. In this paper, we built a mathematical model, based on published data, to study how NHEJ depends on the damage complexity. Under an appropriate set of parameters obtained by minimization technique, we can simulate the kinetics of foci track formation in fluorescently tagged mammalian cells, Ku80-EGFP and DNA-PKcs-YFP for simple and complex DSB repair, respectively, in good agreement with the published experimental data, supporting the notion that simple DSB undergo fast repair in a Ku-dependent, DNA-PKcs-independent manner, while complex DSB repair requires additional DNA-PKcs for end processing, resulting in its slow repair, additionally resulting in slower release rate of Ku and the joining rate of complex DNA ends. Based on the numerous experimental descriptions, we investigated several models to describe the kinetics for complex DSB repair. An important prediction of our model is that the rejoining of complex DSBs is through a process of synapsis formation, similar to a second order reaction between ends, rather than first order break filling/joining. The synapsis formation (SF) model allows for diffusion of ends before the synapsis formation, which is precluded in the first order model by the rapid coupling of ends. Therefore, the SF model also predicts the higher number of chromosomal aberrations observed with high linear energy transfer (LET) radiation due to the higher proportion of complex DSBs compared to low LET radiation, and an increased probability of misrejoin following diffusion before the synapsis is formed, while the first order model does not provide a mechanism for the increased effectiveness in chromosomal aberrations observed.", "link"=>"http://www.mendeley.com/research/modeling-damage-complexitydependent-nonhomologous-endjoining-repair-pathway", "reader_count"=>29, "reader_count_by_academic_status"=>{"Unspecified"=>1, "Researcher"=>6, "Student > Doctoral Student"=>2, "Student > Ph. D. Student"=>13, "Student > Master"=>3, "Other"=>3, "Student > Bachelor"=>1}, "reader_count_by_user_role"=>{"Unspecified"=>1, "Researcher"=>6, "Student > Doctoral Student"=>2, "Student > Ph. D. Student"=>13, "Student > Master"=>3, "Other"=>3, "Student > Bachelor"=>1}, "reader_count_by_subject_area"=>{"Unspecified"=>2, "Environmental Science"=>1, "Biochemistry, Genetics and Molecular Biology"=>5, "Medicine and Dentistry"=>4, "Agricultural and Biological Sciences"=>9, "Neuroscience"=>1, "Pharmacology, Toxicology and Pharmaceutical Science"=>1, "Physics and Astronomy"=>5, "Chemistry"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>4}, "Neuroscience"=>{"Neuroscience"=>1}, "Chemistry"=>{"Chemistry"=>1}, "Physics and Astronomy"=>{"Physics and Astronomy"=>5}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>9}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>5}, "Unspecified"=>{"Unspecified"=>2}, "Environmental Science"=>{"Environmental Science"=>1}, "Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>1}}, "reader_count_by_country"=>{"Spain"=>1}, "group_count"=>0}

Scopus | Further Information

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/1379944"], "description"=>"<p>Let <i>p*</i> be the “optimal” parameter set given in scheme (10) obtained by gradient method. The x-axis presents the variation of the parameter under study, and the y-axis is the resulting variation of the data fitting error when is varied but all others are fixed at the chosen values in scheme (10). Panel (A) shows four parameters whose variation by more than 30% leads to error variation by below 5%, suggesting that the model is robust to these parameters. Panel (B) includes five parameters whose variation by 30% leads to error variation by over 5%.</p>", "links"=>[], "tags"=>["Biochemistry", "Nucleic acids", "dna", "DNA repair", "Biochemistry simulations", "biophysics", "Computational biology", "Biochemical simulations", "Molecular cell biology", "Computerized simulations", "Computing methods", "Mathematical computing", "Applied mathematics", "Mathematical economics", "sf"], "article_id"=>929205, "categories"=>["Biological Sciences", "Mathematics"], "users"=>["Yongfeng Li", "Pamela Reynolds", "Peter O'Neill", "Francis A. Cucinotta"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0085816.g006", "stats"=>{"downloads"=>0, "page_views"=>4, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Sensitivity_analysis_of_parameters_in_the_SF_Model_1_/929205", "title"=>"Sensitivity analysis of parameters in the SF Model 1.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-10 03:14:39"}
  • {"files"=>["https://ndownloader.figshare.com/files/1379943"], "description"=>"<p>Panel (A) is for Ku80-EGFP and panel (B) for DNA-PKcs-YFP. The first row is for the overall kinetics and the second row is for the fast kinetics. The lines with dots are experimental data from <a href=\"http://www.plosone.org/article/info:doi/10.1371/journal.pone.0085816#pone.0085816-Reynolds1\" target=\"_blank\">[1]</a>, and those without dots are numerical simulation of the model. The solid lines are represent calculated normalized fluorescence intensity of the respective fluorescently tagged proteins with control, and the dashed lines are with ATM inhibitor applied.</p>", "links"=>[], "tags"=>["Biochemistry", "Nucleic acids", "dna", "DNA repair", "Biochemistry simulations", "biophysics", "Computational biology", "Biochemical simulations", "Molecular cell biology", "Computerized simulations", "Computing methods", "Mathematical computing", "Applied mathematics", "Mathematical economics", "ku80-egfp", "dna-pkcs-yfp", "dsb", "stripes", "merged", "synapsis", "ends"], "article_id"=>929204, "categories"=>["Biological Sciences", "Mathematics"], "users"=>["Yongfeng Li", "Pamela Reynolds", "Peter O'Neill", "Francis A. Cucinotta"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0085816.g005", "stats"=>{"downloads"=>2, "page_views"=>16, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_SF_Model_Formation_and_loss_of_Ku80_EGFP_and_DNA_PKcs_YFP_at_the_DSB_in_the_radiation_stripes_with_merged_synapsis_formation_and_ends_processing_/929204", "title"=>"SF Model - Formation and loss of Ku80-EGFP and DNA-PKcs-YFP at the DSB in the radiation stripes with merged synapsis formation and ends processing.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-10 03:14:39"}
  • {"files"=>["https://ndownloader.figshare.com/files/1379940"], "description"=>"<p>Panel (A) is for Ku80-EGFP and panel (B) for DNA-PKcs-YFP. The lines with dots are experimental data from <a href=\"http://www.plosone.org/article/info:doi/10.1371/journal.pone.0085816#pone.0085816-Reynolds1\" target=\"_blank\">[1]</a>, and those without dots are numerical simulation of the model. The solid lines are represent calculated normalized fluorescence intensity of the respective fluorescently tagged proteins with control, and the dashed lines are with ATM inhibitor present.</p>", "links"=>[], "tags"=>["Biochemistry", "Nucleic acids", "dna", "DNA repair", "Biochemistry simulations", "biophysics", "Computational biology", "Biochemical simulations", "Molecular cell biology", "Computerized simulations", "Computing methods", "Mathematical computing", "Applied mathematics", "Mathematical economics", "ku80-egfp", "dna-pkcs-yfp", "dsb", "stripes", "ends", "synapsis"], "article_id"=>929201, "categories"=>["Biological Sciences", "Mathematics"], "users"=>["Yongfeng Li", "Pamela Reynolds", "Peter O'Neill", "Francis A. Cucinotta"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0085816.g003", "stats"=>{"downloads"=>0, "page_views"=>9, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_SF_Model_Formation_and_loss_of_Ku80_EGFP_and_DNA_PKcs_YFP_at_the_DSB_in_the_radiation_stripes_with_ends_processing_following_synapsis_formation_/929201", "title"=>"SF Model - Formation and loss of Ku80-EGFP and DNA-PKcs-YFP at the DSB in the radiation stripes with ends processing following synapsis formation.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-10 03:14:39"}
  • {"files"=>["https://ndownloader.figshare.com/files/1379939"], "description"=>"<p>DSBs repair can be modeled in terms of either: (A) break filling in which C<sub>0</sub> represent the complex break, C<sub>2</sub> the break filled by Ku and DNA-PKcs/Artemis and C<sub>3</sub> the filled break after end processing by Artemis, C<sub>4</sub> the filled break bound with XL, and C<sub>5</sub> the filled break with Ku and DNA-PKcs released; or (B) synapsis formation in which C<sub>0</sub> represent the complex free DNA end, C<sub>1</sub> complex DNA end bound with Ku and DNA-PKcs/Artemis, C<sub>2</sub> the synapsis fromed by two complex DNA ends, C<sub>3</sub> the synapsis after end processing by Atemis, C<sub>4</sub> the synapsis with XL recruited, and C<sub>5</sub> the synapsis with Ku and DNA-PKcs released.</p>", "links"=>[], "tags"=>["Biochemistry", "Nucleic acids", "dna", "DNA repair", "Biochemistry simulations", "biophysics", "Computational biology", "Biochemical simulations", "Molecular cell biology", "Computerized simulations", "Computing methods", "Mathematical computing", "Applied mathematics", "Mathematical economics", "strand"], "article_id"=>929200, "categories"=>["Biological Sciences", "Mathematics"], "users"=>["Yongfeng Li", "Pamela Reynolds", "Peter O'Neill", "Francis A. Cucinotta"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0085816.g002", "stats"=>{"downloads"=>0, "page_views"=>6, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Modeling_the_repair_of_complex_DNA_double_strand_breaks_/929200", "title"=>"Modeling the repair of complex DNA double strand breaks.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-10 03:14:39"}
  • {"files"=>["https://ndownloader.figshare.com/files/1379937"], "description"=>"<p>DSBs repair can be modeled in terms of either (A) Break filling in which the break between two nearby DNA ends remains and is filled by NHEJ proteins for ligation and repair. S<sub>0</sub> represents the simple break, S<sub>2</sub> the break filled by Ku and XRCC4/Ligase IV (XL) and S<sub>3</sub> the filled break with Ku released. (B) Synapsis formation in which the break may become a larger gap due to diffusion and requires the extra roles of NHEJ protein to tether and rejoin the DNA ends, and S<sub>0</sub> represent the simple free DNA end, S<sub>1</sub> simple DNA end bound with Ku and XL, S<sub>2</sub> the synapsis fromed by two simple DNA ends and S<sub>3</sub> the synapsis with Ku released.</p>", "links"=>[], "tags"=>["Biochemistry", "Nucleic acids", "dna", "DNA repair", "Biochemistry simulations", "biophysics", "Computational biology", "Biochemical simulations", "Molecular cell biology", "Computerized simulations", "Computing methods", "Mathematical computing", "Applied mathematics", "Mathematical economics", "strand"], "article_id"=>929198, "categories"=>["Biological Sciences", "Mathematics"], "users"=>["Yongfeng Li", "Pamela Reynolds", "Peter O'Neill", "Francis A. Cucinotta"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0085816.g001", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Modeling_the_repair_of_simple_DNA_double_strand_breaks_/929198", "title"=>"Modeling the repair of simple DNA double strand breaks.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-10 03:14:39"}
  • {"files"=>["https://ndownloader.figshare.com/files/1379946"], "description"=>"<p>Notation for the complexes involved in the NHEJ repair of simple and complex DSBs.</p>", "links"=>[], "tags"=>["Biochemistry", "Nucleic acids", "dna", "DNA repair", "Biochemistry simulations", "biophysics", "Computational biology", "Biochemical simulations", "Molecular cell biology", "Computerized simulations", "Computing methods", "Mathematical computing", "Applied mathematics", "Mathematical economics", "complexes", "nhej"], "article_id"=>929207, "categories"=>["Biological Sciences", "Mathematics"], "users"=>["Yongfeng Li", "Pamela Reynolds", "Peter O'Neill", "Francis A. Cucinotta"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0085816.t001", "stats"=>{"downloads"=>0, "page_views"=>2, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Notation_for_the_complexes_involved_in_the_NHEJ_repair_of_simple_and_complex_DSBs_/929207", "title"=>"Notation for the complexes involved in the NHEJ repair of simple and complex DSBs.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2014-02-10 03:14:39"}
  • {"files"=>["https://ndownloader.figshare.com/files/1379947", "https://ndownloader.figshare.com/files/1379948"], "description"=>"<div><p>Non-homologous end joining (NHEJ) is the dominant DNA double strand break (DSB) repair pathway and involves several repair proteins such as Ku, DNA-PKcs, and XRCC4. It has been experimentally shown that the choice of NHEJ proteins is determined by the complexity of DSB. In this paper, we built a mathematical model, based on published data, to study how NHEJ depends on the damage complexity. Under an appropriate set of parameters obtained by minimization technique, we can simulate the kinetics of foci track formation in fluorescently tagged mammalian cells, Ku80-EGFP and DNA-PKcs-YFP for simple and complex DSB repair, respectively, in good agreement with the published experimental data, supporting the notion that simple DSB undergo fast repair in a Ku-dependent, DNA-PKcs-independent manner, while complex DSB repair requires additional DNA-PKcs for end processing, resulting in its slow repair, additionally resulting in slower release rate of Ku and the joining rate of complex DNA ends. Based on the numerous experimental descriptions, we investigated several models to describe the kinetics for complex DSB repair. An important prediction of our model is that the rejoining of complex DSBs is through a process of synapsis formation, similar to a second order reaction between ends, rather than first order break filling/joining. The synapsis formation (SF) model allows for diffusion of ends before the synapsis formation, which is precluded in the first order model by the rapid coupling of ends. Therefore, the SF model also predicts the higher number of chromosomal aberrations observed with high linear energy transfer (LET) radiation due to the higher proportion of complex DSBs compared to low LET radiation, and an increased probability of misrejoin following diffusion before the synapsis is formed, while the first order model does not provide a mechanism for the increased effectiveness in chromosomal aberrations observed.</p></div>", "links"=>[], "tags"=>["Biochemistry", "Nucleic acids", "dna", "DNA repair", "Biochemistry simulations", "biophysics", "Computational biology", "Biochemical simulations", "Molecular cell biology", "Computerized simulations", "Computing methods", "Mathematical computing", "Applied mathematics", "Mathematical economics", "complexity-dependent", "non-homologous", "end-joining"], "article_id"=>929208, "categories"=>["Biological Sciences", "Mathematics"], "users"=>["Yongfeng Li", "Pamela Reynolds", "Peter O'Neill", "Francis A. Cucinotta"], "doi"=>["https://dx.doi.org/10.1371/journal.pone.0085816.s001", "https://dx.doi.org/10.1371/journal.pone.0085816.s002"], "stats"=>{"downloads"=>1, "page_views"=>5, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Modeling_Damage_Complexity_Dependent_Non_Homologous_End_Joining_Repair_Pathway_/929208", "title"=>"Modeling Damage Complexity-Dependent Non-Homologous End-Joining Repair Pathway", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2014-02-10 03:14:39"}
  • {"files"=>["https://ndownloader.figshare.com/files/1379945"], "description"=>"<p>Panel (A) is for Ku80-EGFP and panel (B) for DNA-PKcs-YFP. The lines with dots are experimental data from <a href=\"http://www.plosone.org/article/info:doi/10.1371/journal.pone.0085816#pone.0085816-Reynolds1\" target=\"_blank\">[1]</a>, and those without dots are numerical simulation of the model. The solid lines represent calculated normalized fluorescence intensity of the respective fluorescently tagged proteins with control, and the dashed lines are with ATM inhibitor present.</p>", "links"=>[], "tags"=>["Biochemistry", "Nucleic acids", "dna", "DNA repair", "Biochemistry simulations", "biophysics", "Computational biology", "Biochemical simulations", "Molecular cell biology", "Computerized simulations", "Computing methods", "Mathematical computing", "Applied mathematics", "Mathematical economics"], "article_id"=>929206, "categories"=>["Biological Sciences", "Mathematics"], "users"=>["Yongfeng Li", "Pamela Reynolds", "Peter O'Neill", "Francis A. Cucinotta"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0085816.g007", "stats"=>{"downloads"=>0, "page_views"=>3, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_BF_Model_8211_Break_Filling_/929206", "title"=>"BF Model – Break Filling.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-10 03:14:39"}
  • {"files"=>["https://ndownloader.figshare.com/files/1379942"], "description"=>"<p>Panel (A) is for Ku80-EGFP and panel (B) for DNA-PKcs-YFP. The lines with dots are experimental data from <a href=\"http://www.plosone.org/article/info:doi/10.1371/journal.pone.0085816#pone.0085816-Reynolds1\" target=\"_blank\">[1]</a>, and those without dots are numerical simulation of the model. The solid lines are represent calculated normalized fluorescence intensity of the respective fluorescently tagged proteins with control, and the dashed lines are with ATM inhibitor present.</p>", "links"=>[], "tags"=>["Biochemistry", "Nucleic acids", "dna", "DNA repair", "Biochemistry simulations", "biophysics", "Computational biology", "Biochemical simulations", "Molecular cell biology", "Computerized simulations", "Computing methods", "Mathematical computing", "Applied mathematics", "Mathematical economics", "ku80-egfp", "dna-pkcs-yfp", "dsb", "stripes", "ends", "preceding", "synapsis"], "article_id"=>929203, "categories"=>["Biological Sciences", "Mathematics"], "users"=>["Yongfeng Li", "Pamela Reynolds", "Peter O'Neill", "Francis A. Cucinotta"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0085816.g004", "stats"=>{"downloads"=>0, "page_views"=>21, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_SF_Model_Formation_and_loss_of_Ku80_EGFP_and_DNA_PKcs_YFP_at_the_DSB_in_the_radiation_stripes_with_ends_processing_preceding_synapsis_formation_/929203", "title"=>"SF Model - Formation and loss of Ku80-EGFP and DNA-PKcs-YFP at the DSB in the radiation stripes with ends processing preceding synapsis formation.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-10 03:14:39"}

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Relative Metric

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