The Progeroid Phenotype of Ku80 Deficiency Is Dominant over DNA-PKCS Deficiency
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{"title"=>"The progeroid phenotype of Ku80 deficiency Is dominant over DNA-PK CS deficiency", "type"=>"journal", "authors"=>[{"first_name"=>"Erwin", "last_name"=>"Reiling", "scopus_author_id"=>"15521268600"}, {"first_name"=>"Martijn E T", "last_name"=>"Dollé", "scopus_author_id"=>"56450461400"}, {"first_name"=>"Sameh A.", "last_name"=>"Youssef", "scopus_author_id"=>"56145805600"}, {"first_name"=>"Moonsook", "last_name"=>"Lee", "scopus_author_id"=>"55531879700"}, {"first_name"=>"Bhawani", "last_name"=>"Nagarajah", "scopus_author_id"=>"6506687731"}, {"first_name"=>"Marianne", "last_name"=>"Roodbergen", "scopus_author_id"=>"23971066900"}, {"first_name"=>"Piet", "last_name"=>"De With", "scopus_author_id"=>"56145712600"}, {"first_name"=>"Alain", "last_name"=>"De Bruin", "scopus_author_id"=>"7004759209"}, {"first_name"=>"Jan H.", "last_name"=>"Hoeijmakers", "scopus_author_id"=>"35430855700"}, {"first_name"=>"Jan", "last_name"=>"Vijg", "scopus_author_id"=>"7006875822"}, {"first_name"=>"Harry", "last_name"=>"Van Steeg", "scopus_author_id"=>"7006318945"}, {"first_name"=>"Paul", "last_name"=>"Hasty", "scopus_author_id"=>"7004172435"}], "year"=>2014, "source"=>"PLoS ONE", "identifiers"=>{"scopus"=>"2-s2.0-84899697851", "pmid"=>"24740260", "sgr"=>"84899697851", "doi"=>"10.1371/journal.pone.0093568", "issn"=>"19326203", "pui"=>"372990521"}, "id"=>"2f17c319-b529-35cd-a5fa-443a1a53629d", "abstract"=>"Ku80 and DNA-PKCS are both involved in the repair of double strand DNA breaks via the nonhomologous end joining (NHEJ) pathway. While ku80-/- mice exhibit a severely reduced lifespan and size, this phenotype is less pronounced in dna-pkcs-/- mice. However, these observations are based on independent studies with varying genetic backgrounds. Here, we generated ku80-/-, dna-pkcs-/- and double knock out mice in a C57Bl6/J*FVB F1 hybrid background and compared their lifespan, end of life pathology and mutation frequency in liver and spleen using a lacZ reporter. Our data confirm that inactivation of Ku80 and DNA-PKCS causes reduced lifespan and bodyweights, which is most severe in ku80-/- mice. All mutant mice exhibited a strong increase in lymphoma incidence as well as other aging-related pathology (skin epidermal and adnexal atrophy, trabacular bone reduction, kidney tubular anisokaryosis, and cortical and medullar atrophy) and severe lymphoid depletion. LacZ mutation frequency analysis did not show strong differences in mutation frequencies between knock out and wild type mice. The ku80-/- mice had the most severe phenotype and the Ku80-mutation was dominant over the DNA-PKCS-mutation. Presumably, the more severe degenerative effect of Ku80 inactivation on lifespan compared to DNA-PKCS inactivation is caused by additional functions of Ku80 or activity of free Ku70 since both Ku80 and DNA-PKCS are essential for NHEJ.", "link"=>"http://www.mendeley.com/research/progeroid-phenotype-ku80-deficiency-dominant-dnapk-cs-deficiency", "reader_count"=>10, "reader_count_by_academic_status"=>{"Researcher"=>4, "Student > Ph. D. Student"=>5, "Student > Bachelor"=>1}, "reader_count_by_user_role"=>{"Researcher"=>4, "Student > Ph. D. Student"=>5, "Student > Bachelor"=>1}, "reader_count_by_subject_area"=>{"Biochemistry, Genetics and Molecular Biology"=>2, "Medicine and Dentistry"=>2, "Agricultural and Biological Sciences"=>5, "Unspecified"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>2}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>5}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>2}, "Unspecified"=>{"Unspecified"=>1}}, "group_count"=>0}

Scopus | Further Information

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/1466393"], "description"=>"<p>Mentioned n-numbers are tumor bearing animals available for microscopical examination.</p><p><i>k</i>-/-;<i>d</i>-/-: <i>ku80</i>-/-; <i>dna-pk<sub>cs</sub><sup>−/−</sup></i>.</p><p>mes. lm. nd.: mesenterial lymph node.</p><p>ax. lm. nd.: axillary lymph node.</p><p>*∼5 thymus tumor preparations were microscopically examined per group and found to be all lymphomas. All other macroscopic neoplastic lesions observed in thymus are assumed to be lymphomas as well.</p><p>** analyzed in femur.</p><p>Tumor incidence based on all animals from longevity cohort, including those not microscopically examined.</p>", "links"=>[], "tags"=>["genetics", "Animal genetics", "Cancer genetics", "neoplastic"], "article_id"=>1000928, "categories"=>["Biological Sciences"], "users"=>["Erwin Reiling", "Martijn E. T. Dollé", "Sameh A. Youssef", "Moonsook Lee", "Bhawani Nagarajah", "Marianne Roodbergen", "Piet de With", "Alain de Bruin", "Jan H. Hoeijmakers", "Jan Vijg", "Harry van Steeg", "Paul Hasty"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0093568.t002", "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Histopathology_neoplastic_lesions_/1000928", "title"=>"Histopathology neoplastic lesions.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2014-04-16 02:50:17"}
  • {"files"=>["https://ndownloader.figshare.com/files/1466391"], "description"=>"<p>Error bars represent standard deviation. (A) Mutant frequency in liver. (B) Mutant frequency in spleen.</p>", "links"=>[], "tags"=>["genetics", "Animal genetics", "Cancer genetics", "mutant"], "article_id"=>1000926, "categories"=>["Biological Sciences"], "users"=>["Erwin Reiling", "Martijn E. T. Dollé", "Sameh A. Youssef", "Moonsook Lee", "Bhawani Nagarajah", "Marianne Roodbergen", "Piet de With", "Alain de Bruin", "Jan H. Hoeijmakers", "Jan Vijg", "Harry van Steeg", "Paul Hasty"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0093568.g004", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_LacZ_mutant_frequency_/1000926", "title"=>"LacZ mutant frequency.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-04-16 02:50:17"}
  • {"files"=>["https://ndownloader.figshare.com/files/1466387"], "description"=>"<p><i>Ku80<sup>+/−</sup></i> and <i>dna-pk<sub>cs</sub></i><sup>+/−</sup> animals are backcrossed for multiple generations to C57Bl6/J-pUR288 (left of dashed line) and FVB (right of dashed line) background. Double heterozygous knock out C57BL6/J male mice are crossed with double heterozygous knock out FVB female mice. Using this strategy all four desired cohorts are generated as F1 hybrids (grey boxes).</p>", "links"=>[], "tags"=>["genetics", "Animal genetics", "Cancer genetics", "knockout"], "article_id"=>1000922, "categories"=>["Biological Sciences"], "users"=>["Erwin Reiling", "Martijn E. T. Dollé", "Sameh A. Youssef", "Moonsook Lee", "Bhawani Nagarajah", "Marianne Roodbergen", "Piet de With", "Alain de Bruin", "Jan H. Hoeijmakers", "Jan Vijg", "Harry van Steeg", "Paul Hasty"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0093568.g001", "stats"=>{"downloads"=>0, "page_views"=>8, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Breeding_strategy_to_generate_the_knockout_cohorts_/1000922", "title"=>"Breeding strategy to generate the knockout cohorts.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-04-16 02:50:17"}
  • {"files"=>["https://ndownloader.figshare.com/files/1466390"], "description"=>"<p>Median survivals are shown in the figure legends in parentheses. <i>dna-pk<sub>cs</sub><sup>−/−</sup></i> mice live significantly longer compared to <i>ku80<sup>−/−</sup></i> mice in both male (<i>p</i> = 0.01) and females (<i>p</i> = 8.7*10<sup>−6</sup>) mice. Survival of double knock out mice is identical to <i>ku80<sup>−/−</sup></i>. (A) Males. (B) Females.</p>", "links"=>[], "tags"=>["genetics", "Animal genetics", "Cancer genetics"], "article_id"=>1000925, "categories"=>["Biological Sciences"], "users"=>["Erwin Reiling", "Martijn E. T. Dollé", "Sameh A. Youssef", "Moonsook Lee", "Bhawani Nagarajah", "Marianne Roodbergen", "Piet de With", "Alain de Bruin", "Jan H. Hoeijmakers", "Jan Vijg", "Harry van Steeg", "Paul Hasty"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0093568.g003", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Survival_curves_/1000925", "title"=>"Survival curves.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-04-16 02:50:17"}
  • {"files"=>["https://ndownloader.figshare.com/files/1466389"], "description"=>"<p>(A) Males. (B) Females.</p>", "links"=>[], "tags"=>["genetics", "Animal genetics", "Cancer genetics"], "article_id"=>1000924, "categories"=>["Biological Sciences"], "users"=>["Erwin Reiling", "Martijn E. T. Dollé", "Sameh A. Youssef", "Moonsook Lee", "Bhawani Nagarajah", "Marianne Roodbergen", "Piet de With", "Alain de Bruin", "Jan H. Hoeijmakers", "Jan Vijg", "Harry van Steeg", "Paul Hasty"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0093568.g002", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Mean_body_weights_/1000924", "title"=>"Mean body weights.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-04-16 02:50:17"}
  • {"files"=>["https://ndownloader.figshare.com/files/1466394"], "description"=>"<div><p>Ku80 and DNA-PK<sub>CS</sub> are both involved in the repair of double strand DNA breaks via the nonhomologous end joining (NHEJ) pathway. While <i>ku80<sup>−/−</sup></i> mice exhibit a severely reduced lifespan and size, this phenotype is less pronounced in <i>dna-pk<sub>cs</sub><sup>−/−</sup></i> mice. However, these observations are based on independent studies with varying genetic backgrounds. Here, we generated <i>ku80<sup>−/−</sup></i>, <i>dna-pk<sub>cs</sub><sup>−/−</sup></i> and double knock out mice in a C57Bl6/J*FVB F1 hybrid background and compared their lifespan, end of life pathology and mutation frequency in liver and spleen using a lacZ reporter. Our data confirm that inactivation of Ku80 and DNA-PK<sub>CS</sub> causes reduced lifespan and bodyweights, which is most severe in <i>ku80<sup>−/−</sup></i> mice. All mutant mice exhibited a strong increase in lymphoma incidence as well as other aging-related pathology (skin epidermal and adnexal atrophy, trabacular bone reduction, kidney tubular anisokaryosis, and cortical and medullar atrophy) and severe lymphoid depletion. LacZ mutation frequency analysis did not show strong differences in mutation frequencies between knock out and wild type mice. The <i>ku80<sup>−/−</sup></i> mice had the most severe phenotype and the Ku80-mutation was dominant over the DNA-PK<sub>CS</sub>-mutation. Presumably, the more severe degenerative effect of Ku80 inactivation on lifespan compared to DNA-PK<sub>CS</sub> inactivation is caused by additional functions of Ku80 or activity of free Ku70 since both Ku80 and DNA-PK<sub>CS</sub> are essential for NHEJ.</p></div>", "links"=>[], "tags"=>["genetics", "Animal genetics", "Cancer genetics", "progeroid", "phenotype", "ku80", "deficiency"], "article_id"=>1000929, "categories"=>["Biological Sciences"], "users"=>["Erwin Reiling", "Martijn E. T. Dollé", "Sameh A. Youssef", "Moonsook Lee", "Bhawani Nagarajah", "Marianne Roodbergen", "Piet de With", "Alain de Bruin", "Jan H. Hoeijmakers", "Jan Vijg", "Harry van Steeg", "Paul Hasty"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0093568", "stats"=>{"downloads"=>0, "page_views"=>4, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/The_Progeroid_Phenotype_of_Ku80_Deficiency_Is_Dominant_over_DNA_PK_CS_Deficiency/1000929", "title"=>"The Progeroid Phenotype of Ku80 Deficiency Is Dominant over DNA-PK<sub>CS</sub> Deficiency", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2014-04-16 02:50:17"}
  • {"files"=>["https://ndownloader.figshare.com/files/1466392"], "description"=>"<p>4–5 animals examined per group. All selected mutant mice are at end of life, wild type mice are aged matched to mutant mice.</p><p>Mean age in weeks is shown (w).</p><p>mes ln: mesenterial lymph node.</p><p><i>k</i>-/-;<i>d</i>-/-: <i>ku80</i><sup>−/−</sup>; <i>dna-pk<sub>cs</sub><sup>−/−</sup></i>.</p><p>St. Dev.: Standard deviation.</p><p><i>p</i>-values based on comparison with wild type animals.</p><p>* <i>p</i><0.05.</p><p>** <i>p</i><0.01.</p><p>*** <i>p</i><0.001.</p>", "links"=>[], "tags"=>["genetics", "Animal genetics", "Cancer genetics", "non-neoplastic"], "article_id"=>1000927, "categories"=>["Biological Sciences"], "users"=>["Erwin Reiling", "Martijn E. T. Dollé", "Sameh A. Youssef", "Moonsook Lee", "Bhawani Nagarajah", "Marianne Roodbergen", "Piet de With", "Alain de Bruin", "Jan H. Hoeijmakers", "Jan Vijg", "Harry van Steeg", "Paul Hasty"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0093568.t001", "stats"=>{"downloads"=>0, "page_views"=>2, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Histopathology_non_neoplastic_lesions_/1000927", "title"=>"Histopathology non-neoplastic lesions.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2014-04-16 02:50:17"}

PMC Usage Stats | Further Information

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  • {"unique-ip"=>"5", "full-text"=>"4", "pdf"=>"1", "abstract"=>"0", "scanned-summary"=>"0", "scanned-page-browse"=>"0", "figure"=>"2", "supp-data"=>"0", "cited-by"=>"0", "year"=>"2017", "month"=>"9"}
  • {"unique-ip"=>"3", "full-text"=>"3", "pdf"=>"1", "abstract"=>"0", "scanned-summary"=>"0", "scanned-page-browse"=>"0", "figure"=>"0", "supp-data"=>"0", "cited-by"=>"0", "year"=>"2017", "month"=>"10"}
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Relative Metric

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