Histone Deacetylase Inhibitors Selectively Target Homology Dependent DNA Repair Defective Cells and Elevate Non-Homologous Endjoining Activity
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{"title"=>"Histone deacetylase inhibitors selectively target homology dependent DNA repair defective cells and elevate non-homologous endjoining activity", "type"=>"journal", "authors"=>[{"first_name"=>"Stephanie", "last_name"=>"Smith", "scopus_author_id"=>"57199389438"}, {"first_name"=>"Jennifer", "last_name"=>"Fox", "scopus_author_id"=>"39261226500"}, {"first_name"=>"Marco", "last_name"=>"Mejia", "scopus_author_id"=>"56150227400"}, {"first_name"=>"Wanvipa", "last_name"=>"Ruangpradit", "scopus_author_id"=>"55796132900"}, {"first_name"=>"Alihossein", "last_name"=>"Saberi", "scopus_author_id"=>"10142912500"}, {"first_name"=>"Sunmi", "last_name"=>"Kim", "scopus_author_id"=>"36169889000"}, {"first_name"=>"Yongjun", "last_name"=>"Choi", "scopus_author_id"=>"56456949200"}, {"first_name"=>"Sehyun", "last_name"=>"Oh", "scopus_author_id"=>"51964490700"}, {"first_name"=>"Yucai", "last_name"=>"Wang", "scopus_author_id"=>"37098155500"}, {"first_name"=>"Kyungho", "last_name"=>"Choi", "scopus_author_id"=>"35217582900"}, {"first_name"=>"Lei", "last_name"=>"Li", "scopus_author_id"=>"50561636900"}, {"first_name"=>"Eric A.", "last_name"=>"Hendrickson", "scopus_author_id"=>"7005399990"}, {"first_name"=>"Shunichi", "last_name"=>"Takeda", "scopus_author_id"=>"35428932700"}, {"first_name"=>"Mark", "last_name"=>"Muller", "scopus_author_id"=>"26658530900"}, {"first_name"=>"Kyungjae", "last_name"=>"Myung", "scopus_author_id"=>"57045635100"}], "year"=>2014, "source"=>"PLoS ONE", "identifiers"=>{"issn"=>"19326203", "scopus"=>"2-s2.0-84899847162", "pmid"=>"24466340", "doi"=>"10.1371/journal.pone.0087203", "pui"=>"373020830", "isbn"=>"1932-6203 (Electronic)\\r1932-6203 (Linking)", "sgr"=>"84899847162"}, "id"=>"62c9da10-671e-39c7-a466-5bc0ae116293", "abstract"=>"BACKGROUND: We have previously used the ATAD5-luciferase high-throughput screening assay to identify genotoxic compounds with potential chemotherapeutic capabilities. The successful identification of known genotoxic agents, including the histone deacetylase inhibitor (HDACi) trichostatin A (TSA), confirmed the specificity of the screen since TSA has been widely studied for its ability to cause apoptosis in cancer cells. Because many cancers have acquired mutations in DNA damage checkpoints or repair pathways, we hypothesized that these cancers may be susceptible to treatments that target compensatory pathways. Here, we used a panel of isogenic chicken DT40 B lymphocyte mutant and human cell lines to investigate the ability of TSA to define selective pathways that promote HDACi toxicity.\\n\\nRESULTS: HDACi induced a DNA damage response and reduced viability in all repair deficient DT40 mutants although ATM-nulls were least affected. The most dramatic sensitivity was observed in mutants lacking the homology dependent repair (HDR) factor BLM or the non-homologous end-joining (NHEJ) and HDR factors, KU/RAD54, suggesting an involvement of either HDR or NHEJ in HDACi-induced cell death. To extend these findings, we measured the frequencies of HDR and NHEJ after HDACi treatment and monitored viability in human cell lines comparably deficient in HDR or NHEJ. Although no difference in HDR frequency was observed between HDACi treated and untreated cells, HDR-defective human cell lines were clearly more sensitive than wild type. Unexpectedly, cells treated with HDACis showed a significantly elevated NHEJ frequency.\\n\\nCONCLUSIONS: HDACi targeting drugs induced significant increases in NHEJ activity in human cell lines but did not alter HDR frequency. Moreover, HDR is required for cellular resistance to HDACi therapy; therefore, NHEJ does not appear to be a critical axis for HDACi resistance. Rather, HDACi compounds induced DNA damage, most likely double strand breaks (DSBs), and HDR proficiency is correlated with cell survival.", "link"=>"http://www.mendeley.com/research/histone-deacetylase-inhibitors-selectively-target-homology-dependent-dna-repair-defective-cells-elev", "reader_count"=>30, "reader_count_by_academic_status"=>{"Unspecified"=>2, "Professor > Associate Professor"=>2, "Researcher"=>9, "Student > Doctoral Student"=>2, "Student > Ph. D. Student"=>6, "Student > Postgraduate"=>1, "Student > Master"=>3, "Other"=>2, "Student > Bachelor"=>1, "Professor"=>2}, "reader_count_by_user_role"=>{"Unspecified"=>2, "Professor > Associate Professor"=>2, "Researcher"=>9, "Student > Doctoral Student"=>2, "Student > Ph. D. Student"=>6, "Student > Postgraduate"=>1, "Student > Master"=>3, "Other"=>2, "Student > Bachelor"=>1, "Professor"=>2}, "reader_count_by_subject_area"=>{"Unspecified"=>2, "Environmental Science"=>1, "Biochemistry, Genetics and Molecular Biology"=>4, "Agricultural and Biological Sciences"=>14, "Medicine and Dentistry"=>3, "Pharmacology, Toxicology and Pharmaceutical Science"=>2, "Physics and Astronomy"=>1, "Chemistry"=>1, "Computer Science"=>2}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>3}, "Chemistry"=>{"Chemistry"=>1}, "Physics and Astronomy"=>{"Physics and Astronomy"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>14}, "Computer Science"=>{"Computer Science"=>2}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>4}, "Unspecified"=>{"Unspecified"=>2}, "Environmental Science"=>{"Environmental Science"=>1}, "Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>2}}, "reader_count_by_country"=>{"United Kingdom"=>1, "Indonesia"=>1}, "group_count"=>2}

Scopus | Further Information

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/1358058"], "description"=>"<p>(A) <i>BLM</i> and (B) <i>XPA</i> human lymphocytes were treated with 0 to 1.5 µM TSA or 0 to 100 µM SAHA for 48 hours. (C) <i>SHPRH</i> MEFs were treated with 0 to 1.5 µM TSA or 0 to 100 µM SAHA for 48 hours. (D) <i>FANCM</i> human colorectal cancer cells were treated with 0 to 1.5 µM TSA or 0 to 100 µM SAHA for 48 hr. Viability was determined using CellTiter-Glo. The data represent the average of 3 independent experiments ± SD.</p>", "links"=>[], "tags"=>["genetics", "gene expression", "Histone modification", "Molecular cell biology", "Chromosome biology", "Chromosome structure and function", "Nucleic acids", "dna", "DNA recombination", "DNA repair", "oncology", "Cancer treatment", "Chemotherapy and drug treatment", "hdaci", "viability", "mammalian"], "article_id"=>910304, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Stephanie Smith", "Jennifer Fox", "Marco Mejia", "Wanvipa Ruangpradit", "Alihossein Saberi", "Sunmi Kim", "Yongjun Choi", "Sehyun Oh", "Yucai Wang", "Kyungho Choi", "Lei Li", "Eric A. Hendrickson", "Shunichi Takeda", "Mark Muller", "Kyungjae Myung"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0087203.g007", "stats"=>{"downloads"=>1, "page_views"=>10, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Effect_of_HDACi_on_the_viability_of_mammalian_cell_lines_/910304", "title"=>"Effect of HDACi on the viability of mammalian cell lines.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-01-23 03:35:30"}
  • {"files"=>["https://ndownloader.figshare.com/files/1358056"], "description"=>"<p>The indicated cells were treated for 48 µM TSA, 0 to 100 µM SAHA or 0 to 118 mM MMS. Viability was determined using CellTiter-Glo. The data represent the average of 3 independent experiments ± SD. (A) HCC1937 cells, lacking a functional <i>BRCA1</i> gene, or HC1937 cells complimented by <i>BRCA1</i> cDNA expression (wild-type). EC50 differences between wild-type and <i>BRCA1</i> after treatment with TSA and SAHA were significant at p = 0.0009 and p = 0.02 respectively. EC50 differences between wild-type and <i>BRCA1</i> after MMS treatment were not significant p = 0.07. (B) Hela cells after 2×24 hr transfection with either non-targeting siRNA or siRNA against <i>RAD51</i>. EC50 differences between siNT and siRAD51 after treatment with TSA and SAHA were significant at p<0.0001 and p = 0.03 respectively. EC50 differences between siNT and siRAD51 after MMS treatment were not significant p = 0.07.</p>", "links"=>[], "tags"=>["genetics", "gene expression", "Histone modification", "Molecular cell biology", "Chromosome biology", "Chromosome structure and function", "Nucleic acids", "dna", "DNA recombination", "DNA repair", "oncology", "Cancer treatment", "Chemotherapy and drug treatment", "hdr", "deficient", "cells"], "article_id"=>910302, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Stephanie Smith", "Jennifer Fox", "Marco Mejia", "Wanvipa Ruangpradit", "Alihossein Saberi", "Sunmi Kim", "Yongjun Choi", "Sehyun Oh", "Yucai Wang", "Kyungho Choi", "Lei Li", "Eric A. Hendrickson", "Shunichi Takeda", "Mark Muller", "Kyungjae Myung"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0087203.g006", "stats"=>{"downloads"=>0, "page_views"=>20, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Viability_of_HDR_deficient_cells_after_treatment_with_HDACis_/910302", "title"=>"Viability of HDR deficient cells after treatment with HDACis.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-01-23 03:35:30"}
  • {"files"=>["https://ndownloader.figshare.com/files/1358053"], "description"=>"<p>(A) Representative images of RPE nuclei (blue) with p-53BP1 foci (green) after a 24 hr treatment with 2 mM HU or 1 hr treatment with either 0.5 µM TSA or 32 µM SAHA. (B) The percentage of RPE cells containing the indicated number of p-53BP1 foci following treatment as described in A was determined from at least 145 cells per treatment. (C) Schematic of NHEJ assay. HeLa IHN20.22 cells were pulsed for 24 hr with Dox, washed and chased in the presence of the indicated amounts of TSA (D) or SAHA (E) for 3 days. The graphs represent the average percent GFP ± SD. Significance between +Dox/−TSA or SAHA and +Dox/+TSA or SAHA was calculated using a two-tailed t-test. The percentage of GFP-positive cells was determined by FACS analysis.</p>", "links"=>[], "tags"=>["genetics", "gene expression", "Histone modification", "Molecular cell biology", "Chromosome biology", "Chromosome structure and function", "Nucleic acids", "dna", "DNA recombination", "DNA repair", "oncology", "Cancer treatment", "Chemotherapy and drug treatment", "hdaci"], "article_id"=>910299, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Stephanie Smith", "Jennifer Fox", "Marco Mejia", "Wanvipa Ruangpradit", "Alihossein Saberi", "Sunmi Kim", "Yongjun Choi", "Sehyun Oh", "Yucai Wang", "Kyungho Choi", "Lei Li", "Eric A. Hendrickson", "Shunichi Takeda", "Mark Muller", "Kyungjae Myung"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0087203.g004", "stats"=>{"downloads"=>0, "page_views"=>16, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_The_effect_of_HDACi_on_NHEJ_/910299", "title"=>"The effect of HDACi on NHEJ.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-01-23 03:35:30"}
  • {"files"=>["https://ndownloader.figshare.com/files/1358052"], "description"=>"<p>(A) RPE cells were treated with 0.2 µM TSA for 48 hr. Representative images of metaphase spreads with arrows indicating SCEs (Magnification: 100×). (Inset) Magnification of the boxed region. (B) The graph represents the average number of SCEs per cell ± SD following treatment. Non-significance was determined using a two-tailed t-test. (C) Schematic of DR-GFP HR frequency assay. (D) U2OS DR-GFP cells were transfected with pCGA-I-SCEI and then treated with 0.25 µM TSA for 48 hr. The graph represents the average HR frequency ± SD following treatment determined by FACS analysis. Non-significance was determined using a two-tailed t-test. (E) Schematic of twin reporter DR-GFP HR assay. (F) HeLa iHO4.5GFP cells were pulsed for 24 hr with Dox, washed and chased in the presence of the indicated amounts of TSA. The percentage of GFP-positive cells was determined by FACS analysis. The graph represents the average percent GFP ± SD. The difference between +Dox/−TSA and +Dox/+TSA not significant and was determined using a two-tailed t-test.</p>", "links"=>[], "tags"=>["genetics", "gene expression", "Histone modification", "Molecular cell biology", "Chromosome biology", "Chromosome structure and function", "Nucleic acids", "dna", "DNA recombination", "DNA repair", "oncology", "Cancer treatment", "Chemotherapy and drug treatment", "hdacis", "sce", "hr"], "article_id"=>910298, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Stephanie Smith", "Jennifer Fox", "Marco Mejia", "Wanvipa Ruangpradit", "Alihossein Saberi", "Sunmi Kim", "Yongjun Choi", "Sehyun Oh", "Yucai Wang", "Kyungho Choi", "Lei Li", "Eric A. Hendrickson", "Shunichi Takeda", "Mark Muller", "Kyungjae Myung"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0087203.g003", "stats"=>{"downloads"=>0, "page_views"=>10, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_The_effect_of_HDACis_on_SCE_and_HR_Frequency_/910298", "title"=>"The effect of HDACis on SCE and HR Frequency.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-01-23 03:35:30"}
  • {"files"=>["https://ndownloader.figshare.com/files/1358046"], "description"=>"<p>Viability was determined using CellTiter-Glo. The data represent the average of 3 independent experiments ± SD.</p>", "links"=>[], "tags"=>["genetics", "gene expression", "Histone modification", "Molecular cell biology", "Chromosome biology", "Chromosome structure and function", "Nucleic acids", "dna", "DNA recombination", "DNA repair", "oncology", "Cancer treatment", "Chemotherapy and drug treatment", "isogenic", "dt40", "lymphocyte", "lines", "tsa"], "article_id"=>910292, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Stephanie Smith", "Jennifer Fox", "Marco Mejia", "Wanvipa Ruangpradit", "Alihossein Saberi", "Sunmi Kim", "Yongjun Choi", "Sehyun Oh", "Yucai Wang", "Kyungho Choi", "Lei Li", "Eric A. Hendrickson", "Shunichi Takeda", "Mark Muller", "Kyungjae Myung"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0087203.g002", "stats"=>{"downloads"=>1, "page_views"=>14, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Viability_of_isogenic_chicken_DT40_B_lymphocyte_cell_lines_following_48_A_0_to_0_04_181_M_TSA_and_B_0_to_3_125_181_M_SAHA_/910292", "title"=>"Viability of isogenic chicken DT40 B lymphocyte cell lines following 48(A) 0 to 0.04 µM TSA and (B) 0 to 3.125 µM SAHA.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-01-23 03:35:30"}
  • {"files"=>["https://ndownloader.figshare.com/files/1358060"], "description"=>"<p>EC50 values for isogenic chicken DT40 B lymphocyte cell lines following 48</p>", "links"=>[], "tags"=>["genetics", "gene expression", "Histone modification", "Molecular cell biology", "Chromosome biology", "Chromosome structure and function", "Nucleic acids", "dna", "DNA recombination", "DNA repair", "oncology", "Cancer treatment", "Chemotherapy and drug treatment", "isogenic", "dt40", "lymphocyte", "lines"], "article_id"=>910306, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Stephanie Smith", "Jennifer Fox", "Marco Mejia", "Wanvipa Ruangpradit", "Alihossein Saberi", "Sunmi Kim", "Yongjun Choi", "Sehyun Oh", "Yucai Wang", "Kyungho Choi", "Lei Li", "Eric A. Hendrickson", "Shunichi Takeda", "Mark Muller", "Kyungjae Myung"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0087203.t002", "stats"=>{"downloads"=>2, "page_views"=>16, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_EC50_values_for_isogenic_chicken_DT40_B_lymphocyte_cell_lines_following_48_/910306", "title"=>"EC50 values for isogenic chicken DT40 B lymphocyte cell lines following 48", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2014-01-23 03:35:30"}
  • {"files"=>["https://ndownloader.figshare.com/files/1358055"], "description"=>"<p>The indicated cells were treated for 48 µM TSA, 0 to 100 µM SAHA or 0 to 118 mM MMS. Viability was determined using CellTiter-Glo. The data represent the average of 3 independent experiments ± SD. (A) Hela cells after 24 hr transfection with either non-targeting siRNA or siRNA against <i>KU80</i>. (B) HCT116 <i>LIG4</i>-null or wild-type HCT116 cells. (C) HCC1937 cells, lacking a functional <i>BRCA1</i> gene, or HC1937 cells complimented by <i>BRCA1</i> cDNA expression (wild-type).</p>", "links"=>[], "tags"=>["genetics", "gene expression", "Histone modification", "Molecular cell biology", "Chromosome biology", "Chromosome structure and function", "Nucleic acids", "dna", "DNA recombination", "DNA repair", "oncology", "Cancer treatment", "Chemotherapy and drug treatment", "nhej", "deficient", "cells"], "article_id"=>910301, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Stephanie Smith", "Jennifer Fox", "Marco Mejia", "Wanvipa Ruangpradit", "Alihossein Saberi", "Sunmi Kim", "Yongjun Choi", "Sehyun Oh", "Yucai Wang", "Kyungho Choi", "Lei Li", "Eric A. Hendrickson", "Shunichi Takeda", "Mark Muller", "Kyungjae Myung"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0087203.g005", "stats"=>{"downloads"=>0, "page_views"=>14, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Viability_of_NHEJ_deficient_cells_after_treatment_with_HDACis_/910301", "title"=>"Viability of NHEJ deficient cells after treatment with HDACis.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-01-23 03:35:30"}
  • {"files"=>["https://ndownloader.figshare.com/files/1358062", "https://ndownloader.figshare.com/files/1358063"], "description"=>"<div><p>Background</p><p>We have previously used the ATAD5-luciferase high-throughput screening assay to identify genotoxic compounds with potential chemotherapeutic capabilities. The successful identification of known genotoxic agents, including the histone deacetylase inhibitor (HDACi) trichostatin A (TSA), confirmed the specificity of the screen since TSA has been widely studied for its ability to cause apoptosis in cancer cells. Because many cancers have acquired mutations in DNA damage checkpoints or repair pathways, we hypothesized that these cancers may be susceptible to treatments that target compensatory pathways. Here, we used a panel of isogenic chicken DT40 B lymphocyte mutant and human cell lines to investigate the ability of TSA to define selective pathways that promote HDACi toxicity.</p><p>Results</p><p>HDACi induced a DNA damage response and reduced viability in all repair deficient DT40 mutants although <i>ATM</i>-nulls were least affected. The most dramatic sensitivity was observed in mutants lacking the homology dependent repair (HDR) factor <i>BLM</i> or the non-homologous end-joining (NHEJ) and HDR factors, <i>KU/RAD54</i>, suggesting an involvement of either HDR or NHEJ in HDACi-induced cell death. To extend these findings, we measured the frequencies of HDR and NHEJ after HDACi treatment and monitored viability in human cell lines comparably deficient in HDR or NHEJ. Although no difference in HDR frequency was observed between HDACi treated and untreated cells, HDR-defective human cell lines were clearly more sensitive than wild type. Unexpectedly, cells treated with HDACis showed a significantly elevated NHEJ frequency.</p><p>Conclusions</p><p>HDACi targeting drugs induced significant increases in NHEJ activity in human cell lines but did not alter HDR frequency. Moreover, HDR is required for cellular resistance to HDACi therapy; therefore, NHEJ does not appear to be a critical axis for HDACi resistance. Rather, HDACi compounds induced DNA damage, most likely double strand breaks (DSBs), and HDR proficiency is correlated with cell survival.</p></div>", "links"=>[], "tags"=>["genetics", "gene expression", "Histone modification", "Molecular cell biology", "Chromosome biology", "Chromosome structure and function", "Nucleic acids", "dna", "DNA recombination", "DNA repair", "oncology", "Cancer treatment", "Chemotherapy and drug treatment", "deacetylase", "inhibitors", "selectively", "homology", "defective", "cells", "elevate", "non-homologous", "endjoining"], "article_id"=>910308, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Stephanie Smith", "Jennifer Fox", "Marco Mejia", "Wanvipa Ruangpradit", "Alihossein Saberi", "Sunmi Kim", "Yongjun Choi", "Sehyun Oh", "Yucai Wang", "Kyungho Choi", "Lei Li", "Eric A. Hendrickson", "Shunichi Takeda", "Mark Muller", "Kyungjae Myung"], "doi"=>["https://dx.doi.org/10.1371/journal.pone.0087203.s001", "https://dx.doi.org/10.1371/journal.pone.0087203.s002"], "stats"=>{"downloads"=>0, "page_views"=>16, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Histone_Deacetylase_Inhibitors_Selectively_Target_Homology_Dependent_DNA_Repair_Defective_Cells_and_Elevate_Non_Homologous_Endjoining_Activity_/910308", "title"=>"Histone Deacetylase Inhibitors Selectively Target Homology Dependent DNA Repair Defective Cells and Elevate Non-Homologous Endjoining Activity", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2014-01-23 03:35:30"}
  • {"files"=>["https://ndownloader.figshare.com/files/1358059"], "description"=>"<p>Cell lines used in this study.</p>", "links"=>[], "tags"=>["genetics", "gene expression", "Histone modification", "Molecular cell biology", "Chromosome biology", "Chromosome structure and function", "Nucleic acids", "dna", "DNA recombination", "DNA repair", "oncology", "Cancer treatment", "Chemotherapy and drug treatment", "lines"], "article_id"=>910305, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Stephanie Smith", "Jennifer Fox", "Marco Mejia", "Wanvipa Ruangpradit", "Alihossein Saberi", "Sunmi Kim", "Yongjun Choi", "Sehyun Oh", "Yucai Wang", "Kyungho Choi", "Lei Li", "Eric A. Hendrickson", "Shunichi Takeda", "Mark Muller", "Kyungjae Myung"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0087203.t001", "stats"=>{"downloads"=>0, "page_views"=>14, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Cell_lines_used_in_this_study_/910305", "title"=>"Cell lines used in this study.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2014-01-23 03:35:30"}
  • {"files"=>["https://ndownloader.figshare.com/files/1358044"], "description"=>"<p>(A) HEK293T ELG1-LUC cells were treated with 0.75 µM TSA or 50 µM SAHA for 48 hr. LUC activity was measured using One-Glo. The graph represents average LUC activity ± SD. Significance was calculated using a two-tailed t-test. (B) HEK293T cells were treated with 50 µM TSA for 24 hr. Using the indicated antibodies proteins levels were visualized by Western blot analysis from either the chromatin-bound fraction or total cell lysate. (C) HEK293T cells were treated with 100 uM TSA for 24 hours and then Pulsed-field gel electrophoresis was performed.</p>", "links"=>[], "tags"=>["genetics", "gene expression", "Histone modification", "Molecular cell biology", "Chromosome biology", "Chromosome structure and function", "Nucleic acids", "dna", "DNA recombination", "DNA repair", "oncology", "Cancer treatment", "Chemotherapy and drug treatment"], "article_id"=>910290, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Stephanie Smith", "Jennifer Fox", "Marco Mejia", "Wanvipa Ruangpradit", "Alihossein Saberi", "Sunmi Kim", "Yongjun Choi", "Sehyun Oh", "Yucai Wang", "Kyungho Choi", "Lei Li", "Eric A. Hendrickson", "Shunichi Takeda", "Mark Muller", "Kyungjae Myung"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0087203.g001", "stats"=>{"downloads"=>1, "page_views"=>8, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Trichostatin_A_induces_DNA_damage_/910290", "title"=>"Trichostatin A induces DNA damage.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-01-23 03:35:30"}

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Relative Metric

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