A Synthetic Interaction Screen Identifies Factors Selectively Required for Proliferation and TERT Transcription in p53-Deficient Human Cancer Cells
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{"title"=>"A Synthetic Interaction Screen Identifies Factors Selectively Required for Proliferation and TERT Transcription in p53-Deficient Human Cancer Cells", "type"=>"journal", "authors"=>[{"first_name"=>"Li", "last_name"=>"Xie", "scopus_author_id"=>"55547697600"}, {"first_name"=>"Claude", "last_name"=>"Gazin", "scopus_author_id"=>"6603099263"}, {"first_name"=>"Sung Mi", "last_name"=>"Park", "scopus_author_id"=>"55547414400"}, {"first_name"=>"Lihua J.", "last_name"=>"Zhu", "scopus_author_id"=>"24345727500"}, {"first_name"=>"Marie anne", "last_name"=>"Debily", "scopus_author_id"=>"6507954965"}, {"first_name"=>"Ellen L.W.", "last_name"=>"Kittler", "scopus_author_id"=>"6701742147"}, {"first_name"=>"Maria L.", "last_name"=>"Zapp", "scopus_author_id"=>"6701746805"}, {"first_name"=>"David", "last_name"=>"Lapointe", "scopus_author_id"=>"35965574300"}, {"first_name"=>"Stephane", "last_name"=>"Gobeil", "scopus_author_id"=>"6507992678"}, {"first_name"=>"Ching Man", "last_name"=>"Virbasius", "scopus_author_id"=>"6603081911"}, {"first_name"=>"Michael R.", "last_name"=>"Green", "scopus_author_id"=>"55628582845"}], "year"=>2012, "source"=>"PLoS Genetics", "identifiers"=>{"isbn"=>"1553-7404 (Electronic)\\r1553-7390 (Linking)", "pmid"=>"23284306", "pui"=>"368067356", "issn"=>"15537390", "doi"=>"10.1371/journal.pgen.1003151", "scopus"=>"2-s2.0-84872022032", "sgr"=>"84872022032"}, "id"=>"8a9fd484-534f-3405-b0c4-6209922d6898", "abstract"=>"Numerous genetic and epigenetic alterations render cancer cells selectively dependent on specific genes and regulatory pathways, and represent potential vulnerabilities that can be therapeutically exploited. Here we describe an RNA interference (RNAi)-based synthetic interaction screen to identify genes preferentially required for proliferation of p53-deficient (p53-) human cancer cells. We find that compared to p53-competent (p53+) human cancer cell lines, diverse p53- human cancer cell lines are preferentially sensitive to loss of the transcription factor ETV1 and the DNA damage kinase ATR. In p53- cells, RNAi-mediated knockdown of ETV1 or ATR results in decreased expression of the telomerase catalytic subunit TERT leading to growth arrest, which can be reversed by ectopic TERT expression. Chromatin immunoprecipitation analysis reveals that ETV1 binds to a region downstream of the TERT transcriptional start-site in p53- but not p53+ cells. We find that the role of ATR is to phosphorylate and thereby stabilize ETV1. Our collective results identify a regulatory pathway involving ETV1, ATR, and TERT that is preferentially important for proliferation of diverse p53- cancer cells.", "link"=>"http://www.mendeley.com/research/synthetic-interaction-screen-identifies-factors-selectively-required-proliferation-tert-transcriptio", "reader_count"=>22, "reader_count_by_academic_status"=>{"Professor > Associate Professor"=>1, "Researcher"=>3, "Student > Doctoral Student"=>1, "Student > Ph. D. Student"=>7, "Student > Postgraduate"=>2, "Student > Master"=>2, "Other"=>2, "Student > Bachelor"=>2, "Professor"=>2}, "reader_count_by_user_role"=>{"Professor > Associate Professor"=>1, "Researcher"=>3, "Student > Doctoral Student"=>1, "Student > Ph. D. Student"=>7, "Student > Postgraduate"=>2, "Student > Master"=>2, "Other"=>2, "Student > Bachelor"=>2, "Professor"=>2}, "reader_count_by_subject_area"=>{"Unspecified"=>1, "Environmental Science"=>1, "Biochemistry, Genetics and Molecular Biology"=>1, "Agricultural and Biological Sciences"=>15, "Medicine and Dentistry"=>3, "Physics and Astronomy"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>3}, "Physics and Astronomy"=>{"Physics and Astronomy"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>15}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>1}, "Unspecified"=>{"Unspecified"=>1}, "Environmental Science"=>{"Environmental Science"=>1}}, "group_count"=>0}

Scopus | Further Information

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/280992", "https://ndownloader.figshare.com/files/281027", "https://ndownloader.figshare.com/files/281058", "https://ndownloader.figshare.com/files/281097", "https://ndownloader.figshare.com/files/281136", "https://ndownloader.figshare.com/files/281240", "https://ndownloader.figshare.com/files/281292", "https://ndownloader.figshare.com/files/281329", "https://ndownloader.figshare.com/files/281363", "https://ndownloader.figshare.com/files/281403", "https://ndownloader.figshare.com/files/281429", "https://ndownloader.figshare.com/files/281462", "https://ndownloader.figshare.com/files/281499", "https://ndownloader.figshare.com/files/281548", "https://ndownloader.figshare.com/files/281585", "https://ndownloader.figshare.com/files/281627", "https://ndownloader.figshare.com/files/281655", "https://ndownloader.figshare.com/files/281756", "https://ndownloader.figshare.com/files/281822", "https://ndownloader.figshare.com/files/281876"], "description"=>"<div><p>Numerous genetic and epigenetic alterations render cancer cells selectively dependent on specific genes and regulatory pathways, and represent potential vulnerabilities that can be therapeutically exploited. Here we describe an RNA interference (RNAi)–based synthetic interaction screen to identify genes preferentially required for proliferation of p53-deficient (p53−) human cancer cells. We find that compared to p53-competent (p53+) human cancer cell lines, diverse p53− human cancer cell lines are preferentially sensitive to loss of the transcription factor ETV1 and the DNA damage kinase ATR. In p53− cells, RNAi–mediated knockdown of ETV1 or ATR results in decreased expression of the telomerase catalytic subunit TERT leading to growth arrest, which can be reversed by ectopic <em>TERT</em> expression. Chromatin immunoprecipitation analysis reveals that ETV1 binds to a region downstream of the <em>TERT</em> transcriptional start-site in p53− but not p53+ cells. We find that the role of ATR is to phosphorylate and thereby stabilize ETV1. Our collective results identify a regulatory pathway involving ETV1, ATR, and TERT that is preferentially important for proliferation of diverse p53− cancer cells.</p> </div>", "links"=>[], "tags"=>["synthetic", "identifies", "factors", "selectively", "proliferation", "transcription", "p53-deficient", "cancer", "cells"], "article_id"=>115409, "categories"=>["Molecular Biology", "Biochemistry", "Cell Biology", "Genetics"], "users"=>["Li Xie", "Claude Gazin", "Sung Mi Park", "Lihua J. Zhu", "Marie-Anne Debily", "Ellen L. W. Kittler", "Maria L. Zapp", "David Lapointe", "Stephane Gobeil", "Ching-Man Virbasius", "Michael R. Green"], "doi"=>["https://dx.doi.org/10.1371/journal.pgen.1003151.s001", "https://dx.doi.org/10.1371/journal.pgen.1003151.s002", "https://dx.doi.org/10.1371/journal.pgen.1003151.s003", "https://dx.doi.org/10.1371/journal.pgen.1003151.s004", "https://dx.doi.org/10.1371/journal.pgen.1003151.s005", "https://dx.doi.org/10.1371/journal.pgen.1003151.s006", "https://dx.doi.org/10.1371/journal.pgen.1003151.s007", "https://dx.doi.org/10.1371/journal.pgen.1003151.s008", "https://dx.doi.org/10.1371/journal.pgen.1003151.s009", "https://dx.doi.org/10.1371/journal.pgen.1003151.s010", "https://dx.doi.org/10.1371/journal.pgen.1003151.s011", "https://dx.doi.org/10.1371/journal.pgen.1003151.s012", "https://dx.doi.org/10.1371/journal.pgen.1003151.s013", "https://dx.doi.org/10.1371/journal.pgen.1003151.s014", "https://dx.doi.org/10.1371/journal.pgen.1003151.s015", "https://dx.doi.org/10.1371/journal.pgen.1003151.s016", "https://dx.doi.org/10.1371/journal.pgen.1003151.s017", "https://dx.doi.org/10.1371/journal.pgen.1003151.s018", "https://dx.doi.org/10.1371/journal.pgen.1003151.s019", "https://dx.doi.org/10.1371/journal.pgen.1003151.s020"], "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/A_Synthetic_Interaction_Screen_Identifies_Factors_Selectively_Required_for_Proliferation_and_TERT_Transcription_in_p53_Deficient_Human_Cancer_Cells__/115409", "title"=>"A Synthetic Interaction Screen Identifies Factors Selectively Required for Proliferation and <em>TERT</em> Transcription in p53-Deficient Human Cancer Cells", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2012-12-20 01:30:09"}
  • {"files"=>["https://ndownloader.figshare.com/files/520568"], "description"=>"<p>(A) Schematic summary of the screen. p53+ and p53− HCT116 cells were infected in parallel with a pooled lentiviral human shRNA library. The shRNA population was analyzed by massively parallel sequencing at 40 hours and 10 days post-infection (p.i.). (B) Volcano plot. The horizontal and vertical lines indicate the selection criteria. The red points represent shRNAs diminished ≥4-fold in p53− HCT116 cells and ≤2-fold in p53+ HCT116 cells at 10 days p.i. relative to 40 hours p.i. Blue points represent shRNAs diminished in both p53+ and p53− cells, and black points represent shRNAs not diminished in either p53+ or p53− cells. (C) Colony formation assay. p53+ and p53− HCT116 cells infected with a lentivirus expressing individual candidate shRNAs were selected with puromycin and plated in a serial dilution series in 6-well plates. Only one dilution set is shown. Colonies were fixed and stained with crystal violet. Control refers to the empty lentiviral vector, pGIPZ. (D) Proliferation assay. p53+ and p53− HCT116 cells infected with a lentivirus expressing each individual candidate shRNA, or as a control a non-silencing (NS) shRNA, were selected with puromycin and cell proliferation determined by an Alamar Blue fluorescence assay. The results were normalized to that obtained with a NS shRNA, which was set to 1. Error bars represent SD. (E) Proliferation of p53+ and p53− HCT116 cells transfected with an siRNA directed against an individual candidate gene, or a control lamin A/C (LMNA) siRNA, was determined by an Alamar Blue fluorescence assay. The results were normalized to that obtained with the control shRNA, which was set to 1. Error bars represent SD.</p>", "links"=>[], "tags"=>["genome-wide", "synthetic", "identifies", "genes", "preferentially", "proliferation"], "article_id"=>191048, "categories"=>["Molecular Biology", "Biochemistry", "Cell Biology", "Genetics"], "users"=>["Li Xie", "Claude Gazin", "Sung Mi Park", "Lihua J. Zhu", "Marie-Anne Debily", "Ellen L. W. Kittler", "Maria L. Zapp", "David Lapointe", "Stephane Gobeil", "Ching-Man Virbasius", "Michael R. Green"], "doi"=>["https://dx.doi.org/10.1371/journal.pgen.1003151.g001"], "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_A_genome_wide_shRNA_8211_based_synthetic_interaction_screen_identifies_candidate_genes_preferentially_required_for_proliferation_of_p53_8722_cells_/191048", "title"=>"A genome-wide shRNA–based synthetic interaction screen identifies candidate genes preferentially required for proliferation of p53− cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-12-20 00:17:28"}
  • {"files"=>["https://ndownloader.figshare.com/files/520673"], "description"=>"<p>(A) Proliferation of p53+ and p53− RKO cells expressing an individual candidate shRNA, or as a control a NS shRNA, was determined by an Alamar Blue fluorescence assay. The results were normalized to that obtained with the NS shRNA, which was set to 1. Error bars represent SD. ShRNAs that preferentially affect the proliferation of p53− relative to p53+ cell lines are indicated in red. (B) Proliferation of p53+ and p53− A549 cells transfected with a candidate siRNA, or as a control a LMNA siRNA, was determined by an Alamar Blue fluorescence assay. The results were normalized to that obtained with the LMNA siRNA, which was set to 1. Error bars represent SD. ShRNAs that preferentially affect the proliferation of p53− relative to p53+ cell lines are indicated in red. (C) Proliferation of A549, NCI-H460, NCI-H1299 and NCI-H522 cells expressing a candidate shRNA, or as a control an NS shRNA, was determined by an Alamar Blue fluorescence assay. The results were normalized to that obtained with the NS shRNA, which was set to 1. Error bars represent SD. ShRNAs that preferentially affect the proliferation of p53− relative to p53+ cell lines are indicated in red. (D) p53+ and p53− HCT116 cells expressing an ATR or ETV1 shRNAs or as a control a NS shRNA, were subcutaneously injected into opposite flanks of the same nude mouse, and tumor volume was measured after 4 weeks. The results were normalized to that obtained in p53+ cells expressing a NS shRNA, which was set to 1. Error bars represent SD. * <i>P</i>≤0.0001.</p>", "links"=>[], "tags"=>["atr", "preferentially", "proliferation"], "article_id"=>191162, "categories"=>["Molecular Biology", "Biochemistry", "Cell Biology", "Genetics"], "users"=>["Li Xie", "Claude Gazin", "Sung Mi Park", "Lihua J. Zhu", "Marie-Anne Debily", "Ellen L. W. Kittler", "Maria L. Zapp", "David Lapointe", "Stephane Gobeil", "Ching-Man Virbasius", "Michael R. Green"], "doi"=>["https://dx.doi.org/10.1371/journal.pgen.1003151.g002"], "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_ETV1_and_ATR_are_preferentially_required_for_proliferation_of_diverse_p53_8722_cell_lines_/191162", "title"=>"ETV1 and ATR are preferentially required for proliferation of diverse p53− cell lines.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-12-20 00:19:22"}
  • {"files"=>["https://ndownloader.figshare.com/files/520738"], "description"=>"<p>(A) Immunoblot analysis showing TERT levels in p53+ and p53− HCT116 cells expressing NS, ATR or ETV1 shRNAs. The results using two unrelated ATR or ETV1 shRNAs are shown. β-actin (ACTB) was monitoring as a loading control. (B) qRT-PCR analysis monitoring <i>TERT</i> expression in p53+ and p53− HCT116 cells expressing NS, ATR or ETV1 shRNAs. <i>TERT</i> expression was normalized to that obtained with a NS shRNA, which was set to 1. Error bars represent SD. (C) Immunoblot analysis showing TERT levels in p53+ and p53− HCT116 cells treated with the ATR inhibitor CGK733 (left; 0, 2, 3, 4, and 5 µM) or ETP46464 (right; 0, 0.5, 1, 2, 4 and 8 µM).</p>", "links"=>[], "tags"=>["atr", "preferentially"], "article_id"=>191230, "categories"=>["Molecular Biology", "Biochemistry", "Cell Biology", "Genetics"], "users"=>["Li Xie", "Claude Gazin", "Sung Mi Park", "Lihua J. Zhu", "Marie-Anne Debily", "Ellen L. W. Kittler", "Maria L. Zapp", "David Lapointe", "Stephane Gobeil", "Ching-Man Virbasius", "Michael R. Green"], "doi"=>["https://dx.doi.org/10.1371/journal.pgen.1003151.g003"], "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_ETV1_and_ATR_are_preferentially_required_for_TERT_expression_in_p53_cells_/191230", "title"=>"ETV1 and ATR are preferentially required for <i>TERT</i> expression in p53− cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-12-20 00:20:30"}
  • {"files"=>["https://ndownloader.figshare.com/files/520846"], "description"=>"<p>(A) Senescence-associated β-galactosidase assay in p53+ and p53− HCT116 cells expressing a NS shRNA or one of two unrelated TERT shRNAs. Senescence-associated β-galactosidase activity was normalized to that obtained using a NS shRNA, which was set to 1. Error bars represent SD. (B) Senescence-associated β-galactosidase assay in p53+ and p53− HCT116 cells expressing a NS, ATR or ETV1 shRNA. Senescence-associated β-galactosidase activity was normalized to the level obtained using a NS shRNA, which was set to 1. Error bars represent SD. (C) Table showing the percentage of cells in G1, S and G2/M in p53+ and p53− HCT116 cells expressing a NS shRNA or one of two unrelated TERT shRNAs. (D) Table showing the percentage of cells in G1, S and G2/M in p53+ and p53− HCT116 cells expressing a NS shRNA or one of two unrelated ATR or ETV1 shRNAs. (E) Proliferation of p53+ and p53− HCT116 cells transfected with a control (LMNA), ATR or ETV1 siRNA and stably expressing TERT, or as a control GFP, was determined by an Alamar Blue fluorescence assay. Cell proliferation was normalized to that obtained using a LMNA siRNA, which was set to 1. Error bars represent SD.</p>", "links"=>[], "tags"=>["knockdown", "tert", "induces", "senescence", "prolongs", "preferentially"], "article_id"=>191321, "categories"=>["Molecular Biology", "Biochemistry", "Cell Biology", "Genetics"], "users"=>["Li Xie", "Claude Gazin", "Sung Mi Park", "Lihua J. Zhu", "Marie-Anne Debily", "Ellen L. W. Kittler", "Maria L. Zapp", "David Lapointe", "Stephane Gobeil", "Ching-Man Virbasius", "Michael R. Green"], "doi"=>["https://dx.doi.org/10.1371/journal.pgen.1003151.g004"], "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_RNAi_8211_mediated_knockdown_of_ATR_ETV1_or_TERT_induces_senescence_and_prolongs_G2_M_preferentially_in_p53_8722_cells_/191321", "title"=>"RNAi–mediated knockdown of ATR, ETV1, or TERT induces senescence and prolongs G2/M preferentially in p53− cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-12-20 00:22:01"}
  • {"files"=>["https://ndownloader.figshare.com/files/520947"], "description"=>"<p>(A) Immunoblot analysis showing ETV1 levels in p53+ and p53− HCT116 cells expressing a NS, ATR or ETV1 shRNA. α-tubulin (TUBA) was monitoring as a loading control. (B) qRT-PCR analysis monitoring <i>ETV1</i> expression in p53+ and p53− HCT116 cells expressing a NS, ATR or ETV1 shRNA. <i>ETV1</i> expression was normalized to that obtained with a NS shRNA, which was set to 1. Error bars represent SD. (C) Immunoblot analysis showing ETV1 levels in p53+ and p53− HCT116 cells treated with CGK733 (left; 0, 2, 3, 4 and 5 µM) or ETP46464 (right; 0, 0.5, 1, 2, 4 and 8 µM). (D) Immunoblot analysis showing TERT and ETV1 levels in p53+ and p53− RKO cells, as well as A549, NCI-H460, NCI-H522 and NCI-H1299 cells treated with CGK733 (top; 0, 2 and 4 µM) or ETP46464 (bottom; 0, 0.5, 1, 2, 4 and 8 µM).</p>", "links"=>[], "tags"=>["etv1"], "article_id"=>191437, "categories"=>["Molecular Biology", "Biochemistry", "Cell Biology", "Genetics"], "users"=>["Li Xie", "Claude Gazin", "Sung Mi Park", "Lihua J. Zhu", "Marie-Anne Debily", "Ellen L. W. Kittler", "Maria L. Zapp", "David Lapointe", "Stephane Gobeil", "Ching-Man Virbasius", "Michael R. Green"], "doi"=>["https://dx.doi.org/10.1371/journal.pgen.1003151.g005"], "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_ATR_is_required_for_ETV1_stabilization_/191437", "title"=>"ATR is required for ETV1 stabilization.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-12-20 00:23:57"}
  • {"files"=>["https://ndownloader.figshare.com/files/521068"], "description"=>"<p>(A) (Left) Schematic of the full-length ETV protein, showing the positions of the five potential ATR phosphorylation sites (SQ). (Right) Sequence surrounding each potential phosphorylation site, and the consensus ATR phosphorylation site. (B) Co-immunoprecipitation assay. Cell extract from p53+ or p53− HCT116 cells expressing FLAG-ETV1 was immunoprecipitated using an ATR antibody and the immunoprecipitate analyzed by immunoblotting for FLAG (left), or immunoprecipitated using a FLAG antibody and the immunoprecipitate analyzed by immunoblotting for ATR (right). IgG was used as a specificity control. (C) Extract from p53+ or p53− HCT116 cells expressing FLAG-ETV1 was immunoprecipitated using a FLAG antibody and the immunoprecipitate analyzed by immunoblotting using an antibody that recognizes ETV1 or a phosphorylated SQ motif (P-SQ). (D) In vitro kinase assay monitoring the ability of ATR to phosphorylate a GST-ETV1 (amino acids 1–290) fusion protein containing all five potential SQ phosphorylation sites or, as a control, GST alone. Autoradiographic images (Autorad, top) and corresponding silver-stained gels (SS, bottom) are shown. (E) In vitro kinase assay monitoring the ability of ATR to phosphorylate a series of GST-ETV1 fusion proteins, each containing 15 amino acids encompassing a potential SQ phosphorylation site (sequences shown in A) or, as a control, GST alone. Autoradiographic images (Autorad, top) and corresponding silver-stained gels (SS, bottom) are shown. The position of the <sup>32</sup>P-labeled fusion protein is indicated by the arrow.</p>", "links"=>[], "tags"=>["interacts", "phosphorylates"], "article_id"=>191556, "categories"=>["Molecular Biology", "Biochemistry", "Cell Biology", "Genetics"], "users"=>["Li Xie", "Claude Gazin", "Sung Mi Park", "Lihua J. Zhu", "Marie-Anne Debily", "Ellen L. W. Kittler", "Maria L. Zapp", "David Lapointe", "Stephane Gobeil", "Ching-Man Virbasius", "Michael R. Green"], "doi"=>["https://dx.doi.org/10.1371/journal.pgen.1003151.g006"], "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_ATR_interacts_with_and_phosphorylates_ETV1_/191556", "title"=>"ATR interacts with and phosphorylates ETV1.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-12-20 00:25:56"}
  • {"files"=>["https://ndownloader.figshare.com/files/521154"], "description"=>"<p>(A) ChIP analysis monitoring ETV1 occupancy at two regions of the <i>TERT</i> promoter, in the first intron or 3 kb upstream of the transcription start-site, in p53+ and p53− HCT116 cells treated in the presence or absence of CGK733. The locations of the primer pairs (arrows) and ETV1-binding sites (red rectangles) are shown in the schematic of the <i>TERT</i> promoter (bottom). Error bars represent SD. (B) ChIP analysis monitoring ETV1 occupancy at two regions of the <i>TERT</i> promoter in p53− HCT116 cells expressing wild type p53 (p53-WT) or a vector control (left) and in p53+ HCT116 cells expressing a dominant negative p53 mutant (p53-DD) or a vector control (right). Error bars represent SD. (C) ChIP analysis monitoring ATR occupancy at two regions of the <i>TERT</i> promoter in p53+ and p53− HCT116 cells treated in the presence or absence of CGK733. Error bars represent SD. (D) Proliferation of p53+ and p53− HCT116 cells stably expressing ETV1 or, as a control, empty vector was determined by an Alamar Blue fluorescence assay. Proliferation was normalized to that obtained using a LMNA siRNA, which was set to 1 (not shown). Error bars represent SD.</p>", "links"=>[], "tags"=>["etv1", "bound", "promoter"], "article_id"=>191639, "categories"=>["Molecular Biology", "Biochemistry", "Cell Biology", "Genetics"], "users"=>["Li Xie", "Claude Gazin", "Sung Mi Park", "Lihua J. Zhu", "Marie-Anne Debily", "Ellen L. W. Kittler", "Maria L. Zapp", "David Lapointe", "Stephane Gobeil", "Ching-Man Virbasius", "Michael R. Green"], "doi"=>["https://dx.doi.org/10.1371/journal.pgen.1003151.g007"], "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_ATR_and_ETV1_are_bound_to_the_TERT_promoter_in_p53_but_not_p53_cells_/191639", "title"=>"ATR and ETV1 are bound to the <i>TERT</i> promoter in p53− but not p53+ cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-12-20 00:27:19"}

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