Transcription Factor E2F-1 Is Upregulated in Response to DNA Damage in a Manner Analogous to That of p53

Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from...

Full description

Saved in:

Bibliographic Details
Published in	Molecular and Cellular Biology Vol. 19; no. 5; pp. 3704 - 3713
Main Authors	Blattner, Christine, Sparks, Alison, Lane, David
Format	Journal Article
Language	English
Published	United States American Society for Microbiology 01.05.1999 Taylor & Francis
Subjects	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology Antibodies - pharmacology Carrier Proteins Cell Cycle Proteins Cell Growth and Development Dactinomycin - pharmacology Dichlororibofuranosylbenzimidazole - pharmacology DNA Damage - genetics DNA-Binding Proteins E2F Transcription Factors E2F1 Transcription Factor Enzyme Inhibitors - pharmacology Fluorescent Antibody Technique Gene Expression Regulation - genetics Humans Mutation Nuclear Proteins Oligonucleotides, Antisense - genetics Oligonucleotides, Antisense - pharmacology Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins c-mdm2 Retinoblastoma-Binding Protein 1 RNA, Messenger - metabolism Transcription Factor DP1 Transcription Factors - genetics Transcription, Genetic - radiation effects Tumor Cells, Cultured Tumor Suppressor Protein p53 - genetics Up-Regulation
Online Access	Get full text
ISSN	0270-7306 1098-5549 1067-8824 1098-5549
DOI	10.1128/MCB.19.5.3704

Cover

Abstract	Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology. For an alternate route to MCB .asm.org, visit: MCB
AbstractList	The transcription factor E2F-1 directs the expression of genes that induce or regulate cell division, and a role for E2F-1 in driving cells into apoptosis is the subject of intense discussion. Recently it has been shown that E2F-1 binds and coprecipitates with the mouse double-minute chromosome 2 protein (Mdm2). A domain of E2F-1 (amino acids 390 to 406) shows striking similarity to the Mdm2 binding domain of the tumor suppressor protein p53. It is known that interaction of Mdm2 with p53 through this domain is required for Mdm2-dependent degradation of p53. We show here that E2F-1 protein is upregulated in response to DNA damage. The kinetics of induction are dependent upon the source of DNA damage, i.e., fast and transient after irradiation with X rays and delayed and stable after irradiation with UVC, and thus match the kinetics of p53 induction in response to DNA damage. We show further that E2F-1 is also upregulated by treatment with the transcription inhibitor actinomycin D and with the kinase inhibitor DRB, as well as by high concentrations of the kinase inhibitor H7, all conditions which also upregulate p53. In our experiments we were not able to see an increase in E2F-1 RNA production but did find an increase in protein stability in UVC-irradiated cells. Upregulation of E2F-1 in response to DNA damage seems to require the presence of wild-type p53, since we did not observe an increase in the level of E2F-1 protein in several cell lines which possess mutated p53. Previous experiments showed that p53 is upregulated after microinjection of an antibody which binds to a domain of Mdm2 that is required for the interaction of Mdm2 with p53. Microinjection of the same antibody also increases the expression of E2F-1 protein, while microinjection of a control antibody does not. Furthermore, microinjection of Mdm2 antisense oligonucleotides upregulates E2F-1 protein, while microinjection of an unrelated oligonucleotide does not. These data suggest that E2F-1 is upregulated in a similar way to p53 in response to DNA damage and that Mdm2 appears to play a major role in this pathway. Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology. For an alternate route to MCB .asm.org, visit: MCB The transcription factor E2F-1 directs the expression of genes that induce or regulate cell division, and a role for E2F-1 in driving cells into apoptosis is the subject of intense discussion. Recently it has been shown that E2F-1 binds and coprecipitates with the mouse double-minute chromosome 2 protein (Mdm2). A domain of E2F-1 (amino acids 390 to 406) shows striking similarity to the Mdm2 binding domain of the tumor suppressor protein p53. It is known that interaction of Mdm2 with p53 through this domain is required for Mdm2-dependent degradation of p53. We show here that E2F-1 protein is upregulated in response to DNA damage. The kinetics of induction are dependent upon the source of DNA damage, i.e., fast and transient after irradiation with X rays and delayed and stable after irradiation with UVC, and thus match the kinetics of p53 induction in response to DNA damage. We show further that E2F-1 is also upregulated by treatment with the transcription inhibitor actinomycin D and with the kinase inhibitor DRB, as well as by high concentrations of the kinase inhibitor H7, all conditions which also upregulate p53. In our experiments we were not able to see an increase in E2F-1 RNA production but did find an increase in protein stability in UVC-irradiated cells. Upregulation of E2F-1 in response to DNA damage seems to require the presence of wild-type p53, since we did not observe an increase in the level of E2F-1 protein in several cell lines which possess mutated p53. Previous experiments showed that p53 is upregulated after microinjection of an antibody which binds to a domain of Mdm2 that is required for the interaction of Mdm2 with p53. Microinjection of the same antibody also increases the expression of E2F-1 protein, while microinjection of a control antibody does not. Furthermore, microinjection of Mdm2 antisense oligonucleotides upregulates E2F-1 protein, while microinjection of an unrelated oligonucleotide does not. These data suggest that E2F-1 is upregulated in a similar way to p53 in response to DNA damage and that Mdm2 appears to play a major role in this pathway.The transcription factor E2F-1 directs the expression of genes that induce or regulate cell division, and a role for E2F-1 in driving cells into apoptosis is the subject of intense discussion. Recently it has been shown that E2F-1 binds and coprecipitates with the mouse double-minute chromosome 2 protein (Mdm2). A domain of E2F-1 (amino acids 390 to 406) shows striking similarity to the Mdm2 binding domain of the tumor suppressor protein p53. It is known that interaction of Mdm2 with p53 through this domain is required for Mdm2-dependent degradation of p53. We show here that E2F-1 protein is upregulated in response to DNA damage. The kinetics of induction are dependent upon the source of DNA damage, i.e., fast and transient after irradiation with X rays and delayed and stable after irradiation with UVC, and thus match the kinetics of p53 induction in response to DNA damage. We show further that E2F-1 is also upregulated by treatment with the transcription inhibitor actinomycin D and with the kinase inhibitor DRB, as well as by high concentrations of the kinase inhibitor H7, all conditions which also upregulate p53. In our experiments we were not able to see an increase in E2F-1 RNA production but did find an increase in protein stability in UVC-irradiated cells. Upregulation of E2F-1 in response to DNA damage seems to require the presence of wild-type p53, since we did not observe an increase in the level of E2F-1 protein in several cell lines which possess mutated p53. Previous experiments showed that p53 is upregulated after microinjection of an antibody which binds to a domain of Mdm2 that is required for the interaction of Mdm2 with p53. Microinjection of the same antibody also increases the expression of E2F-1 protein, while microinjection of a control antibody does not. Furthermore, microinjection of Mdm2 antisense oligonucleotides upregulates E2F-1 protein, while microinjection of an unrelated oligonucleotide does not. These data suggest that E2F-1 is upregulated in a similar way to p53 in response to DNA damage and that Mdm2 appears to play a major role in this pathway.
Author	David Lane Christine Blattner Alison Sparks
AuthorAffiliation	Cancer Research Campaign Cell Transformation Group, Department of Biochemistry, Medical Sciences Institute, University of Dundee, Dundee DD1 4HN, United Kingdom
AuthorAffiliation_xml	– name: Cancer Research Campaign Cell Transformation Group, Department of Biochemistry, Medical Sciences Institute, University of Dundee, Dundee DD1 4HN, United Kingdom
Author_xml	– sequence: 1 givenname: Christine surname: Blattner fullname: Blattner, Christine organization: Cancer Research Campaign Cell Transformation Group, Department of Biochemistry, Medical Sciences Institute, University of Dundee – sequence: 2 givenname: Alison surname: Sparks fullname: Sparks, Alison organization: Cancer Research Campaign Cell Transformation Group, Department of Biochemistry, Medical Sciences Institute, University of Dundee – sequence: 3 givenname: David surname: Lane fullname: Lane, David email: dplane@bad.Dundee.ac.uk organization: Cancer Research Campaign Cell Transformation Group, Department of Biochemistry, Medical Sciences Institute, University of Dundee
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/10207094$$D View this record in MEDLINE/PubMed
BookMark	eNqFkktv1DAUhS1URKeFJVtkNuwS7Nh5WGIzTDulUgsSmq6tG8fJGCV2sBNG8-9JlEp9oIqVF_d81rnn3DN0Yp3VCL2nJKY0KT7fbr7GVMRpzHLCX6EVJaKI0pSLE7QiSU6inJHsFJ2F8IsQkgnC3qBTShKSE8FXaL_zYIPyph-Ms3gLanAeXybbiOLrgO96r5uxhUFX2Fj8U4fe2aDx4PDF9zW-gA4aPU8A34K12uO1hdY1bgyzZreHAbsa9yl7i17X0Ab97v49R3fby93mW3Tz4-p6s76JFC_yISo5LTgVipdlkjLNSFWVSuQ8SyvBc604sEoUqq5Vrgtd8VJwNk2TIqlzlmnGzlG8_DvaHo4HaFvZe9OBP0pK5ByZ7FQpqZCpnCObgC8L0I9lpyul7eDhAXJg5NOJNXvZuD9y8lmkE_7pHvfu96jDIDsTlG5bsHpKQWYiE4KmxX-FNE_oVN5s6MNjQ4_sL6VNgmgRKO9C8Lr-Z8PpKJ5syJ7plRlg7nvax7QvUsVCGVs738HB-baSAxxb5-vpaJQJkr2EflzQvWn2B-O1hNA9i_0vll_WOQ
CitedBy_id	crossref_primary_10_1038_sj_onc_1205307 crossref_primary_10_1038_sj_onc_1204734 crossref_primary_10_1016_S0168_8278_01_00106_4 crossref_primary_10_1128_MCB_24_7_2968_2977_2004 crossref_primary_10_1134_S0006297912030042 crossref_primary_10_1083_jcb_200203006 crossref_primary_10_1016_j_ceb_2007_10_006 crossref_primary_10_1038_emboj_2012_17 crossref_primary_10_4161_cc_21665 crossref_primary_10_1158_2767_9764_CRC_22_0003 crossref_primary_10_1038_sj_embor_7401158 crossref_primary_10_1038_sj_emboj_7600999 crossref_primary_10_1074_jbc_M403362200 crossref_primary_10_1128_MCB_20_6_2186_2197_2000 crossref_primary_10_1128_MCB_00938_09 crossref_primary_10_1038_nrc1818 crossref_primary_10_1038_sj_onc_1205541 crossref_primary_10_1038_ncb998 crossref_primary_10_1038_sj_onc_1204055 crossref_primary_10_1242_jcs_164103 crossref_primary_10_1128_JVI_02408_08 crossref_primary_10_1046_j_1365_2184_2003_00267_x crossref_primary_10_1016_j_neulet_2017_02_038 crossref_primary_10_1242_jcs_03293 crossref_primary_10_1158_1078_0432_CCR_1183_3 crossref_primary_10_1269_jrr_08110 crossref_primary_10_1038_sj_onc_1208703 crossref_primary_10_1016_j_yexcr_2014_08_032 crossref_primary_10_1073_pnas_97_15_8501 crossref_primary_10_1016_S0304_419X_02_00051_3 crossref_primary_10_18632_oncotarget_6381 crossref_primary_10_1007_BF03402011 crossref_primary_10_1016_S0026_895X_24_12306_1 crossref_primary_10_1128_MCB_22_1_78_93_2002 crossref_primary_10_1038_onc_2011_603 crossref_primary_10_1101_gad_1221004 crossref_primary_10_1186_s12863_020_00856_0 crossref_primary_10_1016_j_bbcan_2004_09_001 crossref_primary_10_1016_S0006_8993_01_02535_5 crossref_primary_10_1038_sj_onc_1203012 crossref_primary_10_1093_carcin_bgr292 crossref_primary_10_1093_carcin_bgy128 crossref_primary_10_1021_bi0489255 crossref_primary_10_1111_j_1742_4658_2008_06627_x crossref_primary_10_1016_j_biocel_2008_12_005 crossref_primary_10_1038_embor_2012_113 crossref_primary_10_1016_S0304_3835_01_00698_X crossref_primary_10_4161_15384101_2014_985031 crossref_primary_10_1016_j_ejca_2005_08_005 crossref_primary_10_1038_onc_2013_316 crossref_primary_10_1038_sj_cdd_4401324 crossref_primary_10_1038_sj_onc_1209120 crossref_primary_10_1038_s41392_024_01800_9 crossref_primary_10_1006_excr_2000_5141 crossref_primary_10_1038_nrc1435 crossref_primary_10_1038_sj_onc_1203540 crossref_primary_10_1158_1541_7786_203_2_4 crossref_primary_10_1038_sj_onc_1204230 crossref_primary_10_1128_MCB_20_9_3224_3233_2000 crossref_primary_10_1074_jbc_C000781200 crossref_primary_10_1158_1535_7163_577_3_5 crossref_primary_10_1002_cbf_1510 crossref_primary_10_1038_sj_onc_1207516 crossref_primary_10_1158_1541_7786_MCR_08_0359 crossref_primary_10_1016_j_lungcan_2006_12_002 crossref_primary_10_1007_s11010_013_1797_1 crossref_primary_10_3109_10428194_2013_813497 crossref_primary_10_1101_cshperspect_a026138 crossref_primary_10_1080_09553000600930103 crossref_primary_10_1128_MCB_22_17_6170_6182_2002 crossref_primary_10_4161_cc_9_19_13162 crossref_primary_10_1128_MCB_25_16_7170_7180_2005 crossref_primary_10_1038_ncb0703_587 crossref_primary_10_1038_sj_onc_1206144 crossref_primary_10_1093_nar_gkaa965 crossref_primary_10_1038_35037717 crossref_primary_10_1038_sj_onc_1207649 crossref_primary_10_1016_S0003_9861_03_00054_7 crossref_primary_10_1074_jbc_M210327200 crossref_primary_10_1128_MCB_20_20_7624_7633_2000 crossref_primary_10_1073_pnas_97_7_3266 crossref_primary_10_1128_MCB_20_1_273_285_2000 crossref_primary_10_1093_carcin_bgm214 crossref_primary_10_1158_0008_5472_CAN_12_4095 crossref_primary_10_1016_j_dnarep_2004_03_034 crossref_primary_10_1038_sj_onc_1209667 crossref_primary_10_1158_0008_5472_CAN_05_0888 crossref_primary_10_1074_jbc_M107477200 crossref_primary_10_1186_s12885_019_5772_4 crossref_primary_10_1038_sj_onc_1205102 crossref_primary_10_2174_0115665232258528231018113410 crossref_primary_10_1038_sj_onc_1204702 crossref_primary_10_1016_S0378_1119_99_00487_4 crossref_primary_10_1158_0008_5472_CAN_13_3216 crossref_primary_10_1016_S1568_7864_02_00109_X crossref_primary_10_1074_jbc_M211985200 crossref_primary_10_1016_j_molmed_2006_02_002 crossref_primary_10_1002_jcb_24194 crossref_primary_10_1111_j_1582_4934_2007_00030_x crossref_primary_10_1038_s12276_023_00968_4 crossref_primary_10_1128_MCB_20_10_3616_3625_2000 crossref_primary_10_1186_1478_811X_9_15 crossref_primary_10_1074_jbc_R100063200 crossref_primary_10_1074_jbc_M110_121939 crossref_primary_10_1074_jbc_M402403200 crossref_primary_10_1038_ncb1001 crossref_primary_10_1074_jbc_M410493200 crossref_primary_10_1016_S0378_1119_99_00305_4 crossref_primary_10_1038_sj_onc_1205473 crossref_primary_10_1038_sj_onc_1208462 crossref_primary_10_1016_j_tox_2008_02_017 crossref_primary_10_1038_sj_onc_1203623 crossref_primary_10_1021_tx800288v crossref_primary_10_1128_MCB_24_14_6430_6444_2004 crossref_primary_10_1002_ijc_29685 crossref_primary_10_1074_jbc_M206336200 crossref_primary_10_4161_cc_10_8_15341 crossref_primary_10_1016_j_bbrc_2012_03_108 crossref_primary_10_1046_j_0022_202x_2001_01525_x crossref_primary_10_1038_sj_onc_1207829 crossref_primary_10_1038_sj_onc_1207709 crossref_primary_10_1126_science_288_5470_1425 crossref_primary_10_1038_ncb974 crossref_primary_10_1093_nar_gkaa431 crossref_primary_10_3390_biom5042854 crossref_primary_10_1128_MCB_23_24_8960_8969_2003 crossref_primary_10_2174_1381612825666190201120013 crossref_primary_10_1128_MCB_06286_11 crossref_primary_10_1158_1535_7163_MCT_11_0024 crossref_primary_10_1038_sj_cdd_4401536 crossref_primary_10_1073_pnas_0538044100 crossref_primary_10_1128_MCB_22_15_5308_5318_2002 crossref_primary_10_1016_j_bbcan_2013_04_002 crossref_primary_10_1016_j_semcancer_2009_10_004 crossref_primary_10_3390_biomedicines6020039 crossref_primary_10_1053_j_gastro_2004_02_014 crossref_primary_10_1016_S0014_5793_02_03270_2 crossref_primary_10_1158_0008_5472_CAN_11_2196 crossref_primary_10_1073_pnas_081061398 crossref_primary_10_1038_sj_onc_1203593 crossref_primary_10_1038_sj_neo_7900073 crossref_primary_10_1074_jbc_M710296200 crossref_primary_10_1038_nrc2718 crossref_primary_10_18632_oncotarget_19413 crossref_primary_10_4161_cc_11_6_19558 crossref_primary_10_1016_S1097_2765_03_00344_7 crossref_primary_10_1016_S1471_4914_02_02309_2 crossref_primary_10_1038_sj_onc_1205371 crossref_primary_10_1016_j_dnarep_2009_03_003
Cites_doi	10.1038/387299a0 10.1038/sj.onc.1201459 10.1074/jbc.270.41.23922 10.1002/j.1460-2075.1993.tb05678.x 10.1016/S0960-9822(06)00374-5 10.1016/0092-8674(95)90385-2 10.1016/0092-8674(93)90496-D 10.1242/jcs.96.1.121 10.1242/jcs.101.1.183 10.1073/pnas.89.16.7491 10.1038/387296a0 10.1016/S0092-8674(00)80521-8 10.1016/S0959-437X(98)80058-0 10.1074/jbc.272.7.4252 10.1016/S0092-8674(00)81255-6 10.1016/S0014-5793(97)01480-4 10.1083/jcb.106.3.761 10.1016/0092-8674(93)90384-3 10.1128/MCB.15.8.4215 10.1073/pnas.95.1.195 10.1128/jvi.69.4.2491-2500.1995 10.1016/S0092-8674(00)81254-4 10.1128/MCB.4.9.1689 10.1038/sj.onc.1202282 10.1038/sj.onc.1202480 10.1128/MCB.13.10.6501 10.1016/S1097-2765(00)80140-9 10.1038/365349a0 10.1016/0092-8674(92)90593-2 10.1038/sj.onc.1201018 10.1016/0092-8674(95)90412-3 10.1101/gad.7.7a.1126 10.1007/BF03401691 10.1016/0092-8674(93)90499-G 10.1038/sj.onc.1201915 10.1038/ng0498-360 10.1128/MCB.13.7.4107 10.1093/emboj/17.2.554 10.1093/nar/21.22.4998 10.1016/S0955-0674(96)80081-0 10.1101/gad.10.23.2949 10.1002/j.1460-2075.1994.tb06807.x 10.1128/MCB.18.12.7288 10.1038/342705a0 10.1126/science.274.5293.1672 10.1073/pnas.94.6.2221 10.1038/375691a0 10.1093/jnci/86.17.1297 10.1093/nar/13.5.1431 10.1101/gad.10.23.2960 10.1073/pnas.90.15.6914
ContentType	Journal Article
Copyright	Copyright © 1999, American Society for Microbiology 1999
Copyright_xml	– notice: Copyright © 1999, American Society for Microbiology 1999
DBID	AAYXX CITATION CGR CUY CVF ECM EIF NPM 7TM 7TO H94 7X8 5PM ADTOC UNPAY
DOI	10.1128/MCB.19.5.3704
DatabaseName	CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Nucleic Acids Abstracts Oncogenes and Growth Factors Abstracts AIDS and Cancer Research Abstracts MEDLINE - Academic PubMed Central (Full Participant titles) Unpaywall for CDI: Periodical Content Unpaywall
DatabaseTitle	CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Oncogenes and Growth Factors Abstracts AIDS and Cancer Research Abstracts Nucleic Acids Abstracts MEDLINE - Academic
DatabaseTitleList	MEDLINE Oncogenes and Growth Factors Abstracts MEDLINE - Academic
Database_xml	– sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database – sequence: 3 dbid: UNPAY name: Unpaywall url: https://proxy.k.utb.cz/login?url=https://unpaywall.org/ sourceTypes: Open Access Repository
DeliveryMethod	fulltext_linktorsrc
Discipline	Chemistry Biology
EISSN	1098-5549
EndPage	3713
ExternalDocumentID	oai:pubmedcentral.nih.gov:84185 PMC84185 10207094 10_1128_MCB_19_5_3704 12287959 mcb_19_5_3704
Genre	Research Article Research Support, Non-U.S. Gov't Journal Article
GroupedDBID	--- -DZ -~X .55 .GJ 0R~ 123 18M 29M 2WC 39C 3O- 4.4 53G 5RE 5VS 9M8 AAGFI ABJNI ACGFO ACKIV ACNCT ADBBV ADIYS ADXHL AENEX AEOZL AFFNX AGHSJ ALMA_UNASSIGNED_HOLDINGS AOIJS AQTUD BAWUL BTFSW C1A CS3 DIK DU5 E3Z EBS EJD F5P GX1 H13 HH5 HYE HZ~ IH2 KQ8 L7B M4Z MVM N9A O9- OK1 P2P RHI RNS RPM TASJS TDBHL TFL TFW TR2 UDS W8F WH7 WOQ X7M Y6R YYP ZCA ZGI ZXP AAYXX CITATION ABRLO ABTAH AGVNZ CGR CUY CVF ECM EIF EMOBN NPM PKN RHF RSF UCJ VQA WHG YIN ZY4 7TM 7TO H94 7X8 5PM ADTOC UNPAY
ID	FETCH-LOGICAL-c487t-b418419c4bb253e30ddbc97465d947ec4a3d98cffc7e8ed4b943746282f736e33
IEDL.DBID	UNPAY
ISSN	0270-7306 1098-5549 1067-8824
IngestDate	Sun Oct 26 03:10:34 EDT 2025 Thu Aug 21 17:34:22 EDT 2025 Thu Oct 02 12:00:35 EDT 2025 Wed Aug 20 00:25:48 EDT 2025 Wed Feb 19 02:32:28 EST 2025 Thu Apr 24 23:05:48 EDT 2025 Wed Oct 01 02:23:16 EDT 2025 Mon Oct 20 23:47:09 EDT 2025 Wed May 18 15:28:01 EDT 2016
IsDoiOpenAccess	false
IsOpenAccess	true
IsPeerReviewed	true
IsScholarly	true
Issue	5
Language	English
LinkModel	DirectLink
MergedId	FETCHMERGED-LOGICAL-c487t-b418419c4bb253e30ddbc97465d947ec4a3d98cffc7e8ed4b943746282f736e33
Notes	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 Corresponding author. Mailing address: Cancer Research Campaign Cell Transformation Group, Department of Biochemistry, Medical Sciences Institute, University of Dundee, Dundee DD1 4HN, United Kingdom. Phone: 44-1382-344920. Fax: 44-1382-224117. E-mail: dplane@bad.Dundee.ac.uk.
OpenAccessLink	https://proxy.k.utb.cz/login?url=https://www.ncbi.nlm.nih.gov/pmc/articles/84185
PMID	10207094
PQID	17211094
PQPubID	23462
PageCount	10
ParticipantIDs	informaworld_taylorfrancis_310_1128_MCB_19_5_3704 highwire_asm_mcb_19_5_3704 unpaywall_primary_10_1128_mcb_19_5_3704 proquest_miscellaneous_69699158 pubmedcentral_primary_oai_pubmedcentral_nih_gov_84185 crossref_primary_10_1128_MCB_19_5_3704 proquest_miscellaneous_17211094 pubmed_primary_10207094 crossref_citationtrail_10_1128_MCB_19_5_3704
ProviderPackageCode	CITATION AAYXX
PublicationCentury	1900
PublicationDate	1999-05-01
PublicationDateYYYYMMDD	1999-05-01
PublicationDate_xml	– month: 05 year: 1999 text: 1999-05-01 day: 01
PublicationDecade	1990
PublicationPlace	United States
PublicationPlace_xml	– name: United States
PublicationTitle	Molecular and Cellular Biology
PublicationTitleAlternate	Mol Cell Biol
PublicationYear	1999
Publisher	American Society for Microbiology Taylor & Francis
Publisher_xml	– name: American Society for Microbiology – name: Taylor & Francis
References	B20 B21 B22 Hunt K. K. (B31) 1997; 57 B23 B24 B25 B26 B27 B28 B29 Kowalik T. F. (B34) 1998; 9 Bartek J. (B3) 1992; 7 Huang Y. Y. (B30) 1997; 57 Eldeiry W. S. (B12) 1994; 54 B32 B33 B35 B36 B37 B38 B6a B1 B2 B4 B5 B6 B7 B8 B9 B40 Maki C. G. (B39) 1996; 56 B41 B42 B43 B44 B45 B47 B48 B49 B50 B52 B53 B10 B54 B11 B55 B56 B13 B57 B14 B58 B15 B59 B16 B17 B18 B19 B4a Nip J. (B46) 1997; 90 Shan B. (B51) 1994; 14
References_xml	– ident: B36 doi: 10.1038/387299a0 – ident: B43 doi: 10.1038/sj.onc.1201459 – ident: B59 doi: 10.1074/jbc.270.41.23922 – ident: B1 doi: 10.1002/j.1460-2075.1993.tb05678.x – ident: B6 doi: 10.1016/S0960-9822(06)00374-5 – ident: B54 doi: 10.1016/0092-8674(95)90385-2 – ident: B38 doi: 10.1016/0092-8674(93)90496-D – volume: 57 start-page: 4722 year: 1997 ident: B31 publication-title: Cancer Res. – ident: B53 doi: 10.1242/jcs.96.1.121 – ident: B42 doi: 10.1242/jcs.101.1.183 – ident: B37 doi: 10.1073/pnas.89.16.7491 – ident: B23 doi: 10.1038/387296a0 – ident: B19 doi: 10.1016/S0092-8674(00)80521-8 – ident: B24 doi: 10.1016/S0959-437X(98)80058-0 – ident: B48 doi: 10.1074/jbc.272.7.4252 – ident: B13 doi: 10.1016/S0092-8674(00)81255-6 – ident: B29 doi: 10.1016/S0014-5793(97)01480-4 – ident: B7 doi: 10.1083/jcb.106.3.761 – ident: B6a – ident: B50 doi: 10.1016/0092-8674(93)90384-3 – ident: B11 doi: 10.1128/MCB.15.8.4215 – ident: B10 doi: 10.1073/pnas.95.1.195 – ident: B35 doi: 10.1128/jvi.69.4.2491-2500.1995 – ident: B58 doi: 10.1016/S0092-8674(00)81254-4 – volume: 14 start-page: 8166 year: 1994 ident: B51 publication-title: Mol. Cell. Biol. – ident: B40 doi: 10.1128/MCB.4.9.1689 – ident: B26 doi: 10.1038/sj.onc.1202282 – volume: 57 start-page: 3640 year: 1997 ident: B30 publication-title: Cancer Res. – ident: B4 doi: 10.1038/sj.onc.1202480 – ident: B4a – ident: B25 doi: 10.1128/MCB.13.10.6501 – volume: 56 start-page: 2649 year: 1996 ident: B39 publication-title: Cancer Res. – ident: B18 doi: 10.1016/S1097-2765(00)80140-9 – ident: B32 doi: 10.1038/365349a0 – ident: B33 doi: 10.1016/0092-8674(92)90593-2 – ident: B5 doi: 10.1038/sj.onc.1201018 – ident: B44 doi: 10.1016/0092-8674(95)90412-3 – ident: B56 doi: 10.1101/gad.7.7a.1126 – ident: B55 doi: 10.1007/BF03401691 – volume: 54 start-page: 1169 year: 1994 ident: B12 publication-title: Cancer Res. – ident: B21 doi: 10.1016/0092-8674(93)90499-G – ident: B28 doi: 10.1038/sj.onc.1201915 – ident: B57 doi: 10.1038/ng0498-360 – ident: B9 doi: 10.1128/MCB.13.7.4107 – volume: 90 start-page: 205 year: 1997 ident: B46 publication-title: Blood – ident: B49 doi: 10.1093/emboj/17.2.554 – ident: B20 doi: 10.1093/nar/21.22.4998 – ident: B2 doi: 10.1016/S0955-0674(96)80081-0 – volume: 7 start-page: 101 year: 1992 ident: B3 publication-title: Oncogene – ident: B27 doi: 10.1101/gad.10.23.2949 – ident: B47 doi: 10.1002/j.1460-2075.1994.tb06807.x – ident: B17 doi: 10.1128/MCB.18.12.7288 – ident: B45 doi: 10.1038/342705a0 – ident: B52 doi: 10.1126/science.274.5293.1672 – ident: B8 doi: 10.1073/pnas.94.6.2221 – ident: B41 doi: 10.1038/375691a0 – ident: B15 doi: 10.1093/jnci/86.17.1297 – ident: B16 doi: 10.1093/nar/13.5.1431 – ident: B22 doi: 10.1101/gad.10.23.2960 – volume: 9 start-page: 113 year: 1998 ident: B34 publication-title: Cell Growth Differ. – ident: B14 doi: 10.1073/pnas.90.15.6914
SSID	ssj0006903
Score	2.062462
Snippet	Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... The transcription factor E2F-1 directs the expression of genes that induce or regulate cell division, and a role for E2F-1 in driving cells into apoptosis is...
SourceID	unpaywall pubmedcentral proquest pubmed crossref informaworld highwire
SourceType	Open Access Repository Aggregation Database Index Database Enrichment Source Publisher
StartPage	3704
SubjectTerms	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology Antibodies - pharmacology Carrier Proteins Cell Cycle Proteins Cell Growth and Development Dactinomycin - pharmacology Dichlororibofuranosylbenzimidazole - pharmacology DNA Damage - genetics DNA-Binding Proteins E2F Transcription Factors E2F1 Transcription Factor Enzyme Inhibitors - pharmacology Fluorescent Antibody Technique Gene Expression Regulation - genetics Humans Mutation Nuclear Proteins Oligonucleotides, Antisense - genetics Oligonucleotides, Antisense - pharmacology Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins c-mdm2 Retinoblastoma-Binding Protein 1 RNA, Messenger - metabolism Transcription Factor DP1 Transcription Factors - genetics Transcription, Genetic - radiation effects Tumor Cells, Cultured Tumor Suppressor Protein p53 - genetics Up-Regulation
Title	Transcription Factor E2F-1 Is Upregulated in Response to DNA Damage in a Manner Analogous to That of p53
URI	http://mcb.asm.org/content/19/5/3704.abstract https://www.tandfonline.com/doi/abs/10.1128/MCB.19.5.3704 https://www.ncbi.nlm.nih.gov/pubmed/10207094 https://www.proquest.com/docview/17211094 https://www.proquest.com/docview/69699158 https://pubmed.ncbi.nlm.nih.gov/PMC84185 https://www.ncbi.nlm.nih.gov/pmc/articles/84185
UnpaywallVersion	submittedVersion
Volume	19
hasFullText	1
inHoldings	1
isFullTextHit
isPrint
journalDatabaseRights	– providerCode: PRVFSB databaseName: Free Full-Text Journals in Chemistry customDbUrl: eissn: 1098-5549 dateEnd: 20250428 omitProxy: true ssIdentifier: ssj0006903 issn: 1098-5549 databaseCode: HH5 dateStart: 19810101 isFulltext: true titleUrlDefault: http://abc-chemistry.org/ providerName: ABC ChemistRy – providerCode: PRVAFT databaseName: Open Access Digital Library customDbUrl: eissn: 1098-5549 dateEnd: 99991231 omitProxy: true ssIdentifier: ssj0006903 issn: 1098-5549 databaseCode: KQ8 dateStart: 19890101 isFulltext: true titleUrlDefault: http://grweb.coalliance.org/oadl/oadl.html providerName: Colorado Alliance of Research Libraries – providerCode: PRVAFT databaseName: Open Access Digital Library customDbUrl: eissn: 1098-5549 dateEnd: 99991231 omitProxy: true ssIdentifier: ssj0006903 issn: 1098-5549 databaseCode: KQ8 dateStart: 19810101 isFulltext: true titleUrlDefault: http://grweb.coalliance.org/oadl/oadl.html providerName: Colorado Alliance of Research Libraries – providerCode: PRVBFR databaseName: Free Medical Journals customDbUrl: eissn: 1098-5549 dateEnd: 20250428 omitProxy: true ssIdentifier: ssj0006903 issn: 1098-5549 databaseCode: DIK dateStart: 19810101 isFulltext: true titleUrlDefault: http://www.freemedicaljournals.com providerName: Flying Publisher – providerCode: PRVFQY databaseName: GFMER Free Medical Journals customDbUrl: eissn: 1098-5549 dateEnd: 20250428 omitProxy: true ssIdentifier: ssj0006903 issn: 1098-5549 databaseCode: GX1 dateStart: 19810101 isFulltext: true titleUrlDefault: http://www.gfmer.ch/Medical_journals/Free_medical.php providerName: Geneva Foundation for Medical Education and Research – providerCode: PRVAQN databaseName: Consulter via PubMed Central customDbUrl: eissn: 1098-5549 dateEnd: 99991231 omitProxy: true ssIdentifier: ssj0006903 issn: 1098-5549 databaseCode: RPM dateStart: 19810101 isFulltext: true titleUrlDefault: https://www.ncbi.nlm.nih.gov/pmc/ providerName: National Library of Medicine
link	http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1db9MwFL3aOqHxwsdg0AHDDwheSNrETuw8lm7VAK0aaJXGk2U7Dq1okqpNhcavx46bqt0YgmfffDg-9r3XuT4H4I3JGAQR0kRuONGe8dDCM7Mo9RiTJE5NgI6F_aN7PozPRuTTVXS1A53mLExdtK_kxC-muV9MxnVt5SxXnaZOrMMs3cou7MWRCb5bsDcaXvS-1TsptGueWKtpWl408zgnaWsZM43TTBqGzZB1ciX9IPEjH9OVQtvaIzUswTeoS_8UgN6uo9xfFjNx_VNMpxtOavAQLpruudqUH_6ykr76dYP58T_6_wgerAJW1HMNj2FHFwdwz0lYXh_Afr9RjHsC49rxNcsQGtRSPug0HHgB-rhAo9ncCd_rFE0K9NVV52pUlehk2EMnIjdrm20RyEo36zmyjCnl93K5sDaXY1GhMkOzCD-F0eD0sn_mrZQcPGUSosqT5p1JkCgiZRhhjbtpKpXJZOIoTQjVigicJkxlmaKa6ZTIhGBqT82GGcWxxvgQWkVZ6OeAmGBEhCEVWMREEyqEzkRXK0q1oBinbXjfjCZXK5pzq7Yx5XW6EzJ-3v_Ag4RH3A5-G96uzWeO3-Muw6MGGlwscm4gtNkYbIKFV_VuS-akUTi-44avG0RxM072P40otPmk3GXlyV8s4iQ2cX3E2vDMIXDj3UOziNtroy1srg0snfh2i0FZTSteA6sN79YYvvVBtvp89M-WL-C-I7uwZaIvoVXNl_qVCeUqeQy7n7-w49Uk_g2b2UZO
linkProvider	Unpaywall
linkToUnpaywall	http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1bb9MwFLZGJzReuAwGHTc_IHghaRM7sf1YulUDadWEVmk8Wbbj0IrmojYVGr8eO66rdmMInn1ycfzZ5xzn-PsAeGcyBoGFNJEbYjowHloEZhZlAaUSp5kJ0JGwf3TPx-nZBH-5Sq72QM-fhWmL9pWcheW8CMvZtK2trAvV83ViPWrpVu6B_TQxwXcH7E_GF4Nv7U4K6ZsntmqalhfNPM5J2lrGTOM0mWfYjGmvUDKMWJiEiKwV2jYeybME36Au_VMAeruO8mBV1uL6p5jPt5zU6BG48N1ztSk_wlUjQ_XrBvPjf_T_MXi4DljhwDU8AXu6PAT3nYTl9SE4GHrFuKdg2jo-vwzBUSvlA0_jURDBz0s4qRdO-F5ncFbCr646V8OmgifjATwRhVnbbIuAVrpZL6BlTKm-V6ultbmcigZWOawT9AxMRqeXw7NgreQQKJMQNYE074wjprCUcYI06meZVCaTSZOMYaIVFihjVOW5IprqDEuGEbGnZuOcoFQjdAQ6ZVXqFwBSQbGIYyKQSLHGRAidi75WhGhBEMq64KMfTa7WNOdWbWPO23Qnpvx8-IlHjCfcDn4XvN-Y147f4y7DYw8NLpYFNxDaboy2wcKbdrcld9IoHN1xw7ceUdyMk_1PI0ptPil3WTn7i0XKUhPXJ7QLnjsEbr17bBZxe22yg82NgaUT320xKGtpxVtgdcGHDYZvfZCdPh__s-VL8MCRXdgy0Veg0yxW-rUJ5Rr5Zj19fwP7okVZ
openUrl	ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Transcription+Factor+E2F-1+Is+Upregulated+in+Response+to+DNA+Damage+in+a+Manner+Analogous+to+That+of+p53&rft.jtitle=Molecular+and+cellular+biology&rft.au=Blattner%2C+Christine&rft.au=Sparks%2C+Alison&rft.au=Lane%2C+David&rft.date=1999-05-01&rft.pub=American+Society+for+Microbiology&rft.issn=0270-7306&rft.eissn=1098-5549&rft.volume=19&rft.issue=5&rft.spage=3704&rft.epage=3713&rft_id=info:doi/10.1128%2FMCB.19.5.3704&rft_id=info%3Apmid%2F10207094&rft.externalDocID=PMC84185
thumbnail_l	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0270-7306&client=summon
thumbnail_m	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0270-7306&client=summon
thumbnail_s	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0270-7306&client=summon