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Adenovirus small e1a alters global patterns of histone modification (2008)

G. A. Horwitz ; K. Zhang ; M. A. McBrian ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 321(5892): 1084-5. doi: 10.1126/science.1155544.

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Publication Date: 2008-08-23

Description: Adenovirus small early region 1a (e1a) protein drives cells into S phase by binding RB family proteins and the closely related histone acetyl transferases p300 and CBP. The interaction with RB proteins displaces them from DNA-bound E2F transcription factors, reversing their repression of cell cycle genes. However, it has been unclear how the e1a interaction with p300 and CBP promotes passage through the cell cycle. We show that this interaction causes a threefold reduction in total cellular histone H3 lysine 18 acetylation (H3K18ac). CBP and p300 are required for acetylation at this site because their knockdown causes specific hypoacetylation at H3K18. SV40 T antigen also induces H3K18 hypoacetylation. Because global hypoacetylation at this site is observed in prostate carcinomas with poor prognosis, this suggests that processes resulting in global H3K18 hypoacetylation may be linked to oncogenic transformation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756290/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756290/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horwitz, Gregory A -- Zhang, Kangling -- McBrian, Matthew A -- Grunstein, Michael -- Kurdistani, Siavash K -- Berk, Arnold J -- CA25235/CA/NCI NIH HHS/ -- R37 CA025235/CA/NCI NIH HHS/ -- R37 CA025235-30/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Aug 22;321(5892):1084-5. doi: 10.1126/science.1155544.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18719283" target="_blank"〉PubMed〈/a〉

Keywords: Acetylation ; Adenovirus E1A Proteins/genetics/*metabolism ; Adenoviruses, Human/*metabolism ; Antigens, Polyomavirus Transforming/metabolism ; CREB-Binding Protein/metabolism ; *Cell Cycle ; Cell Line ; Cell Transformation, Viral ; Cells, Cultured ; HeLa Cells ; Histones/*metabolism ; Humans ; Lysine/metabolism ; Mutation ; p300-CBP Transcription Factors/metabolism

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics

Published by American Association for the Advancement of Science (AAAS)

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Epigenetic reprogramming by adenovirus e1a (2008)

R. Ferrari ; M. Pellegrini ; G. A. Horwitz ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 321(5892): 1086-8. doi: 10.1126/science.1155546.

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Publication Date: 2008-08-23

Description: Adenovirus e1a induces quiescent human cells to replicate. We found that e1a causes global relocalization of the RB (retinoblastoma) proteins (RB, p130, and p107) and p300/CBP histone acetyltransferases on promoters, the effect of which is to restrict the acetylation of histone 3 lysine-18 (H3K18ac) to a limited set of genes, thereby stimulating cell cycling and inhibiting antiviral responses and cellular differentiation. Soon after expression, e1a binds transiently to promoters of cell cycle and growth genes, causing enrichment of p300/CBP, PCAF (p300/CBP-associated factor), and H3K18ac; depletion of RB proteins; and transcriptional activation. e1a also associates transiently with promoters of antiviral genes, causing enrichment for RB, p130, and H4K16ac; increased nucleosome density; and transcriptional repression. At later times, e1a and p107 bind mainly to promoters of development and differentiation genes, repressing transcription. The temporal order of e1a binding requires its interactions with p300/CBP and RB proteins. Our data uncover a defined epigenetic reprogramming leading to cellular transformation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2693122/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2693122/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferrari, Roberto -- Pellegrini, Matteo -- Horwitz, Gregory A -- Xie, Wei -- Berk, Arnold J -- Kurdistani, Siavash K -- CA25235/CA/NCI NIH HHS/ -- R37 CA025235/CA/NCI NIH HHS/ -- R37 CA025235-30/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Aug 22;321(5892):1086-8. doi: 10.1126/science.1155546.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18719284" target="_blank"〉PubMed〈/a〉

Keywords: Adenovirus E1A Proteins/genetics/*metabolism ; Adenoviruses, Human/genetics/*metabolism ; CREB-Binding Protein/metabolism ; Cell Transformation, Viral ; Crk-Associated Substrate Protein/genetics/metabolism ; *Epigenesis, Genetic ; Gene Expression Profiling ; Gene Expression Regulation ; Histones/metabolism ; Humans ; Mutation ; Promoter Regions, Genetic ; Protein Binding ; RNA, Messenger/genetics/metabolism ; Retinoblastoma Protein/genetics/metabolism ; Retinoblastoma-Like Protein p107/genetics/metabolism ; Transcription, Genetic ; p300-CBP Transcription Factors/metabolism

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics

Published by American Association for the Advancement of Science (AAAS)

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Transcription control by E1A and MAP kinase pathway via Sur2 mediator subunit (2002)

J. L. Stevens ; G. T. Cantin ; G. Wang ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 296(5568): 755-8. doi: 10.1126/science.1068943.

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Publication Date: 2002-04-06

Description: Sur2 is a metazoan Mediator subunit that interacts with the adenovirus E1A protein and functions in a mitogen-activated protein kinase pathway required for vulva development in Caenorhabditis elegans. We generated sur2-/- embryonic stem cells to analyze its function as a mammalian Mediator component. Our results show that Sur2 forms a subcomplex of the Mediator with two other subunits, TRAP/Med100 and 95. Knock-out of Sur2 prevents activation by E1A-CR3 and the mitogen-activated protein kinase-regulated ETS transcription factor Elk-1, but not by multiple other transcription factors. These results imply that specific activation domains stimulate transcription by binding to distinct Mediator subunits. Activation by E1A and Elk-1 requires recruitment of Mediator to a promoter by binding to its Sur2 subunit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stevens, Jennitte L -- Cantin, Greg T -- Wang, Gang -- Shevchenko, Andrej -- Shevchenko, Anna -- Berk, Arnold J -- CA25235/CA/NCI NIH HHS/ -- GM07185/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Apr 26;296(5568):755-8. Epub 2002 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Institute, University of California, Los Angeles, 611 Charles Young Drive East, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11934987" target="_blank"〉PubMed〈/a〉

Keywords: Adenovirus E1A Proteins/*metabolism ; Adenoviruses, Human/physiology ; Animals ; Carrier Proteins/genetics/*metabolism ; Cells, Cultured ; *DNA-Binding Proteins ; Genes, Immediate-Early ; HeLa Cells ; Humans ; *MAP Kinase Signaling System ; Mediator Complex ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/metabolism ; Stem Cells/*metabolism ; *Trans-Activators ; Transcription Factors/metabolism ; *Transcription, Genetic ; *Transcriptional Activation ; Transfection ; ets-Domain Protein Elk-1

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Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics

Published by American Association for the Advancement of Science (AAAS)

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Mismatch repair deficiency in phenotypically normal human cells (1995)

R. Parsons ; G. M. Li ; M. Longley ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 268(5211): 738-40.

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Publication Date: 1995-05-05

Description: Tumor cells in patients with hereditary nonpolyposis colorectal cancer (HNPCC) are characterized by a genetic hypermutability caused by defects in DNA mismatch repair. A subset of HNPCC patients was found to have widespread mutations not only in their tumors, but also in their non-neoplastic cells. Although these patients had numerous mutations in all tissues examined, they had very few tumors. The hypermutability was associated with a profound defect in mismatch repair at the biochemical level. These results have implications for the relation between mutagenesis and carcinogenesis, and they suggest that mismatch repair deficiency is compatible with normal human development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parsons, R -- Li, G M -- Longley, M -- Modrich, P -- Liu, B -- Berk, T -- Hamilton, S R -- Kinzler, K W -- Vogelstein, B -- CA35494/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- GM45190/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 May 5;268(5211):738-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins Oncology Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7632227" target="_blank"〉PubMed〈/a〉

Keywords: Base Sequence ; Cell Line, Transformed ; Clone Cells ; Colorectal Neoplasms, Hereditary Nonpolyposis/*genetics ; DNA Repair/*genetics ; DNA, Satellite/analysis ; Humans ; Intestinal Mucosa/chemistry ; Lymphocytes/chemistry ; Molecular Sequence Data ; Mutation ; Phenotype ; Repetitive Sequences, Nucleic Acid

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics

Published by American Association for the Advancement of Science (AAAS)

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