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  • 1
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    Tet-mediated formation of 5-carboxylcytosine and its excision by TDG in mammalian DNA (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-06
    Description: The prevalent DNA modification in higher organisms is the methylation of cytosine to 5-methylcytosine (5mC), which is partially converted to 5-hydroxymethylcytosine (5hmC) by the Tet (ten eleven translocation) family of dioxygenases. Despite their importance in epigenetic regulation, it is unclear how these cytosine modifications are reversed. Here, we demonstrate that 5mC and 5hmC in DNA are oxidized to 5-carboxylcytosine (5caC) by Tet dioxygenases in vitro and in cultured cells. 5caC is specifically recognized and excised by thymine-DNA glycosylase (TDG). Depletion of TDG in mouse embyronic stem cells leads to accumulation of 5caC to a readily detectable level. These data suggest that oxidation of 5mC by Tet proteins followed by TDG-mediated base excision of 5caC constitutes a pathway for active DNA demethylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3462231/" 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/PMC3462231/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Yu-Fei -- Li, Bin-Zhong -- Li, Zheng -- Liu, Peng -- Wang, Yang -- Tang, Qingyu -- Ding, Jianping -- Jia, Yingying -- Chen, Zhangcheng -- Li, Lin -- Sun, Yan -- Li, Xiuxue -- Dai, Qing -- Song, Chun-Xiao -- Zhang, Kangling -- He, Chuan -- Xu, Guo-Liang -- 1S10RR027643-01/RR/NCRR NIH HHS/ -- GM071440/GM/NIGMS NIH HHS/ -- R01 GM071440/GM/NIGMS NIH HHS/ -- S10 RR027643/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1303-7. doi: 10.1126/science.1210944. Epub 2011 Aug 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Group of DNA Metabolism, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai 200031, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21817016" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/metabolism ; Animals ; Cell Line ; Cytosine/*analogs & derivatives/metabolism ; DNA/*metabolism ; DNA Methylation ; DNA-Binding Proteins/genetics/*metabolism ; Embryonic Stem Cells ; HEK293 Cells ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Mice ; Oxidation-Reduction ; Proto-Oncogene Proteins/genetics/*metabolism ; RNA, Small Interfering ; Thymine DNA Glycosylase/genetics/*metabolism ; Transfection
    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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  • 2
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    Glioma-derived mutations in IDH1 dominantly inhibit IDH1 catalytic activity and induce HIF-1alpha (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-11
    Description: Heterozygous mutations in the gene encoding isocitrate dehydrogenase-1 (IDH1) occur in certain human brain tumors, but their mechanistic role in tumor development is unknown. We have shown that tumor-derived IDH1 mutations impair the enzyme's affinity for its substrate and dominantly inhibit wild-type IDH1 activity through the formation of catalytically inactive heterodimers. Forced expression of mutant IDH1 in cultured cells reduces formation of the enzyme product, alpha-ketoglutarate (alpha-KG), and increases the levels of hypoxia-inducible factor subunit HIF-1alpha, a transcription factor that facilitates tumor growth when oxygen is low and whose stability is regulated by alpha-KG. The rise in HIF-1alpha levels was reversible by an alpha-KG derivative. HIF-1alpha levels were higher in human gliomas harboring an IDH1 mutation than in tumors without a mutation. Thus, IDH1 appears to function as a tumor suppressor that, when mutationally inactivated, contributes to tumorigenesis in part through induction of the HIF-1 pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251015/" 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/PMC3251015/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Shimin -- Lin, Yan -- Xu, Wei -- Jiang, Wenqing -- Zha, Zhengyu -- Wang, Pu -- Yu, Wei -- Li, Zhiqiang -- Gong, Lingling -- Peng, Yingjie -- Ding, Jianping -- Lei, Qunying -- Guan, Kun-Liang -- Xiong, Yue -- R01 CA068377/CA/NCI NIH HHS/ -- R01 CA068377-14/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 10;324(5924):261-5. doi: 10.1126/science.1170944.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cell Biology Laboratory, Institute of Biomedical Sciences, Fudan University, 130 Dong-An Road, Shanghai 200032, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19359588" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Astrocytoma/genetics/metabolism ; Biocatalysis ; Brain Neoplasms/*genetics/metabolism ; Cell Line ; Child ; Female ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Glioblastoma/genetics/metabolism ; Glioma/*genetics/metabolism ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & ; inhibitors/genetics/*metabolism ; Isocitrate Dehydrogenase/chemistry/*genetics/*metabolism ; Ketoglutaric Acids/metabolism ; Male ; Middle Aged ; Mutant Proteins/chemistry/metabolism ; Oligodendroglioma/genetics/metabolism ; Oxalates/pharmacology ; Protein Multimerization
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Recurrent hemizygous deletions in cancers may optimize proliferative potential (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-26
    Description: Tumors exhibit numerous recurrent hemizygous focal deletions that contain no known tumor suppressors and are poorly understood. To investigate whether these regions contribute to tumorigenesis, we searched genetically for genes with cancer-relevant properties within these hemizygous deletions. We identified STOP and GO genes, which negatively and positively regulate proliferation, respectively. STOP genes include many known tumor suppressors, whereas GO genes are enriched for essential genes. Analysis of their chromosomal distribution revealed that recurring deletions preferentially overrepresent STOP genes and underrepresent GO genes. We propose a hypothesis called the cancer gene island model, whereby gene islands encompassing high densities of STOP genes and low densities of GO genes are hemizygously deleted to maximize proliferative fitness through cumulative haploinsufficiencies. Because hundreds to thousands of genes are hemizygously deleted per tumor, this mechanism may help to drive tumorigenesis across many cancer types.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4027969/" 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/PMC4027969/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Solimini, Nicole L -- Xu, Qikai -- Mermel, Craig H -- Liang, Anthony C -- Schlabach, Michael R -- Luo, Ji -- Burrows, Anna E -- Anselmo, Anthony N -- Bredemeyer, Andrea L -- Li, Mamie Z -- Beroukhim, Rameen -- Meyerson, Matthew -- Elledge, Stephen J -- T32 GM007753/GM/NIGMS NIH HHS/ -- T32GM07753/GM/NIGMS NIH HHS/ -- U54CA143798/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jul 6;337(6090):104-9. doi: 10.1126/science.1219580. Epub 2012 May 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard University Medical School, and Division of Genetics, Howard Hughes Medical Institute, Brigham and Women's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22628553" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; *Cell Transformation, Neoplastic ; Chromosome Mapping ; Genes, Essential ; *Genes, Neoplasm ; Genes, Recessive ; Genes, Tumor Suppressor ; *Haploinsufficiency ; Hemizygote ; Humans ; Models, Genetic ; Neoplasms/*genetics/*pathology ; Oncogenes ; *Sequence Deletion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    RAG mutations in human B cell-negative SCID (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-04
    Description: Patients with human severe combined immunodeficiency (SCID) can be divided into those with B lymphocytes (B+ SCID) and those without (B- SCID). Although several genetic causes are known for B+ SCID, the etiology of B- SCID has not been defined. Six of 14 B- SCID patients tested were found to carry a mutation of the recombinase activating gene 1 (RAG-1), RAG-2, or both. This mutation resulted in a functional inability to form antigen receptors through genetic recombination and links a defect in one of the site-specific recombination systems to a human disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwarz, K -- Gauss, G H -- Ludwig, L -- Pannicke, U -- Li, Z -- Lindner, D -- Friedrich, W -- Seger, R A -- Hansen-Hagge, T E -- Desiderio, S -- Lieber, M R -- Bartram, C R -- New York, N.Y. -- Science. 1996 Oct 4;274(5284):97-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Molecular Biology, University of Ulm, D-89070 Ulm, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8810255" target="_blank"〉PubMed〈/a〉
    Keywords: B-Lymphocytes/immunology ; Cell Line ; Consanguinity ; *DNA-Binding Proteins ; Female ; Genes, Immunoglobulin ; Genes, Recessive ; *Homeodomain Proteins ; Humans ; Immunophenotyping ; Male ; Mutation ; Nuclear Proteins ; Polymorphism, Single-Stranded Conformational ; Proteins/*genetics ; Receptors, Antigen, T-Cell/genetics ; Recombination, Genetic ; Sequence Deletion ; Severe Combined Immunodeficiency/*genetics/immunology ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Germline allele-specific expression of TGFBR1 confers an increased risk of colorectal cancer (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-16
    Description: Much of the genetic predisposition to colorectal cancer (CRC) in humans is unexplained. Studying a Caucasian-dominated population in the United States, we showed that germline allele-specific expression (ASE) of the gene encoding transforming growth factor-beta (TGF-beta) type I receptor, TGFBR1, is a quantitative trait that occurs in 10 to 20% of CRC patients and 1 to 3% of controls. ASE results in reduced expression of the gene, is dominantly inherited, segregates in families, and occurs in sporadic CRC cases. Although subtle, the reduction in constitutive TGFBR1 expression alters SMAD-mediated TGF-beta signaling. Two major TGFBR1 haplotypes are predominant among ASE cases, which suggests ancestral mutations, but causative germline changes have not been identified. Conservative estimates suggest that ASE confers a substantially increased risk of CRC (odds ratio, 8.7; 95% confidence interval, 2.6 to 29.1), but these estimates require confirmation and will probably show ethnic differences.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2672914/" 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/PMC2672914/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Valle, Laura -- Serena-Acedo, Tarsicio -- Liyanarachchi, Sandya -- Hampel, Heather -- Comeras, Ilene -- Li, Zhongyuan -- Zeng, Qinghua -- Zhang, Hong-Tao -- Pennison, Michael J -- Sadim, Maureen -- Pasche, Boris -- Tanner, Stephan M -- de la Chapelle, Albert -- CA108741/CA/NCI NIH HHS/ -- CA112520/CA/NCI NIH HHS/ -- CA16058/CA/NCI NIH HHS/ -- CA67941/CA/NCI NIH HHS/ -- R01 CA108741/CA/NCI NIH HHS/ -- R01 CA108741-01A2/CA/NCI NIH HHS/ -- R01 CA112520/CA/NCI NIH HHS/ -- R01 CA112520-01A1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1361-5. doi: 10.1126/science.1159397. Epub 2008 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Cancer Genetics Program, Comprehensive Cancer Center, Ohio State University, Columbus, OH 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18703712" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Adult ; Aged ; Aged, 80 and over ; Alleles ; Cell Line ; Colorectal Neoplasms/*genetics ; Female ; *Gene Expression ; *Genetic Predisposition to Disease ; Haplotypes ; Heterozygote ; Humans ; Linkage Disequilibrium ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Protein-Serine-Threonine Kinases/*genetics ; Quantitative Trait, Heritable ; Receptors, Transforming Growth Factor beta/*genetics ; Risk Factors ; Signal Transduction ; Smad3 Protein/metabolism ; Transforming Growth Factor beta/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Cancer proliferation gene discovery through functional genomics (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-02
    Description: Retroviral short hairpin RNA (shRNA)-mediated genetic screens in mammalian cells are powerful tools for discovering loss-of-function phenotypes. We describe a highly parallel multiplex methodology for screening large pools of shRNAs using half-hairpin barcodes for microarray deconvolution. We carried out dropout screens for shRNAs that affect cell proliferation and viability in cancer cells and normal cells. We identified many shRNAs to be antiproliferative that target core cellular processes, such as the cell cycle and protein translation, in all cells examined. Moreover, we identified genes that are selectively required for proliferation and survival in different cell lines. Our platform enables rapid and cost-effective genome-wide screens to identify cancer proliferation and survival genes for target discovery. Such efforts are complementary to the Cancer Genome Atlas and provide an alternative functional view of cancer cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2981870/" 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/PMC2981870/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schlabach, Michael R -- Luo, Ji -- Solimini, Nicole L -- Hu, Guang -- Xu, Qikai -- Li, Mamie Z -- Zhao, Zhenming -- Smogorzewska, Agata -- Sowa, Mathew E -- Ang, Xiaolu L -- Westbrook, Thomas F -- Liang, Anthony C -- Chang, Kenneth -- Hackett, Jennifer A -- Harper, J Wade -- Hannon, Gregory J -- Elledge, Stephen J -- F31 NS054507-01/NS/NINDS NIH HHS/ -- P01 CA013106/CA/NCI NIH HHS/ -- P01 CA013106-36/CA/NCI NIH HHS/ -- P01 CA013106-37/CA/NCI NIH HHS/ -- R01 AG011085/AG/NIA NIH HHS/ -- T32CA09216/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Feb 1;319(5863):620-4. doi: 10.1126/science.1149200.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Genetics, Center for Genetics and Genomics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18239126" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics/pathology ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Cell Survival/genetics ; Colonic Neoplasms/*genetics/pathology ; Gene Library ; *Genes, Neoplasm ; Genetic Vectors ; Genome, Human ; Genomics/*methods ; Humans ; MicroRNAs ; Oligonucleotide Array Sequence Analysis ; RNA, Small Interfering ; Retroviridae/genetics
    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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