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Pesquisa : G05.200.210.220 [Categoria DeCS]
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  1 / 5618 MEDLINE  
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[PMID]:28453388
[Au] Autor:Ayars M; Eshleman J; Goggins M
[Ad] Endereço:a Department of Pathology , The Johns Hopkins University School of Medicine , Baltimore , MD, USA.
[Ti] Título:Susceptibility of ATM-deficient pancreatic cancer cells to radiation.
[So] Source:Cell Cycle;16(10):991-998, 2017 May 19.
[Is] ISSN:1551-4005
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ataxia telangiectasia mutated (ATM) is inactivated in a significant minority of pancreatic ductal adenocarcinomas and may be predictor of treatment response. We determined if ATM deficiency renders pancreatic cancer cells more sensitive to fractionated radiation or commonly used chemotherapeutics. ATM expression was knocked down in three pancreatic cancer cell lines using ATM-targeting shRNA. Isogenic cell lines were tested for sensitivity to several chemotherapeutic agents and radiation. DNA repair kinetics were analyzed in irradiated cells using the comet assay. We find that while rendering pancreatic cancer cells ATM-deficient did not significantly change their sensitivity to several chemotherapeutics, it did render them exquisitely sensitized to radiation. Pancreatic cancer ATM status may help predict response to radiotherapy.
[Mh] Termos MeSH primário: Adenocarcinoma/radioterapia
Proteínas Mutadas de Ataxia Telangiectasia/genética
Carcinoma Ductal Pancreático/radioterapia
Tolerância a Radiação/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Adenocarcinoma/patologia
Carcinoma Ductal Pancreático/genética
Carcinoma Ductal Pancreático/patologia
Linhagem Celular Tumoral
Quebras de DNA de Cadeia Dupla
Dano ao DNA/efeitos da radiação
Reparo do DNA/efeitos da radiação
Regulação Neoplásica da Expressão Gênica/efeitos da radiação
Seres Humanos
Fosforilação/efeitos da radiação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.11.1 (ATM protein, human); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1080/15384101.2017.1312236


  2 / 5618 MEDLINE  
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[PMID]:28743762
[Au] Autor:Hum YF; Jinks-Robertson S
[Ad] Endereço:Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina 27710.
[Ti] Título:Mitotic Gene Conversion Tracts Associated with Repair of a Defined Double-Strand Break in .
[So] Source:Genetics;207(1):115-128, 2017 09.
[Is] ISSN:1943-2631
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitotic recombination between homologous chromosomes leads to the uncovering of recessive alleles through loss of heterozygosity. In the current study, a defined double-strand break was used to initiate reciprocal loss of heterozygosity between diverged homologs of chromosome IV in These events resulted from the repair of two broken chromatids, one of which was repaired as a crossover and the other as a noncrossover. Associated gene conversion tracts resulting from the donor-directed repair of mismatches formed during strand exchange (heteroduplex DNA) were mapped using microarrays. Gene conversion tracts associated with individual crossover and noncrossover events were similar in size and position, with half of the tracts being unidirectional and mapping to only one side of the initiating break. Among crossover events, this likely reflected gene conversion on only one side of the break, with restoration-type repair occurring on the other side. For noncrossover events, an ectopic system was used to directly compare gene conversion tracts produced in a wild-type strain to heteroduplex DNA tracts generated in the absence of the Mlh1 mismatch-repair protein. There was a strong bias for unidirectional tracts in the absence, but not in the presence, of Mlh1 This suggests that mismatch repair acts on heteroduplex DNA that is only transiently present in noncrossover intermediates of the synthesis dependent strand annealing pathway. Although the molecular features of events associated with loss of heterozygosity generally agreed with those predicted by current recombination models, there were unexpected complexities in associated gene conversion tracts.
[Mh] Termos MeSH primário: Quebras de DNA de Cadeia Dupla
Conversão Gênica
Mitose/genética
Reparo de DNA por Recombinação
Saccharomyces cerevisiae/genética
[Mh] Termos MeSH secundário: Troca Genética
Saccharomyces cerevisiae/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1534/genetics.117.300057


  3 / 5618 MEDLINE  
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[PMID]:28467943
[Au] Autor:Tian X; Seluanov A; Gorbunova V
[Ad] Endereço:Department of Biology, University of Rochester, Rochester, NY 14627, USA.
[Ti] Título:Beyond Making Ends Meet: DNA-PK, Metabolism, and Aging.
[So] Source:Cell Metab;25(5):991-992, 2017 May 02.
[Is] ISSN:1932-7420
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA-dependent protein kinase (DNA-PK), a central player in DNA double-strand break (DSB) repair, shows emerging roles in metabolic regulation. In this issue of Cell Metabolism, Park et al. (2017) elucidate a molecular mechanism whereby DNA-PK negatively regulates AMPK, contributing to metabolic and fitness decline during aging.
[Mh] Termos MeSH primário: Envelhecimento
Dano ao DNA
Proteína Quinase Ativada por DNA/metabolismo
[Mh] Termos MeSH secundário: Animais
Quebras de DNA de Cadeia Dupla
Proteínas de Choque Térmico HSP90/metabolismo
Seres Humanos
Redes e Vias Metabólicas
Proteínas Quinases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HSP90 Heat-Shock Proteins); EC 2.7.- (Protein Kinases); EC 2.7.1.- (AMP-activated protein kinase kinase); EC 2.7.11.1 (DNA-Activated Protein Kinase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  4 / 5618 MEDLINE  
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[PMID]:29284038
[Au] Autor:Bauer RJ; Zhelkovsky A; Bilotti K; Crowell LE; Evans TC; McReynolds LA; Lohman GJS
[Ad] Endereço:Research Division, New England Biolabs, Inc., Ipswich, MA, United States of America.
[Ti] Título:Comparative analysis of the end-joining activity of several DNA ligases.
[So] Source:PLoS One;12(12):e0190062, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA ligases catalyze the repair of phosphate backbone breaks in DNA, acting with highest activity on breaks in one strand of duplex DNA. Some DNA ligases have also been observed to ligate two DNA fragments with short complementary overhangs or blunt-ended termini. In this study, several wild-type DNA ligases (phage T3, T4, and T7 DNA ligases, Paramecium bursaria chlorella virus 1 (PBCV1) DNA ligase, human DNA ligase 3, and Escherichia coli DNA ligase) were tested for their ability to ligate DNA fragments with several difficult to ligate end structures (blunt-ended termini, 3'- and 5'- single base overhangs, and 5'-two base overhangs). This analysis revealed that T4 DNA ligase, the most common enzyme utilized for in vitro ligation, had its greatest activity on blunt- and 2-base overhangs, and poorest on 5'-single base overhangs. Other ligases had different substrate specificity: T3 DNA ligase ligated only blunt ends well; PBCV1 DNA ligase joined 3'-single base overhangs and 2-base overhangs effectively with little blunt or 5'- single base overhang activity; and human ligase 3 had highest activity on blunt ends and 5'-single base overhangs. There is no correlation of activity among ligases on blunt DNA ends with their activity on single base overhangs. In addition, DNA binding domains (Sso7d, hLig3 zinc finger, and T4 DNA ligase N-terminal domain) were fused to PBCV1 DNA ligase to explore whether modified binding to DNA would lead to greater activity on these difficult to ligate substrates. These engineered ligases showed both an increased binding affinity for DNA and increased activity, but did not alter the relative substrate preferences of PBCV1 DNA ligase, indicating active site structure plays a role in determining substrate preference.
[Mh] Termos MeSH primário: DNA Ligases/metabolismo
[Mh] Termos MeSH secundário: Quebras de DNA de Cadeia Dupla
Eletroforese Capilar
Seres Humanos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 6.5.1.- (DNA Ligases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171229
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190062


  5 / 5618 MEDLINE  
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[PMID]:29352017
[Au] Autor:Gnügge R; Symington LS
[Ad] Endereço:Department of Microbiology and Immunology, Columbia University Medical Center, New York, New York 10032, USA.
[Ti] Título:Keeping it real: MRX-Sae2 clipping of natural substrates.
[So] Source:Genes Dev;31(23-24):2311-2312, 2017 12 01.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The yeast Mre11-Rad50-Xrs2 (MRX) complex and Sae2 function together to initiate DNA end resection, an essential early step in homology-dependent repair of DNA double-strand breaks (DSBs). In this issue of , Wang and colleagues (pp. 2331-2336) and Reginato and colleagues (pp. 2325-2330) report that a variety of physiological protein blocks, including Ku, RPA, and nucleosomes, stimulate MRX-Sae2 endonuclease cleavage in vitro. These studies have important implications for how cells deal with a range of barriers to end resection and highlight the crucial role of Sae2 in activating MRX cleavage at the correct cell cycle stage.
[Mh] Termos MeSH primário: Endodesoxirribonucleases/genética
Proteínas de Saccharomyces cerevisiae/genética
[Mh] Termos MeSH secundário: Quebras de DNA de Cadeia Dupla
Reparo do DNA
Proteínas de Ligação a DNA/genética
Exodesoxirribonucleases/genética
Saccharomyces cerevisiae/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW; COMMENT
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Saccharomyces cerevisiae Proteins); EC 3.1.- (Endodeoxyribonucleases); EC 3.1.- (Exodeoxyribonucleases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180121
[St] Status:MEDLINE
[do] DOI:10.1101/gad.310771.117


  6 / 5618 MEDLINE  
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[PMID]:29182755
[Au] Autor:Kochan JA; Desclos ECB; Bosch R; Meister L; Vriend LEM; van Attikum H; Krawczyk PM
[Ad] Endereço:Department of Medical Biology and Laboratory of Experimental Oncology and Radiobiology (LEXOR), Cancer Center Amsterdam, Academic Medical Center, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands.
[Ti] Título:Meta-analysis of DNA double-strand break response kinetics.
[So] Source:Nucleic Acids Res;45(22):12625-12637, 2017 Dec 15.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Most proteins involved in the DNA double-strand break response (DSBR) accumulate at the damage sites, where they perform functions related to damage signaling, chromatin remodeling and repair. Over the last two decades, studying the accumulation of many DSBR proteins provided information about their functionality and underlying mechanisms of action. However, comparison and systemic interpretation of these data is challenging due to their scattered nature and differing experimental approaches. Here, we extracted, analyzed and compared the available results describing accumulation of 79 DSBR proteins at sites of DNA damage, which can be further explored using Cumulus (http://www.dna-repair.live/cumulus/)-the accompanying interactive online application. Despite large inter-study variability, our analysis revealed that the accumulation of most proteins starts immediately after damage induction, occurs in parallel and peaks within 15-20 min. Various DSBR pathways are characterized by distinct accumulation kinetics with major non-homologous end joining proteins being generally faster than those involved in homologous recombination, and signaling and chromatin remodeling factors accumulating with varying speeds. Our meta-analysis provides, for the first time, comprehensive overview of the temporal organization of the DSBR in mammalian cells and could serve as a reference for future mechanistic studies of this complex process.
[Mh] Termos MeSH primário: Quebras de DNA de Cadeia Dupla
Reparo do DNA
Proteínas de Ligação a DNA/metabolismo
DNA/genética
Recombinação Homóloga
[Mh] Termos MeSH secundário: Animais
DNA/metabolismo
Seres Humanos
Cinética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 9007-49-2 (DNA)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180115
[Lr] Data última revisão:
180115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx1128


  7 / 5618 MEDLINE  
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[PMID]:28740117
[Au] Autor:Glover TW; Wilson TE; Arlt MF
[Ad] Endereço:Department of Human Genetics; the Department of Pathology; and the Department of Pediatrics and Communicable Diseases, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA.
[Ti] Título:Fragile sites in cancer: more than meets the eye.
[So] Source:Nat Rev Cancer;17(8):489-501, 2017 07 25.
[Is] ISSN:1474-1768
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ever since initial suggestions that instability at common fragile sites (CFSs) could be responsible for chromosome rearrangements in cancers, CFSs and associated genes have been the subject of numerous studies, leading to questions and controversies about their role and importance in cancer. It is now clear that CFSs are not frequently involved in translocations or other cancer-associated recurrent gross chromosome rearrangements. However, recent studies have provided new insights into the mechanisms of CFS instability, their effect on genome instability, and their role in generating focal copy number alterations that affect the genomic landscape of many cancers.
[Mh] Termos MeSH primário: Instabilidade Cromossômica
Sítios Frágeis do Cromossomo
Variações do Número de Cópias de DNA
Neoplasias/genética
Oncogenes/genética
[Mh] Termos MeSH secundário: Anáfase
Animais
Quebra Cromossômica
Quebras de DNA de Cadeia Dupla
Replicação do DNA
Rearranjo Gênico
Seres Humanos
Metáfase
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1038/nrc.2017.52


  8 / 5618 MEDLINE  
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[PMID]:28746375
[Au] Autor:Markowitz TE; Suarez D; Blitzblau HG; Patel NJ; Markhard AL; MacQueen AJ; Hochwagen A
[Ad] Endereço:Department of Biology; New York University; New York, NY; United States of America.
[Ti] Título:Reduced dosage of the chromosome axis factor Red1 selectively disrupts the meiotic recombination checkpoint in Saccharomyces cerevisiae.
[So] Source:PLoS Genet;13(7):e1006928, 2017 Jul.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Meiotic chromosomes assemble characteristic "axial element" structures that are essential for fertility and provide the chromosomal context for meiotic recombination, synapsis and checkpoint signaling. Whether these meiotic processes are equally dependent on axial element integrity has remained unclear. Here, we investigated this question in S. cerevisiae using the putative condensin allele ycs4S. We show that the severe axial element assembly defects of this allele are explained by a linked mutation in the promoter of the major axial element gene RED1 that reduces Red1 protein levels to 20-25% of wild type. Intriguingly, the Red1 levels of ycs4S mutants support meiotic processes linked to axis integrity, including DNA double-strand break formation and deposition of the synapsis protein Zip1, at levels that permit 70% gamete survival. By contrast, the ability to elicit a meiotic checkpoint arrest is completely eliminated. This selective loss of checkpoint function is supported by a RED1 dosage series and is associated with the loss of most of the cytologically detectable Red1 from the axial element. Our results indicate separable roles for Red1 in building the structural axis of meiotic chromosomes and mounting a sustained recombination checkpoint response.
[Mh] Termos MeSH primário: Dosagem de Genes/genética
Meiose/genética
Recombinação Genética
Proteínas de Saccharomyces cerevisiae/genética
[Mh] Termos MeSH secundário: Pareamento Cromossômico
Cromossomos Fúngicos/genética
Quebras de DNA de Cadeia Dupla
Mutação
Saccharomyces cerevisiae/genética
Esporos Fúngicos/genética
Complexo Sinaptonêmico/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RED1 protein, S cerevisiae); 0 (Saccharomyces cerevisiae Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006928


  9 / 5618 MEDLINE  
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[PMID]:29220655
[Au] Autor:Pannunzio NR; Lieber MR
[Ad] Endereço:USC Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, 1441 Eastlake Avenue, Rm. 5428, Los Angeles, CA 90089, USA.
[Ti] Título:AID and Reactive Oxygen Species Can Induce DNA Breaks within Human Chromosomal Translocation Fragile Zones.
[So] Source:Mol Cell;68(5):901-912.e3, 2017 Dec 07.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA double-strand breaks (DSBs) occurring within fragile zones of less than 200 base pairs account for the formation of the most common human chromosomal translocations in lymphoid malignancies, yet the mechanism of how breaks occur remains unknown. Here, we have transferred human fragile zones into S. cerevisiae in the context of a genetic assay to understand the mechanism leading to DSBs at these sites. Our findings indicate that a combination of factors is required to sensitize these regions. Foremost, DNA strand separation by transcription or increased torsional stress can expose these DNA regions to damage from either the expression of human AID or increased oxidative stress. This damage causes DNA lesions that, if not repaired quickly, are prone to nuclease cleavage, resulting in DSBs. Our results provide mechanistic insight into why human neoplastic translocation fragile DNA sequences are more prone to enzymes or agents that cause longer-lived DNA lesions.
[Mh] Termos MeSH primário: Cromossomos Humanos/genética
Citidina Desaminase/genética
Quebras de DNA de Cadeia Dupla
DNA Fúngico/genética
Estresse Oxidativo
Espécies Reativas de Oxigênio/metabolismo
Saccharomyces cerevisiae/genética
Translocação Genética
[Mh] Termos MeSH secundário: Cromossomos Humanos/química
Cromossomos Humanos/metabolismo
Citidina Desaminase/metabolismo
DNA Fúngico/química
DNA Fúngico/metabolismo
Endonucleases/genética
Endonucleases/metabolismo
Regulação Enzimológica da Expressão Gênica
Regulação Fúngica da Expressão Gênica
Seres Humanos
Conformação de Ácido Nucleico
Peroxidases/genética
Peroxidases/metabolismo
Saccharomyces cerevisiae/enzimologia
Proteínas de Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/metabolismo
Relação Estrutura-Atividade
Transcrição Genética
Uracila-DNA Glicosidase/genética
Uracila-DNA Glicosidase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Fungal); 0 (Reactive Oxygen Species); 0 (Saccharomyces cerevisiae Proteins); EC 1.11.1.- (Peroxidases); EC 1.11.1.- (Tsa1 protein, S cerevisiae); EC 3.1.- (Endonucleases); EC 3.1.- (artemis nuclease, human); EC 3.2.2.- (Uracil-DNA Glycosidase); EC 3.5.4.- (AICDA (activation-induced cytidine deaminase)); EC 3.5.4.5 (Cytidine Deaminase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE


  10 / 5618 MEDLINE  
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[PMID]:29184180
[Au] Autor:Storici F; Tichon AE
[Ad] Endereço:School of Biological Sciences, Georgia Institute of Technology, Atlanta, Georgia 30332, USA.
[Ti] Título:RNA takes over control of DNA break repair.
[So] Source:Nat Cell Biol;19(12):1382-1384, 2017 Nov 29.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Small RNAs generated at DNA break sites are implicated in mammalian DNA repair. Now, a study shows that following the formation of DNA double-strand breaks, bidirectional transcription events adjacent to the break generate small RNAs that trigger the DNA damage response by local RNA:RNA interactions.
[Mh] Termos MeSH primário: Quebras de DNA de Cadeia Dupla
Reparo do DNA
RNA/genética
RNA/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Biológicos
RNA Polimerase II/metabolismo
RNA Longo não Codificante/genética
RNA Longo não Codificante/metabolismo
Pequeno RNA não Traduzido/genética
Pequeno RNA não Traduzido/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Long Noncoding); 0 (RNA, Small Untranslated); 63231-63-0 (RNA); EC 2.7.7.- (RNA Polymerase II)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3645



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