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[PMID]:29309426
[Au] Autor:McDonald JS; McDonald RJ; Ekins JB; Tin AS; Costes S; Hudson TM; Schroeder DJ; Kallmes K; Kaufmann SH; Young PM; Lu A; Kadirvel R; Kallmes DF
[Ad] Endereço:Department of Radiology, College of Medicine, Mayo Clinic, Rochester, MN, United States of America.
[Ti] Título:Gadolinium-enhanced cardiac MR exams of human subjects are associated with significant increases in the DNA repair marker 53BP1, but not the damage marker γH2AX.
[So] Source:PLoS One;13(1):e0190890, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Magnetic resonance imaging is considered low risk, yet recent studies have raised a concern of potential damage to DNA in peripheral blood leukocytes. This prospective Institutional Review Board-approved study examined potential double-strand DNA damage by analyzing changes in the DNA damage and repair markers γH2AX and 53BP1 in patients who underwent a 1.5 T gadolinium-enhanced cardiac magnetic resonance (MR) exam. Sixty patients were enrolled (median age 55 years, 39 males). Patients with history of malignancy or who were receiving chemotherapy, radiation therapy, or steroids were excluded. MR sequence data were recorded and blood samples obtained immediately before and after MR exposure. An automated immunofluorescence assay quantified γH2AX or 53BP1 foci number in isolated peripheral blood mononuclear cells. Changes in foci number were analyzed using the Wilcoxon signed-rank test. Clinical and MR procedural characteristics were compared between patients who had a >10% increase in γH2AX or 53BP1 foci numbers and patients who did not. The number of γH2AX foci did not significantly change following cardiac MR (median foci per cell pre-MR = 0.11, post-MR = 0.11, p = .90), but the number of 53BP1 foci significantly increased following MR (median foci per cell pre-MR = 0.46, post-MR = 0.54, p = .0140). Clinical and MR characteristics did not differ significantly between patients who had at least a 10% increase in foci per cell and those who did not. We conclude that MR exposure leads to a small (median 25%) increase in 53BP1 foci, however the clinical relevance of this increase is unknown and may be attributable to normal variation instead of MR exposure.
[Mh] Termos MeSH primário: Biomarcadores/metabolismo
Dano ao DNA
Reparo do DNA
Gadolínio/administração & dosagem
Coração/diagnóstico por imagem
Histonas/metabolismo
Imagem por Ressonância Magnética/métodos
Proteína 1 de Ligação à Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Prospectivos
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (H2AFX protein, human); 0 (Histones); 0 (TP53BP1 protein, human); 0 (Tumor Suppressor p53-Binding Protein 1); AU0V1LM3JT (Gadolinium)
[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:180109
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190890


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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


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[PMID]:28458064
[Au] Autor:Nagel ZD; Engelward BP; Brenner DJ; Begley TJ; Sobol RW; Bielas JH; Stambrook PJ; Wei Q; Hu JJ; Terry MB; Dilworth C; McAllister KA; Reinlib L; Worth L; Shaughnessy DT
[Ad] Endereço:Department of Environmental Health, Harvard School of Public Health, Boston, MA, 02115, USA.
[Ti] Título:Towards precision prevention: Technologies for identifying healthy individuals with high risk of disease.
[So] Source:Mutat Res;800-802:14-28, 2017 08.
[Is] ISSN:1873-135X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The rise of advanced technologies for characterizing human populations at the molecular level, from sequence to function, is shifting disease prevention paradigms toward personalized strategies. Because minimization of adverse outcomes is a key driver for treatment decisions for diseased populations, developing personalized therapy strategies represent an important dimension of both precision medicine and personalized prevention. In this commentary, we highlight recently developed enabling technologies in the field of DNA damage, DNA repair, and mutagenesis. We propose that omics approaches and functional assays can be integrated into population studies that fuse basic, translational and clinical research with commercial expertise in order to accelerate personalized prevention and treatment of cancer and other diseases linked to aberrant responses to DNA damage. This collaborative approach is generally applicable to efforts to develop data-driven, individualized prevention and treatment strategies for other diseases. We also recommend strategies for maximizing the use of biological samples for epidemiological studies, and for applying emerging technologies to clinical applications.
[Mh] Termos MeSH primário: Neoplasias/diagnóstico
Neoplasias/prevenção & controle
Medicina de Precisão
[Mh] Termos MeSH secundário: Dano ao DNA
Reparo do DNA
Seres Humanos
Mutagênese
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:29295984
[Au] Autor:Goyal N; Rossi MJ; Mazina OM; Chi Y; Moritz RL; Clurman BE; Mazin AV
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, PA, 19102, USA.
[Ti] Título:RAD54 N-terminal domain is a DNA sensor that couples ATP hydrolysis with branch migration of Holliday junctions.
[So] Source:Nat Commun;9(1):34, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In eukaryotes, RAD54 catalyzes branch migration (BM) of Holliday junctions, a basic process during DNA repair, replication, and recombination. RAD54 also stimulates RAD51 recombinase and has other activities. Here, we investigate the structural determinants for different RAD54 activities. We find that the RAD54 N-terminal domain (NTD) is responsible for initiation of BM through two coupled, but distinct steps; specific binding to Holliday junctions and RAD54 oligomerization. Furthermore, we find that the RAD54 oligomeric state can be controlled by NTD phosphorylation at S49, a CDK2 consensus site, which inhibits RAD54 oligomerization and, consequently, BM. Importantly, the effect of phosphorylation on RAD54 oligomerization is specific for BM, as it does not affect stimulation of RAD51 recombinase by RAD54. Thus, the transition of the oligomeric states provides an important control of the biological functions of RAD54 and, likely, other multifunctional proteins.
[Mh] Termos MeSH primário: Adenosina Trifosfatases/metabolismo
DNA Helicases/metabolismo
DNA Cruciforme/metabolismo
Proteínas Nucleares/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sítios de Ligação/genética
Linhagem Celular
DNA Helicases/química
DNA Helicases/genética
Reparo do DNA
DNA Cruciforme/química
DNA Cruciforme/genética
Seres Humanos
Hidrólise
Proteínas Nucleares/química
Proteínas Nucleares/genética
Conformação de Ácido Nucleico
Fosforilação
Multimerização Proteica
Recombinação Genética
Homologia de Sequência de Aminoácidos
Células Sf9
Spodoptera
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (DNA, Cruciform); 0 (Nuclear Proteins); 0 (RAD54L protein, human); EC 3.6.1.- (Adenosine Triphosphatases); EC 3.6.4.- (DNA Helicases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02497-x


  5 / 45187 MEDLINE  
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[PMID]:29421518
[Au] Autor:Luo H; Liang H; Chen Y; Chen S; Xu Y; Xu L; Liu J; Zhou K; Peng J; Guo G; Lai B; Song L; Yang H; Liu L; Peng J; Liu Z; Tang L; Chen W; Tang H
[Ad] Endereço:Department of Environmental and Occupational Health, Dongguan Key Laboratory of Environmental Medicine, School of Public Health, Guangdong Medical University, Dongguan, China.
[Ti] Título:miR-7-5p overexpression suppresses cell proliferation and promotes apoptosis through inhibiting the ability of DNA damage repair of PARP-1 and BRCA1 in TK6 cells exposed to hydroquinone.
[So] Source:Chem Biol Interact;283:84-90, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Hydroquinone (HQ), one of the major metabolic products of benzene, is a carcinogen, which induces apoptosis and inhibit proliferation in lymphoma cells. microRNA-7-5p (miR-7-5p), a tumor suppressor, participates in various biological processes including cell proliferation and apoptosis regulation by repressing expression of specific oncogenic target genes. To explore whether miR-7-5p is involved in HQ-induced cell proliferation and apoptosis, we assessed the effect of miR-7-5p overexpression on induction of apoptosis analyzed by FACSCalibur flow cytometer in transfection of TK6 cells with miR-7-5p mimic (TK6- miR-7-5p). We observed an increased apoptosis by 25.43% and decreased proliferation by 28.30% in TK6-miR-7-5p cells compared to those negative control cells (TK6-shNC) in response to HQ treatment. Furthermore, HQ might active the apoptotic pathway via partly downregulation the expression of BRCA1 and PARP-1, followed by p53 activation, in TK6-miR-7-5p cells. In contrast, attenuated p53 and BRCA1 expression was observed in shPARP-1 cells than in NC cells after HQ treatment. Therefore, we conclude that HQ may activate apoptotic signals via inhibiting the tumor suppressive effects of miR-7-5p, which may be mediated partly by upregulating the expression of PARP-1 and BRCA1 in control cells. The increase of miR-7-5p expression further intensified downregulation of PARP-1 and BRCA1 in TK6-miR-7-5p cells, resulting in an increase of apoptosis and proliferation inhibited.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Proteína BRCA1/metabolismo
Proliferação Celular/efeitos dos fármacos
Reparo do DNA/efeitos dos fármacos
Hidroquinonas/farmacologia
MicroRNAs/metabolismo
Poli(ADP-Ribose) Polimerase-1/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Antagomirs/metabolismo
Proteína BRCA1/genética
Caspase 3/metabolismo
Linhagem Celular Tumoral
Regulação para Baixo/efeitos dos fármacos
Seres Humanos
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Poli(ADP-Ribose) Polimerase-1/antagonistas & inibidores
Poli(ADP-Ribose) Polimerase-1/genética
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Antagomirs); 0 (BRCA1 Protein); 0 (BRCA1 protein, human); 0 (Hydroquinones); 0 (MicroRNAs); 0 (RNA, Small Interfering); 0 (Tumor Suppressor Protein p53); EC 2.4.2.30 (PARP1 protein, human); EC 2.4.2.30 (Poly (ADP-Ribose) Polymerase-1); EC 3.4.22.- (Caspase 3); XV74C1N1AE (hydroquinone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE


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[PMID]:29412148
[Au] Autor:Hou J; Cui C; Kim S; Sung C; Choi C
[Ad] Endereço:Intelligent Synthetic Biology Center, Daejeon 34141, Republic of Korea.
[Ti] Título:Ginsenoside F1 suppresses astrocytic senescence-associated secretory phenotype.
[So] Source:Chem Biol Interact;283:75-83, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Senescence is one of the hallmarks of aging and identified as a potential therapeutic target in the treatment of aging and aging-related diseases. Senescent cells accumulate with age in a variety of human tissues where they develop a complex senescence-associated secretory phenotype (SASP). SASP in brain could contribute to age-related inflammation and chronic neurodegenerative diseases. We confirmed that senescent astrocytes express a characteristic of SASP in vitro by human cytokine antibody array. Ginsenoside F1 suppresses the SASP from astrocytes induced by d-galactose via suppressing p38MAPK-dependent NF-κB activity. A specific inhibitor of p38MAPK, SB203580 significantly decreased the secretion of IL-6 and IL-8, the major components of SASPs. Additionally, treatment of senescent astrocytes with NF-κB inhibitor, BAY 11-7092, also suppressed the secretion of IL-6 and IL-8, suggesting NF-κB was required for SASP. Importantly, conditioned media from senescent astrocytes promoted the migration of glioblastoma cells, such as U373-MG, U251-MG and U87-MG assessed by scratch wound healing. This migration was significantly decreased by F1 treatment in senescent astrocytes. Interestingly, IL-8, the main mediator regulating glioblastoma cell invasion, was suppressed in both transcriptional and protein level. Herein, we propose ginsenoside F1 as a potential therapeutic strategy for reducing the deleterious contribution of senescent astrocytes in aged brain and related diseases.
[Mh] Termos MeSH primário: Senescência Celular/efeitos dos fármacos
Ginsenosídeos/farmacologia
[Mh] Termos MeSH secundário: Astrócitos/citologia
Astrócitos/efeitos dos fármacos
Astrócitos/metabolismo
Linhagem Celular
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Reparo do DNA/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Imidazóis/farmacologia
Interleucina-6/análise
Interleucina-6/metabolismo
Interleucina-8/análise
Interleucina-8/metabolismo
NF-kappa B/antagonistas & inibidores
NF-kappa B/metabolismo
Fosforilação/efeitos dos fármacos
Piridinas/farmacologia
Transdução de Sinais/efeitos dos fármacos
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ginsenosides); 0 (Imidazoles); 0 (Interleukin-6); 0 (Interleukin-8); 0 (NF-kappa B); 0 (Pyridines); 53963-43-2 (ginsenoside F1); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); OU13V1EYWQ (SB 203580)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE


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[PMID]:29335415
[Au] Autor:Uckelmann M; Densham RM; Baas R; Winterwerp HHK; Fish A; Sixma TK; Morris JR
[Ad] Endereço:Division of Biochemistry and Cancer Genomics Centre, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands.
[Ti] Título:USP48 restrains resection by site-specific cleavage of the BRCA1 ubiquitin mark from H2A.
[So] Source:Nat Commun;9(1):229, 2018 01 15.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BRCA1-BARD1-catalyzed ubiquitination of histone H2A is an important regulator of the DNA damage response, priming chromatin for repair by homologous recombination. However, no specific deubiquitinating enzymes (DUBs) are known to antagonize this function. Here we identify ubiquitin specific protease-48 (USP48) as a H2A DUB, specific for the C-terminal BRCA1 ubiquitination site. Detailed biochemical analysis shows that an auxiliary ubiquitin, an additional ubiquitin that itself does not get cleaved, modulates USP48 activity, which has possible implications for its regulation in vivo. In cells we reveal that USP48 antagonizes BRCA1 E3 ligase function and in BRCA1-proficient cells loss of USP48 results in positioning 53BP1 further from the break site and in extended resection lengths. USP48 repression confers a survival benefit to cells treated with camptothecin and its activity acts to restrain gene conversion and mutagenic single-strand annealing. We propose that USP48 promotes genome stability by antagonizing BRCA1 E3 ligase function.
[Mh] Termos MeSH primário: Proteína BRCA1/metabolismo
Histonas/metabolismo
Proteases Específicas de Ubiquitina/metabolismo
Ubiquitina/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteína BRCA1/genética
Sequência de Bases
Linhagem Celular Tumoral
Células Cultivadas
Reparo do DNA
Células HeLa
Seres Humanos
Cinética
Camundongos Knockout
Interferência de RNA
Proteína 1 de Ligação à Proteína Supressora de Tumor p53/metabolismo
Ubiquitina-Proteína Ligases/genética
Ubiquitina-Proteína Ligases/metabolismo
Proteases Específicas de Ubiquitina/genética
Ubiquitinação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BRCA1 Protein); 0 (BRCA1 protein, human); 0 (Histones); 0 (TP53BP1 protein, human); 0 (Tumor Suppressor p53-Binding Protein 1); 0 (Ubiquitin); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 3.4.19.12 (USP48 protein, human); EC 3.4.19.12 (Ubiquitin-Specific Proteases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02653-3


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[PMID]:29295983
[Au] Autor:Flett FJ; Ruksenaite E; Armstrong LA; Bharati S; Carloni R; Morris ER; Mackay CL; Interthal H; Richardson JM
[Ad] Endereço:Institute of Cell Biology, School of Biological Sciences, University of Edinburgh, The King's Buildings, Roger Land Building, Alexander Crum Brown Road, Edinburgh, EH9 3FF, UK.
[Ti] Título:Structural basis for DNA 3'-end processing by human tyrosyl-DNA phosphodiesterase 1.
[So] Source:Nat Commun;9(1):24, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tyrosyl-DNA phosphodiesterase (Tdp1) is a DNA 3'-end processing enzyme that repairs topoisomerase 1B-induced DNA damage. We use a new tool combining site-specific DNA-protein cross-linking with mass spectrometry to identify Tdp1 interactions with DNA. A conserved phenylalanine (F259) of Tdp1, required for efficient DNA processing in biochemical assays, cross-links to defined positions in DNA substrates. Crystal structures of Tdp1-DNA complexes capture the DNA repair machinery after 3'-end cleavage; these reveal how Tdp1 coordinates the 3'-phosphorylated product of nucleosidase activity and accommodates duplex DNA. A hydrophobic wedge splits the DNA ends, directing the scissile strand through a channel towards the active site. The F259 side-chain stacks against the -3 base pair, delimiting the junction of duplexed and melted DNA, and fixes the scissile strand in the channel. Our results explain why Tdp1 cleavage is non-processive and provide a molecular basis for DNA 3'-end processing by Tdp1.
[Mh] Termos MeSH primário: Dano ao DNA
Reparo do DNA
DNA/metabolismo
Diester Fosfórico Hidrolases/metabolismo
[Mh] Termos MeSH secundário: Sequência de Bases
Domínio Catalítico
Cristalografia por Raios X
DNA/química
DNA/genética
Seres Humanos
Modelos Moleculares
Conformação de Ácido Nucleico
Diester Fosfórico Hidrolases/química
Ligação Proteica
Domínios Proteicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
9007-49-2 (DNA); EC 3.1.4.- (Phosphoric Diester Hydrolases); EC 3.1.4.- (tyrosyl-DNA phosphodiesterase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02530-z


  9 / 45187 MEDLINE  
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[PMID]:28460465
[Au] Autor:McCormick A; Earp E; Elliot K; Cuthbert G; O'Donnell R; Wilson BT; Sutton R; Leeson C; Thomas HD; Blair H; Fordham S; Lunec J; Allan J; Edmondson RJ
[Ad] Endereço:Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, UK.
[Ti] Título:Functional characterisation of a novel ovarian cancer cell line, NUOC-1.
[So] Source:Oncotarget;8(16):26832-26844, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cell lines provide a powerful model to study cancer and here we describe a new spontaneously immortalised epithelial ovarian cancer cell line (NUOC-1) derived from the ascites collected at a time of primary debulking surgery for a mixed endometrioid / clear cell / High Grade Serous (HGS) histology. RESULTS: This spontaneously immortalised cell line was found to maintain morphology and epithelial markers throughout long-term culture. NUOC-1 cells grow as an adherent monolayer with a doubling time of 58 hours. The cells are TP53 wildtype, positive for PTEN, HER2 and HER3 expression but negative for oestrogen, progesterone and androgen receptor expression. NUOC-1 cells are competent in homologous recombination and non-homologous end joining, but base excision repair defective. Karyotype analysis demonstrated a complex tetraploid karyotype. SNP array analysis of parent and derived subpopulations (NUOC-1-A1 and NUOC-1-A2) cells demonstrated heterogeneous cell populations with numerous copy number alterations and a pro-amplification phenotype. The characteristics of this new cell line lends it to be an excellent model for investigation of a number of the identified targets. MATERIALS AND METHODS: The cell line has been characterised for growth, drug sensitivity, expression of common ovarian markers and mutations, clonogenic potential and ability to form xenografts in SCID mice. Copy number changes and clonal evolution were assessed by SNP arrays.
[Mh] Termos MeSH primário: Linhagem Celular Tumoral
Neoplasias Ovarianas/genética
Neoplasias Ovarianas/patologia
[Mh] Termos MeSH secundário: Animais
Bandeamento Cromossômico
Evolução Clonal/genética
Variações do Número de Cópias de DNA
Reparo do DNA
Modelos Animais de Doenças
Feminino
Amplificação de Genes
Genes myc
Xenoenxertos
Seres Humanos
Hibridização in Situ Fluorescente
Camundongos
Camundongos SCID
Meia-Idade
Mutação
Gradação de Tumores
Células-Tronco Neoplásicas/metabolismo
Proteína Supressora de Tumor p53/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tumor Suppressor Protein p53)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15821


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[PMID]:29281624
[Au] Autor:Lafuente-Barquero J; Luke-Glaser S; Graf M; Silva S; Gómez-González B; Lockhart A; Lisby M; Aguilera A; Luke B
[Ad] Endereço:Andalusian Center for Molecular Biology and Regenerative Medicine-CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, Avda. Americo Vespucio 24, Seville, Spain.
[Ti] Título:The Smc5/6 complex regulates the yeast Mph1 helicase at RNA-DNA hybrid-mediated DNA damage.
[So] Source:PLoS Genet;13(12):e1007136, 2017 12.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RNA-DNA hybrids are naturally occurring obstacles that must be overcome by the DNA replication machinery. In the absence of RNase H enzymes, RNA-DNA hybrids accumulate, resulting in replication stress, DNA damage and compromised genomic integrity. We demonstrate that Mph1, the yeast homolog of Fanconi anemia protein M (FANCM), is required for cell viability in the absence of RNase H enzymes. The integrity of the Mph1 helicase domain is crucial to prevent the accumulation of RNA-DNA hybrids and RNA-DNA hybrid-dependent DNA damage, as determined by Rad52 foci. Mph1 forms foci when RNA-DNA hybrids accumulate, e.g. in RNase H or THO-complex mutants and at short telomeres. Mph1, however is a double-edged sword, whose action at hybrids must be regulated by the Smc5/6 complex. This is underlined by the observation that simultaneous inactivation of RNase H2 and Smc5/6 results in Mph1-dependent synthetic lethality, which is likely due to an accumulation of toxic recombination intermediates. The data presented here support a model, where Mph1's helicase activity plays a crucial role in responding to persistent RNA-DNA hybrids.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/genética
RNA Helicases DEAD-box/genética
RNA Helicases DEAD-box/metabolismo
Dano ao DNA
RNA Fúngico/genética
Proteínas de Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Ciclo Celular/metabolismo
DNA/metabolismo
Reparo do DNA
Replicação do DNA/genética
Replicação do DNA/fisiologia
RNA Helicases/metabolismo
RNA Fúngico/metabolismo
Ribonuclease H/genética
Saccharomyces cerevisiae/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (RNA, Fungal); 0 (SMC5 protein, S cerevisiae); 0 (SMC6 protein, S cerevisiae); 0 (Saccharomyces cerevisiae Proteins); 9007-49-2 (DNA); EC 3.1.26.4 (Ribonuclease H); EC 3.6.1.- (MPH1 protein, S cerevisiae); EC 3.6.4.13 (DEAD-box RNA Helicases); EC 3.6.4.13 (RNA Helicases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171228
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007136



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