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Pesquisa : D02.065.064.150.100 [Categoria DeCS]
Referências encontradas : 335 [refinar]
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[PMID]:21487018
[Au] Autor:Kemp MG; Lindsey-Boltz LA; Sancar A
[Ad] Endereço:Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599, USA.
[Ti] Título:The DNA damage response kinases DNA-dependent protein kinase (DNA-PK) and ataxia telangiectasia mutated (ATM) Are stimulated by bulky adduct-containing DNA.
[So] Source:J Biol Chem;286(22):19237-46, 2011 Jun 03.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A variety of environmental, carcinogenic, and chemotherapeutic agents form bulky lesions on DNA that activate DNA damage checkpoint signaling pathways in human cells. To identify the mechanisms by which bulky DNA adducts induce damage signaling, we developed an in vitro assay using mammalian cell nuclear extract and plasmid DNA containing bulky adducts formed by N-acetoxy-2-acetylaminofluorene or benzo(a)pyrene diol epoxide. Using this cell-free system together with a variety of pharmacological, genetic, and biochemical approaches, we identified the DNA damage response kinases DNA-dependent protein kinase (DNA-PK) and ataxia telangiectasia mutated (ATM) as bulky DNA damage-stimulated kinases that phosphorylate physiologically important residues on the checkpoint proteins p53, Chk1, and RPA. Consistent with these results, purified DNA-PK and ATM were directly stimulated by bulky adduct-containing DNA and preferentially associated with damaged DNA in vitro. Because the DNA damage response kinase ATM and Rad3-related (ATR) is also stimulated by bulky DNA adducts, we conclude that a common biochemical mechanism exists for activation of DNA-PK, ATM, and ATR by bulky adduct-containing DNA.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/metabolismo
Adutos de DNA/metabolismo
Dano ao DNA/fisiologia
Proteína Quinase Ativada por DNA/metabolismo
Proteínas de Ligação a DNA/metabolismo
Proteínas Nucleares/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas Supressoras de Tumor/metabolismo
[Mh] Termos MeSH secundário: Acetoxiacetilaminofluoreno/farmacologia
Alquilantes/farmacologia
Animais
Proteínas Mutadas de Ataxia Telangiectasia
Benzo(a)pireno/farmacologia
Células CHO
Proteínas de Ciclo Celular/genética
Quinase do Ponto de Checagem 1
Cricetinae
Cricetulus
Adutos de DNA/genética
Dano ao DNA/efeitos dos fármacos
Proteína Quinase Ativada por DNA/genética
Proteínas de Ligação a DNA/genética
Seres Humanos
Proteínas Nucleares/genética
Fosforilação/efeitos dos fármacos
Fosforilação/fisiologia
Proteínas Quinases/genética
Proteínas Quinases/metabolismo
Proteínas Serina-Treonina Quinases/genética
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Alkylating Agents); 0 (Cell Cycle Proteins); 0 (DNA Adducts); 0 (DNA-Binding Proteins); 0 (Nuclear Proteins); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 0 (Tumor Suppressor Proteins); 3417WMA06D (Benzo(a)pyrene); 6098-44-8 (Acetoxyacetylaminofluorene); EC 2.7.- (Protein Kinases); EC 2.7.11.1 (ATM protein, human); EC 2.7.11.1 (ATR protein, human); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins); EC 2.7.11.1 (CHEK1 protein, human); EC 2.7.11.1 (Checkpoint Kinase 1); EC 2.7.11.1 (DNA-Activated Protein Kinase); EC 2.7.11.1 (PRKDC protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1108
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110414
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M111.235036


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[PMID]:20067618
[Au] Autor:Mahabir AG; Schaap MM; Pennings JL; van Benthem J; Hendriksen CF; van Steeg H
[Ad] Endereço:National Institute for Public Health and the Environment (RIVM), Laboratory for Health Protection Research (GBO), NL-3720 BA Bilthoven, the Netherlands.
[Ti] Título:Comparison of clastogen-induced gene expression profiles in wild-type and DNA repair-deficient Rad54/Rad54B cells.
[So] Source:BMC Genomics;11:24, 2010 Jan 12.
[Is] ISSN:1471-2164
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Previously we found that Rad54/Rad54B cells are more sensitive towards mitomycin C (MMC) as compared to wild-type (WT) cells. This difference in sensitivity was absent upon exposure to other clastogens like bleomycin (BLM) and gamma-radiation. In order to get further insight into possible underlying mechanisms, gene expression changes in WT and Rad54/Rad54B MEFs (mouse embryonic fibroblasts) after exposure to the clastogens MMC and BLM were investigated. Exposures of these cells to mutagens (N-ac-AAF and ENU) and vehicle were taken as controls. RESULTS: Most exposures resulted in an induction of DNA damage signaling and apoptosis genes and a reduced expression of cell division genes in cells of both genotypes. As expected, responses to N-ac-AAF were very similar in both genotypes. ENU exposure did not lead to significant gene expression changes in cells of both genotypes, presumably due to its short half-life. Gene expression responses to clastogens, however, showed a genotype-dependent effect for BLM and MMC. MMC treated Rad54/Rad54B MEFs showed no induction of p53-signaling, DNA damage response and apoptosis as seen for all the other treatments. CONCLUSION: These data support our finding that different types of clastogens exist and that responses to these types depend on the DNA repair status of the cells.
[Mh] Termos MeSH primário: Bleomicina/farmacologia
Reparo do DNA
Perfilação da Expressão Gênica
Mitomicina/farmacologia
Mutagênicos/farmacologia
[Mh] Termos MeSH secundário: Acetoxiacetilaminofluoreno/farmacologia
Animais
Apoptose
Linhagem Celular
Dano ao DNA
Etilnitrosoureia/farmacologia
Genótipo
Camundongos
Análise de Sequência com Séries de Oligonucleotídeos
Análise de Componente Principal
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mutagens); 11056-06-7 (Bleomycin); 50SG953SK6 (Mitomycin); 6098-44-8 (Acetoxyacetylaminofluorene); P8M1T4190R (Ethylnitrosourea)
[Em] Mês de entrada:1005
[Cu] Atualização por classe:141204
[Lr] Data última revisão:
141204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100114
[St] Status:MEDLINE
[do] DOI:10.1186/1471-2164-11-24


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[PMID]:19053159
[Au] Autor:Liao Q; Shen C; Vouros P
[Ad] Endereço:Mass Spectrometry Center, FAS Center for System Biology, Harvard University, Cambridge, MA 02138, USA.
[Ti] Título:GenoMass--a computer software for automated identification of oligonucleotide DNA adducts from LC-MS analysis of DNA digests.
[So] Source:J Mass Spectrom;44(4):549-60, 2009 Apr.
[Is] ISSN:1096-9888
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In the investigation of oligonucleotides, DNA and their adducts by LC-MS, a myriad of data are generated that make manual data processing quite difficult. This paper describes a 'reversed pseudo-combinatorial' approach for fragment identification and the software implementation of this approach. Combinatorial isomer libraries are generated in silico to represent the digestion products of oligonucleotides, DNA or DNA adducts of various sizes. The software automatically calculates ion masses of each isomeric segment of the library, searches for them in complicated LC-MS data, lists their intensities and plots extracted ion chromatograms (EIC). This customized new data analysis tool has enabled a study of the enzymatic behavior of a nuclease system in the digestion of normal and adducted DNA, and in the recognition of oligomers containing a carcinogen bound to a nucleobase. The software program potentially can be further expanded to postulate unknown DNA sequences and recognize the adduction sites.
[Mh] Termos MeSH primário: DNA/análise
Espectrometria de Massas/métodos
Oligonucleotídeos/análise
Software
[Mh] Termos MeSH secundário: 2-Acetilaminofluoreno/metabolismo
Acetoxiacetilaminofluoreno/metabolismo
Fosfatase Alcalina/metabolismo
Sequência de Bases
Cromatografia Líquida de Alta Pressão/métodos
DNA/metabolismo
Endodesoxirribonucleases/metabolismo
Endorribonucleases/metabolismo
Dados de Sequência Molecular
Oligonucleotídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Oligonucleotides); 6098-44-8 (Acetoxyacetylaminofluorene); 9007-49-2 (DNA); 9M98QLJ2DL (2-Acetylaminofluorene); EC 3.1.- (Endodeoxyribonucleases); EC 3.1.- (Endoribonucleases); EC 3.1.3.1 (Alkaline Phosphatase); EC 3.1.30.2 (Serratia marcescens nuclease)
[Em] Mês de entrada:0907
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:081205
[St] Status:MEDLINE
[do] DOI:10.1002/jms.1532


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[PMID]:17143337
[Au] Autor:Pietrowska M; Kolodziejczyk I; Widlak P
[Ad] Endereço:Department of Experimental and Clinical Radiobiology, Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Gliwice, Poland. m_pietrowska@io.gliwice.pl
[Ti] Título:Mitochondrial transcription factor A is the major protein in rodent hepatocytes that recognizes DNA lesions induced by N-acetoxy-acetylaminofluorene.
[So] Source:Acta Biochim Pol;53(4):777-82, 2006.
[Is] ISSN:0001-527X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Extracts from rodent liver cells contain an abundant protein that recognizes DNA adducts induced by the chemical carcinogen N-acetoxy-acetylaminofluorene (AAAF). This protein also has a strong affinity for DNA damaged by cisplatin (DDP), but not by benzo(a)pyrene diolepoxide or UV-radiation, and has been termed AAAF/DDP-DDB. Here we purified this protein from rat tissue and analyzed it by mass spectrometry and identified it as mitochondrial transcription factor A (TFAM). Experiments with bacterially expressed recombinant TFAM confirmed its high affinity for DNA damaged by AAAF. Assuming its abundance and specificity for AAAF induced lesions, TFAM may significantly impede recognition and repair of DNA adducts induced by AAAF and other derivatives of 2-aminofluorene.
[Mh] Termos MeSH primário: Acetoxiacetilaminofluoreno/efeitos adversos
Dano ao DNA
Proteínas de Ligação a DNA/fisiologia
Hepatócitos/química
Proteínas Mitocondriais/fisiologia
Fatores de Transcrição/fisiologia
[Mh] Termos MeSH secundário: Animais
Adutos de DNA
Proteínas de Ligação a DNA/isolamento & purificação
Proteínas Mitocondriais/isolamento & purificação
Ratos
Fatores de Transcrição/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA Adducts); 0 (DNA-Binding Proteins); 0 (Mitochondrial Proteins); 0 (Transcription Factors); 0 (mitochondrial transcription factor A); 6098-44-8 (Acetoxyacetylaminofluorene)
[Em] Mês de entrada:0710
[Cu] Atualização por classe:070103
[Lr] Data última revisão:
070103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:061205
[St] Status:MEDLINE


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[PMID]:16222506
[Au] Autor:Wagner ED; McMillan SM; Plewa MJ
[Ad] Endereço:Department of Crop Sciences, College of Agricultural, Consumer and Environmental Sciences, University of Illinois at Urbana-Champaign, 366 NSRC MC-635, 1101 West Peabody Drive, Urbana, IL 61801, USA.
[Ti] Título:Cytotoxicity of organophosphorus ester (OP) insecticides and cytotoxic synergism of 2-acetoxyacetylaminofluorene (2AAAF) in Chinese hamster ovary (CHO) cells.
[So] Source:Bull Environ Contam Toxicol;75(2):329-34, 2005 Aug.
[Is] ISSN:0007-4861
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Acetoxiacetilaminofluoreno/toxicidade
Inseticidas/toxicidade
[Mh] Termos MeSH secundário: Animais
Células CHO
Sobrevivência Celular/efeitos dos fármacos
Cricetinae
Sinergismo Farmacológico
Compostos Organofosforados/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Insecticides); 0 (Organophosphorus Compounds); 6098-44-8 (Acetoxyacetylaminofluorene)
[Em] Mês de entrada:0510
[Cu] Atualização por classe:091111
[Lr] Data última revisão:
091111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:051014
[St] Status:MEDLINE


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[PMID]:15940347
[Au] Autor:Pietrowska M; Widlak P
[Ad] Endereço:Department of Experimental and Clinical Radiobiology, Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Gliwice, Poland.
[Ti] Título:Characterization of a novel protein that specifically binds to DNA modified by N-acetoxy-acetylaminofluorene and cis-diamminedichloroplatinum.
[So] Source:Acta Biochim Pol;52(4):867-74, 2005.
[Is] ISSN:0001-527X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Proteins recognizing DNA damaged by the chemical carcinogen N-acetoxy-acetylaminofluorene (AAAF) were analyzed in nuclear extracts from rat tissues, using a 36 bp oligonucleotide as a substrate and electrophoretic mobility shift and Southwestern blot assays. One major damage-recognizing protein was detected, whose amount was estimated as at least 10(5) copies per cell. Levels of this protein were similar in extracts from brain, kidney and liver, but much lower in extracts from testis. The affinity of the detected protein for DNA damaged by AAAF was about 70-fold higher than for undamaged DNA. DNA damaged by cis-diamminedichloroplatinum (cis-DDP), benzo(a)pyrene diolepoxide (BPDE) or UV-radiation also bound this protein with an increased affinity, the former more strongly and the latter two more weakly as compared to AAAF-damaged DNA. The detected AAAF/DDP-damaged-DNA-binding (AAAF/DDP-DDB) protein had a molecular mass of about 25 kDa and was distinct from histone H1 or HMGB proteins, which are known to have a high affinity for cis-DDP-damaged DNA. The level of this damage-recognizing protein was not affected in rats treated with the carcinogen 2-acetylaminofluorene. The activity of an AAAF/DDP-DDB protein could also be detected in extracts from mouse liver cells but not from the Hep2G human hepatocellular carcinoma.
[Mh] Termos MeSH primário: Acetoxiacetilaminofluoreno/farmacologia
Cisplatino/farmacologia
Dano ao DNA/efeitos dos fármacos
Proteínas de Ligação a DNA/metabolismo
DNA/metabolismo
[Mh] Termos MeSH secundário: Animais
DNA/efeitos dos fármacos
Proteínas de Grupo de Alta Mobilidade/metabolismo
Histonas/metabolismo
Cinética
Fígado/metabolismo
Masculino
Ligação Proteica
Ratos
Ratos Endogâmicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (High Mobility Group Proteins); 0 (Histones); 6098-44-8 (Acetoxyacetylaminofluorene); 9007-49-2 (DNA); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:0607
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050609
[St] Status:MEDLINE


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[PMID]:15828769
[Au] Autor:Flarakos J; Xiong W; Glick J; Vouros P
[Ad] Endereço:Barnett Institute and Department of Chemistry and Chemical Biology, Northeastern University, Boston, Massachusetts 02115, USA.
[Ti] Título:A deoxynucleotide derivatization methodology for improving LC-ESI-MS detection.
[So] Source:Anal Chem;77(8):2373-80, 2005 Apr 15.
[Is] ISSN:0003-2700
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have developed a novel LC-UV-MS derivatization method for the analysis of deoxyguanosine monophosphate adducts that demonstrates enhanced signal intensities relative to underivatized analytes in positive ion mode electrospray ionization MS. Detection of DNA nucleotide adducts is normally conducted in negative ion mode, which requires basic mobile phases that make chromatographic separations difficult and reduce MS sensitivity. Utilizing coupling reagents typically employed in peptide synthesis, several different deoxyguanosine nucleotide phosphoramidates and phosphomonoesters were synthesized in high conversion yield and under mild reaction conditions. The derivatives were characterized by MS/MS and reaction conversion yields determined from the DAD-UV traces. The derivatives were evaluated for ionization efficiencies, fragmentation patterns, and reversed-phase chromatographic properties by LC/ESI-MS/MS. Overall, the hydrophobic derivatives showed increases in ionization efficiency and improved peak shape. Rank ordering of the derivatizing agents was initially established using the dGp-modified derivatives. The best derivatizing agent, hexamethyleneimine, showed a 3-4-fold signal enhancement compared to underivatized dGp and was selected for additional evaluation. A model system using the carcinogen, N-acetoxy-2-acetylaminofluorene (AAAF), was used to synthesize a N-acetyl-(2-aminofluorenyl)-guanosine 5'-monophosphate (dGpAAF) adduct, which was subsequently derivatized with hexamethyleneimine. Detection limits for dGphex and dGpAAFhex, purified by HPLC, were 10- and 3-fold higher (S/N) than their respective underivatized analogues. Practical applicability, with similar improvements in sensitivity, was established by derivatizing adducts isolated from calf thymus DNA exposed to AAAF. Our results demonstrate the utility of simple reactions for the enhanced detection of a mononucleotide in positive ion mode ESI MS and the application of this technique for the detection of dGp-DNA adducts at the low-femtomole level.
[Mh] Termos MeSH primário: Cromatografia Líquida de Alta Pressão/métodos
Adutos de DNA/análise
Desoxiguanosina/química
Espectrometria de Massas por Ionização por Electrospray/métodos
[Mh] Termos MeSH secundário: Acetoxiacetilaminofluoreno/toxicidade
Animais
Carcinógenos/toxicidade
Bovinos
Adutos de DNA/efeitos dos fármacos
Sensibilidade e Especificidade
Timo/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Carcinogens); 0 (DNA Adducts); 6098-44-8 (Acetoxyacetylaminofluorene); G9481N71RO (Deoxyguanosine)
[Em] Mês de entrada:0703
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050415
[St] Status:MEDLINE


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[PMID]:15380103
[Au] Autor:Iwamoto TA; Kobayashi N; Imoto K; Yamamoto A; Nakamura Y; Yamauchi Y; Okumura H; Tanaka A; Hanaoka F; Shibutani S; Miyagawa S; Mori T
[Ad] Endereço:Radioisotope Research Center, Department of Dermatology, Nara Medical University, Kashihara, Nara 634-8521, Japan.
[Ti] Título:In situ detection of acetylaminofluorene-DNA adducts in human cells using monoclonal antibodies.
[So] Source:DNA Repair (Amst);3(11):1475-82, 2004 Nov 02.
[Is] ISSN:1568-7864
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The present study was performed to generate monoclonal antibodies capable of detecting N-acetoxy-2-acetylaminofluorene (NA-AAF)-derived DNA adducts in human cells in situ. As an immunogen, we employed NA-AAF-modified single-stranded DNA coupled electrostatically to methylated protein and we produced five different monoclonal antibodies. All of them showed strong binding to NA-AAF-modified DNA, but had undetectable or minimal binding to undamaged DNA. Competitive inhibition experiments revealed that the epitope recognized by these antibodies is N-(deoxyguanosin-8-yl)-2-acetylaminofluorene (dG-C8-AAF) in DNA, although deacetylated N-(deoxyguanosin-8-yl)-2-aminofluorene in DNA is also recognized with slightly less efficiency. In contrast, these antibodies did not bind to 3-(deoxyguanosin-N(2)-yl)-2-acetylaminofluorene in DNA or to UV-induced lesions in DNA. Interestingly, they showed only minimal binding to small AAF-nucleoside adducts (dG-C8-AAF), indicating that DNA regions flanking a DNA-bound adduct, in addition to the adduct itself, are essential for the stable binding of the antibodies. Using an enzyme-linked immunosorbent assay with the most promising antibody (AAF-1), we detected the concentration-dependent induction of NA-AAF-modified adducts in DNA from repair deficient xeroderma pigmentosum (XP) cells treated with physiological concentrations of NA-AAF. Moreover, the assay enabled to confirm that normal human cells efficiently repaired NA-AAF-induced DNA adducts but not XP-A cells. Most importantly, the formation of NA-AAF-induced DNA adducts in individual nuclei of XP cells could be clearly visualized using indirect immunofluorescence. Thus, we succeeded in establishing novel monoclonal antibodies capable of the in situ detection of NA-AAF-induced DNA adducts in human cells.
[Mh] Termos MeSH primário: Acetoxiacetilaminofluoreno/análise
Acetoxiacetilaminofluoreno/imunologia
Anticorpos Monoclonais
Adutos de DNA/análise
Adutos de DNA/imunologia
[Mh] Termos MeSH secundário: Animais
Bovinos
Linhagem Celular
Dano ao DNA
Reparo do DNA
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Hibridomas/imunologia
Camundongos
Microscopia de Fluorescência
Xeroderma Pigmentoso/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (DNA Adducts); 6098-44-8 (Acetoxyacetylaminofluorene)
[Em] Mês de entrada:0503
[Cu] Atualização por classe:071114
[Lr] Data última revisão:
071114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:040924
[St] Status:MEDLINE


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[PMID]:12888115
[Au] Autor:van Gijssel HE; Mullenders LH; van Oosterwijk MF; Meerman JH
[Ad] Endereço:Division of Toxicology, Leiden/Amsterdam Center for Drug Research, Leiden University, Leiden, The Netherlands.
[Ti] Título:Blockage of transcription as a trigger for p53 accumulation by 2-acetylaminofluorene DNA-adducts.
[So] Source:Life Sci;73(14):1759-71, 2003 Aug 22.
[Is] ISSN:0024-3205
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The hepatocarcinogen 2-acetylaminofluorene is one of the most studied experimental carcinogens. We have shown previously that normal rat hepatocytes accumulate the tumour suppressor p53 after exposure to this compound while preneoplastic rat hepatocytes do not. We suggested that the lack of p53 response may confer a growth advantage on preneoplastic hepatocytes and may be an important factor in hepatic tumor promotion by 2-acetylaminofluorene and other genotoxic compounds. Inhibition of RNA polymerase II driven transcription by DNA lesions may constitute one of the mechanisms leading to accumulation of the tumour suppressor p53. We have investigated the accumulation of p53 by structurally different DNA lesions of 2-acetylaminofluorene for which the rate of nucleotide excision repair (NER) and inhibition of transcription are known. Experiments were performed with NER proficient human fibroblasts as well as repair deficient xeroderma pigmentosum group A (XPA) cells, XPC cells [only transcription coupled repair (TCR)] and Cockayne syndrome (CS)B cells [only global genome repair (GGR)]. The cells were exposed to N-acetoxy-acetylaminofluorene (NAAAF) in the presence or absence of paraoxon inducing dG-C8-AAF or dG-C8-AF adducts respectively. Both treatments led to accumulation of p53 in all cells. However, dG-C8-AAF adducts produced greater p53 induction than dG-C8-AF adducts. The percentage p53-positive cells was highest and the threshold for p53 accumulation was lowest in XPA and CSB cells. Our results further demonstrate that both the potency of a lesion to inhibit transcription as well as the restoration of RNA synthesis determines the magnitude of p53 induction.
[Mh] Termos MeSH primário: Acetoxiacetilaminofluoreno/toxicidade
Adutos de DNA/metabolismo
Reparo do DNA
Transcrição Genética
Proteína Supressora de Tumor p53/biossíntese
[Mh] Termos MeSH secundário: Linhagem Celular
Síndrome de Cockayne/genética
Síndrome de Cockayne/metabolismo
Adutos de DNA/genética
Dano ao DNA
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Seres Humanos
Proteína Supressora de Tumor p53/genética
Xeroderma Pigmentoso/genética
Xeroderma Pigmentoso/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA Adducts); 0 (Tumor Suppressor Protein p53); 6098-44-8 (Acetoxyacetylaminofluorene)
[Em] Mês de entrada:0308
[Cu] Atualização por classe:051117
[Lr] Data última revisão:
051117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:030731
[St] Status:MEDLINE


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[PMID]:12815074
[Au] Autor:Ng JM; Vermeulen W; van der Horst GT; Bergink S; Sugasawa K; Vrieling H; Hoeijmakers JH
[Ad] Endereço:MGC-Department of Cell Biology & Genetics, Centre for Biomedical Genetics, Erasmus Medical Center, Rotterdam, The Netherlands.
[Ti] Título:A novel regulation mechanism of DNA repair by damage-induced and RAD23-dependent stabilization of xeroderma pigmentosum group C protein.
[So] Source:Genes Dev;17(13):1630-45, 2003 Jul 01.
[Is] ISSN:0890-9369
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Primary DNA damage sensing in mammalian global genome nucleotide excision repair (GG-NER) is performed by the xeroderma pigmentosum group C (XPC)/HR23B protein complex. HR23B and HR23A are human homologs of the yeast ubiquitin-domain repair factor RAD23, the function of which is unknown. Knockout mice revealed that mHR23A and mHR23B have a fully redundant role in NER, and a partially redundant function in embryonic development. Inactivation of both genes causes embryonic lethality, but appeared still compatible with cellular viability. Analysis of mHR23A/B double-mutant cells showed that HR23 proteins function in NER by governing XPC stability via partial protection against proteasomal degradation. Interestingly, NER-type DNA damage further stabilizes XPC and thereby enhances repair. These findings resolve the primary function of RAD23 in repair and reveal a novel DNA-damage-dependent regulation mechanism of DNA repair in eukaryotes, which may be part of a more global damage-response circuitry.
[Mh] Termos MeSH primário: Dano ao DNA
Reparo do DNA
Proteínas de Ligação a DNA/metabolismo
[Mh] Termos MeSH secundário: Acetoxiacetilaminofluoreno/farmacologia
Animais
Linhagem Celular
Cisteína Endopeptidases/metabolismo
Enzimas Reparadoras do DNA
Proteínas de Ligação a DNA/genética
Feminino
Marcação de Genes
Temperatura Alta
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Complexos Multienzimáticos/metabolismo
Complexo de Endopeptidases do Proteassoma
Proteínas Recombinantes de Fusão/metabolismo
Transcrição Genética/efeitos dos fármacos
Transcrição Genética/efeitos da radiação
Transfecção
Ubiquitina/metabolismo
Raios Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Multienzyme Complexes); 0 (RAD23B protein, human); 0 (Rad23a protein, mouse); 0 (Rad23b protein, mouse); 0 (Recombinant Fusion Proteins); 0 (Ubiquitin); 0 (Xpc protein, mouse); 156533-33-4 (RAD23A protein, human); 156533-34-5 (XPC protein, human); 6098-44-8 (Acetoxyacetylaminofluorene); EC 3.4.22.- (Cysteine Endopeptidases); EC 3.4.25.1 (Proteasome Endopeptidase Complex); EC 6.5.1.- (DNA Repair Enzymes)
[Em] Mês de entrada:0307
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:030620
[St] Status:MEDLINE



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