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[PMID]:29220449
[Au] Autor:Choi JA; Wyrick JJ
[Ad] Endereço:School of Molecular Biosciences.
[Ti] Título:RegulatorDB: a resource for the analysis of yeast transcriptional regulation.
[So] Source:Database (Oxford);2017, 2017 Jan 01.
[Is] ISSN:1758-0463
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Database URL: http://wyrickbioinfo2.smb.wsu.edu/RegulatorDB.
[Mh] Termos MeSH primário: DNA Fúngico
Proteínas de Ligação a DNA
Bases de Dados Genéticas
Proteínas Fúngicas
Regulação Fúngica da Expressão Gênica/genética
Saccharomyces cerevisiae
[Mh] Termos MeSH secundário: Sítios de Ligação
DNA Fúngico/genética
DNA Fúngico/metabolismo
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Proteínas Fúngicas/genética
Proteínas Fúngicas/metabolismo
Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Fungal); 0 (DNA-Binding Proteins); 0 (Fungal Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE
[do] DOI:10.1093/database/bax058


  2 / 139316 MEDLINE  
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[PMID]:29205966
[Au] Autor:Deng XD; Zhang W; Zhang B; Ma Y; Muer CE; Zhang LX; Xie Y; Liu Y
[Ad] Endereço:Department of Forensic Medicine, North Sichuan Medical College, Nanchong 637000, China.
[Ti] Título:[Expression of XPG Gene in Forensic Age Estimation].
[So] Source:Fa Yi Xue Za Zhi;32(6):415-419, 2016 Dec.
[Is] ISSN:1004-5619
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVES: To explore the expression of xeroderma pigmentosum complementation group G ( ) gene in healthy Han population of different ages and to analysis the relationship between the mRNA and protein expression levels of XPG and age, which may provide a new molecular-biological indicator for forensic age determination. METHODS: Total 150 samples of peripheral blood were collected from healthy Han population of different ages. Total RNA of peripheral blood mononuclear cell (PBMC) were extracted by TRIzol method, and the relative expression of mRNA in PBMC was detected by quantitative real-time PCR, and the protein expression levels of XPG in plasma were detected by ELISA. RESULTS: The mRNA and protein expression levels of XPG in ≤18 years old group were significantly different from 19-45 years old group and ≥46 years old group ( <0.05), while there was no significant difference between 19-45 years old group and ≥46 years old group ( >0.05). No significant sex differences were observed in mRNA and protein expression levels of XPG ( >0.05). CONCLUSIONS: The relative expression level of mRNA in PBMC declines with the increase of age in younger age, while the protein expression level in plasma increases with age, and gene can be used as one of new markers for forensic age estimation.
[Mh] Termos MeSH primário: Fatores Etários
Proteínas de Ligação a DNA/genética
Endonucleases/genética
Proteínas Nucleares/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Adulto
Grupo com Ancestrais do Continente Asiático
Genética Forense
Seres Humanos
Leucócitos Mononucleares
Meia-Idade
RNA Mensageiro
Reação em Cadeia da Polimerase em Tempo Real
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA excision repair protein ERCC-5); 0 (DNA-Binding Proteins); 0 (Nuclear Proteins); 0 (RNA, Messenger); 0 (Transcription Factors); EC 3.1.- (Endonucleases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.3969/j.issn.1004-5619.2016.06.005


  3 / 139316 MEDLINE  
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[PMID]:29178831
[Au] Autor:Myschyshyn M; Farren-Dai M; Chuang TJ; Vocadlo D
[Ad] Endereço:Department of Molecular Biology and Biochemistry, 8888 University Drive, Burnaby, BC, V5A 1S6, Canada. mmyschyshyn@gmail.com.
[Ti] Título:Software for rapid time dependent ChIP-sequencing analysis (TDCA).
[So] Source:BMC Bioinformatics;18(1):521, 2017 Nov 25.
[Is] ISSN:1471-2105
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) and associated methods are widely used to define the genome wide distribution of chromatin associated proteins, post-translational epigenetic marks, and modifications found on DNA bases. An area of emerging interest is to study time dependent changes in the distribution of such proteins and marks by using serial ChIP-seq experiments performed in a time resolved manner. Despite such time resolved studies becoming increasingly common, software to facilitate analysis of such data in a robust automated manner is limited. RESULTS: We have designed software called Time-Dependent ChIP-Sequencing Analyser (TDCA), which is the first program to automate analysis of time-dependent ChIP-seq data by fitting to sigmoidal curves. We provide users with guidance for experimental design of TDCA for modeling of time course (TC) ChIP-seq data using two simulated data sets. Furthermore, we demonstrate that this fitting strategy is widely applicable by showing that automated analysis of three previously published TC data sets accurately recapitulates key findings reported in these studies. Using each of these data sets, we highlight how biologically relevant findings can be readily obtained by exploiting TDCA to yield intuitive parameters that describe behavior at either a single locus or sets of loci. TDCA enables customizable analysis of user input aligned DNA sequencing data, coupled with graphical outputs in the form of publication-ready figures that describe behavior at either individual loci or sets of loci sharing common traits defined by the user. TDCA accepts sequencing data as standard binary alignment map (BAM) files and loci of interest in browser extensible data (BED) file format. CONCLUSIONS: TDCA accurately models the number of sequencing reads, or coverage, at loci from TC ChIP-seq studies or conceptually related TC sequencing experiments. TC experiments are reduced to intuitive parametric values that facilitate biologically relevant data analysis, and the uncovering of variations in the time-dependent behavior of chromatin. TDCA automates the analysis of TC ChIP-seq experiments, permitting researchers to easily obtain raw and modeled data for specific loci or groups of loci with similar behavior while also enhancing consistency of data analysis of TC data within the genomics field.
[Mh] Termos MeSH primário: Imunoprecipitação da Cromatina/métodos
Sequenciamento de Nucleotídeos em Larga Escala/métodos
Software
[Mh] Termos MeSH secundário: Algoritmos
Animais
Linhagem Celular
Cromossomos/química
Cromossomos/metabolismo
DNA/química
DNA/isolamento & purificação
DNA/metabolismo
Proteínas de Ligação a DNA/química
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Histonas/química
Histonas/genética
Histonas/metabolismo
Seres Humanos
Saccharomyces cerevisiae/metabolismo
Proteínas de Saccharomyces cerevisiae/química
Proteínas de Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/metabolismo
Análise de Sequência de DNA
Fatores de Transcrição/química
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABF1 protein, S cerevisiae); 0 (DNA-Binding Proteins); 0 (Histones); 0 (Saccharomyces cerevisiae Proteins); 0 (Transcription Factors); 9007-49-2 (DNA)
[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:171128
[St] Status:MEDLINE
[do] DOI:10.1186/s12859-017-1936-x


  4 / 139316 MEDLINE  
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[PMID]:29178651
[Au] Autor:Laurino MY; Truitt AR; Tenney L; Fisher D; Lindor NM; Veenstra D; Jarvik GP; Newcomb PA; Fullerton SM
[Ad] Endereço:Cancer Prevention Program, Seattle Cancer Care Alliance, Seattle, Washington, USA.
[Ti] Título:Clinical verification of genetic results returned to research participants: findings from a Colon Cancer Family Registry.
[So] Source:Mol Genet Genomic Med;5(6):700-708, 2017 11.
[Is] ISSN:2324-9269
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The extent to which participants act to clinically verify research results is largely unknown. This study examined whether participants who received Lynch syndrome (LS)-related findings pursued researchers' recommendation to clinically verify results with testing performed by a CLIA-certified laboratory. METHODS: The Fred Hutchinson Cancer Research Center site of the multinational Colon Cancer Family Registry offered non-CLIA individual genetic research results to select registry participants (cases and their enrolled relatives) from 2011 to 2013. Participants who elected to receive results were counseled on the importance of verifying results at a CLIA-certified laboratory. Twenty-six (76.5%) of the 34 participants who received genetic results completed 2- and 12-month postdisclosure surveys; 42.3% of these (11/26) participated in a semistructured follow-up interview. RESULTS: Within 12 months of result disclosure, only 4 (15.4%) of 26 participants reported having verified their results in a CLIA-certified laboratory; of these four cases, all research and clinical results were concordant. Reasons for pursuing clinical verification included acting on the recommendation of the research team and informing future clinical care. Those who did not verify results cited lack of insurance coverage and limited perceived personal benefit of clinical verification as reasons for inaction. CONCLUSION: These findings suggest researchers will need to address barriers to seeking clinical verification in order to ensure that the intended benefits of returning genetic research results are realized.
[Mh] Termos MeSH primário: Neoplasias Colorretais Hereditárias sem Polipose/diagnóstico
Testes Genéticos
[Mh] Termos MeSH secundário: Adulto
Idoso
Neoplasias Colorretais Hereditárias sem Polipose/genética
Neoplasias Colorretais Hereditárias sem Polipose/psicologia
Proteínas de Ligação a DNA/genética
Família
Feminino
Pesquisa em Genética
Testes Genéticos/normas
Seres Humanos
Cobertura do Seguro
Laboratórios/normas
Masculino
Meia-Idade
Endonuclease PMS2 de Reparo de Erro de Pareamento/genética
Proteína 1 Homóloga a MutL/genética
Proteína 2 Homóloga a MutS/genética
Sistema de Registros
Inquéritos e Questionários
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (MLH1 protein, human); 0 (Msh6 protein, mouse); EC 3.6.1.- (PMS2 protein, human); EC 3.6.1.3 (MSH2 protein, human); EC 3.6.1.3 (Mismatch Repair Endonuclease PMS2); EC 3.6.1.3 (MutL Protein Homolog 1); EC 3.6.1.3 (MutS Homolog 2 Protein)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1002/mgg3.328


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[PMID]:28452714
[Au] Autor:Li D; Palanca AMS; Won SY; Gao L; Feng Y; Vashisht AA; Liu L; Zhao Y; Liu X; Wu X; Li S; Le B; Kim YJ; Yang G; Li S; Liu J; Wohlschlegel JA; Guo H; Mo B; Chen X; Law JA
[Ad] Endereço:Department of Botany and Plant Sciences, Institute of Integrative Genome Biology, University of California, Riverside, United States.
[Ti] Título:The MBD7 complex promotes expression of methylated transgenes without significantly altering their methylation status.
[So] Source:Elife;6, 2017 04 28.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:DNA methylation is associated with gene silencing in eukaryotic organisms. Although pathways controlling the establishment, maintenance and removal of DNA methylation are known, relatively little is understood about how DNA methylation influences gene expression. Here we identified a METHYL-CpG-BINDING DOMAIN 7 (MBD7) complex in that suppresses the transcriptional silencing of two ( reporters via a mechanism that is largely downstream of DNA methylation. Although mutations in components of the MBD7 complex resulted in modest increases in DNA methylation concomitant with decreased expression, we found that these hyper-methylation and gene expression phenotypes can be genetically uncoupled. This finding, along with genome-wide profiling experiments showing minimal changes in DNA methylation upon disruption of the MBD7 complex, places the MBD7 complex amongst a small number of factors acting downstream of DNA methylation. This complex, however, is unique as it functions to suppress, rather than enforce, DNA methylation-mediated gene silencing.
[Mh] Termos MeSH primário: Arabidopsis
Metilação de DNA
Proteínas de Ligação a DNA/metabolismo
Regulação da Expressão Gênica de Plantas
Proteínas de Plantas/metabolismo
[Mh] Termos MeSH secundário: Genes Reporter
Luciferases/análise
Transgenes
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Plant Proteins); EC 1.13.12.- (Luciferases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


  6 / 139316 MEDLINE  
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[PMID]:27778395
[Au] Autor:Michailidou I; Naessens DM; Hametner S; Guldenaar W; Kooi EJ; Geurts JJ; Baas F; Lassmann H; Ramaglia V
[Ad] Endereço:Department of Genome Analysis, Academic Medical Center, Meibergdreef 9, Amsterdam, 1105, The Netherlands.
[Ti] Título:Complement C3 on microglial clusters in multiple sclerosis occur in chronic but not acute disease: Implication for disease pathogenesis.
[So] Source:Glia;65(2):264-277, 2017 02.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microglial clusters with C3d deposits are observed in the periplaque of multiple sclerosis (MS) brains and were proposed as early stage of lesion formation. As such they should appear in the brain of MS donors with acute disease but thus far this has not been shown. Using postmortem brain tissue from acute (n = 10) and chronic (n = 15) MS cases we investigated whether C3d+ microglial clusters are part of an acute attack against myelinated axons, which could have implications for disease pathogenesis. The specificity of our findings to MS was tested in ischemic stroke cases (n = 8) with initial or advanced lesions and further analyzed in experimental traumatic brain injury (TBI, n = 26), as both conditions are primarily nondemyelinating but share essential features of neurodegeneration with MS lesions. C3d+ microglial clusters were found in chronic but not acute MS. They were not associated with antibody deposits or terminal complement activation. They were linked to slowly expanding lesions, localized on axons with impaired transport and associated with neuronal C3 production. C3d+ microglial clusters were not specific to MS as they were also found in stroke and experimental TBI. We conclude that C3d+ microglial clusters in MS are not part of an acute attack against myelinated axons. As such it is unlikely that they drive formation of new lesions but could represent a physiological mechanism to remove irreversibly damaged axons in chronic disease. GLIA 2017;65:264-277.
[Mh] Termos MeSH primário: Complemento C3/metabolismo
Microglia/metabolismo
Esclerose Múltipla/patologia
[Mh] Termos MeSH secundário: Doença Aguda
Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Autopsia
Doença Crônica
Complemento C3/genética
Citocinas/metabolismo
Proteínas de Ligação a DNA/metabolismo
Modelos Animais de Doenças
Feminino
Traumatismos Cranianos Fechados/patologia
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Meia-Idade
Proteínas da Mielina/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Neurônios/patologia
Acidente Vascular Cerebral/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AIF1 protein, human); 0 (C3 protein, human); 0 (Complement C3); 0 (Cytokines); 0 (DNA-Binding Proteins); 0 (Myelin Proteins); 0 (Nerve Tissue Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23090


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[PMID]:29307819
[Au] Autor:Kong L; Murata MM; Digman MA
[Ad] Endereço:Laboratory for Fluorescence Dynamics, Department of Biomedical Engineering, University of California, Irvine, CA 92697, USA; University High School, Irvine, CA 92612, USA.
[Ti] Título:Absence of REV3L promotes p53-regulated cancer cell metabolism in cisplatin-treated lung carcinoma cells.
[So] Source:Biochem Biophys Res Commun;496(1):199-204, 2018 01 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lung cancer is one of the deadliest cancers in the world because of chemo-resistance to the commonly used cisplatin-based treatments. The use of low fidelity DNA polymerases in the translesional synthesis (TLS) DNA damage response pathway that repairs lesions caused by cisplatin also presents a mutational carcinogenic burden on cells that needs to be regulated by the tumor suppressor protein p53. However, there is much debate over the roles of the reversionless 3-like (REV3L) protein responsible for TLS and p53 in regulating cancer cell metabolism. In this study, the fluorescence lifetime of the metabolic coenzyme NADH reveals that the absence of REV3L can promote the p53-mediated upregulation of oxidative phosphorylation in cisplatin-treated H1299 lung carcinoma cells and increases cancer cell sensitivity to this platinum-based chemotherapy. These results demonstrate a previously unrecognized relationship between p53 and REV3L in cancer cell metabolism and may lead to improvements in chemotherapy treatment plans that reduce cisplatin resistance in lung cancer.
[Mh] Termos MeSH primário: Cisplatino/administração & dosagem
Proteínas de Ligação a DNA/metabolismo
DNA Polimerase Dirigida por DNA/metabolismo
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos/administração & dosagem
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Proteínas de Ligação a DNA/genética
DNA Polimerase Dirigida por DNA/genética
Relação Dose-Resposta a Droga
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Inativação Gênica
Seres Humanos
Neoplasias Pulmonares/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (DNA-Binding Proteins); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); EC 2.7.7.7 (DNA-Directed DNA Polymerase); EC 2.7.7.7 (REV3L protein, human); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180303
[Lr] Data última revisão:
180303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE


  8 / 139316 MEDLINE  
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[PMID]:27771340
[Au] Autor:Ambrosini A; Gracia M; Proag A; Rayer M; Monier B; Suzanne M
[Ad] Endereço:LBCMCP UMR5088, Centre de Biologie Integrative (CBI), Université de Toulouse, CNRS, UPS, France.
[Ti] Título:Apoptotic forces in tissue morphogenesis.
[So] Source:Mech Dev;144(Pt A):33-42, 2017 04.
[Is] ISSN:1872-6356
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:It is now well established that apoptosis is induced in response to mechanical strain. Indeed, increasing compressive forces induces apoptosis in confined spheroids of tumour cells, whereas releasing stress reduces apoptosis in spheroids cultivated in free suspension (Cheng et al., 2009). Apoptosis can also be induced by applying a 100 to 250MPa pressure, as shown in different cultured cells (for review, see (Frey et al., 2008)). During epithelium development, the pressure caused by a fast-growing clone can trigger apoptosis at the vicinity of the clone, mediating mechanical cell competition (Levayer et al., 2016). While the effect of strain has long been known for its role in apoptosis induction, the reciprocal mechanism has only recently been highlighted. First demonstrated at the cellular level, the effect of an apoptotic cell on its direct neighbours has been analysed in different kinds of monolayer epithelium (Gu et al., 2011; Rosenblatt et al., 2001; Kuipers et al., 2014; Lubkov & Bar-Sagi, 2014). More recently, the concept of a broader impact of apoptotic cell behaviours on tissue mechanical strain has emerged from the characterisation of tissue remodelling during Drosophila development (Toyama et al., 2008; Monier et al., 2015). In the present review, we summarize our current knowledge on the mechanical impact of apoptosis during tissue remodelling.
[Mh] Termos MeSH primário: Apoptose/genética
Drosophila melanogaster/crescimento & desenvolvimento
Células Epiteliais/citologia
Regulação da Expressão Gênica no Desenvolvimento
Morfogênese/genética
[Mh] Termos MeSH secundário: Abdome/crescimento & desenvolvimento
Animais
Divisão Celular
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Proteínas de Drosophila/genética
Proteínas de Drosophila/metabolismo
Drosophila melanogaster/genética
Drosophila melanogaster/metabolismo
Células Epiteliais/metabolismo
Matriz Extracelular/metabolismo
Larva/genética
Larva/crescimento & desenvolvimento
Larva/metabolismo
Modelos Biológicos
Pupa/genética
Pupa/crescimento & desenvolvimento
Pupa/metabolismo
Estresse Mecânico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Drosophila Proteins); 0 (dwg protein, Drosophila); 0 (reaper protein, Drosophila)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  9 / 139316 MEDLINE  
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[PMID]:29367528
[Au] Autor:Oshima S
[Ad] Endereço:Department of Gastroenterology and Hepatology, Tokyo Medical and Dental University (TMDU).
[Ti] Título:[Autoimmune diseases and ubiquitin system].
[So] Source:Nihon Rinsho Meneki Gakkai Kaishi;40(6):442-449, 2017.
[Is] ISSN:1349-7413
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:  Cytokines play important roles in the pathogenesis of autoimmune diseases. Anti-TNFα antibody therapy for rheumatoid arthritis, Crohn's disease, and psoriasis has made enough progress to change its treatment goal. This review focuses on the recent advances that have been made in understanding TNFR signaling through ubiquitin system. Genome-wide association studies (GWAS) identified numerous susceptibility loci associated with autoimmune diseases. Ubiquitin related genes TNFAIP3 and TNIP1 have been linked to multiple autoimmune diseases. Here, we review the importance of TNFAIP3 and TNIP1-mediated regulation of ubiquitin-dependent signaling. To monitor the dynamics of ubiquitin chain formation in vivo, we have developed a polyubiquitin-mediated fluorescence complementation (PolyUb-FC) assay. The PolyUb-FC assay has the advantage that monoubiquitination is non-fluorescent and chain-specific poly-ubiquitination can be directly visualized in living cells without using antibodies. The PolyUb-FC will be a useful tool for analyzing the dynamics of polyubiquitin chain generation.
[Mh] Termos MeSH primário: Doenças Autoimunes/etiologia
Ubiquitina/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/uso terapêutico
Doenças Autoimunes/tratamento farmacológico
Doenças Autoimunes/genética
Proteínas de Ligação a DNA/fisiologia
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Seres Humanos
Camundongos
Imagem Molecular/métodos
Transdução de Sinais/genética
Proteína 3 Induzida por Fator de Necrose Tumoral alfa/fisiologia
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (DNA-Binding Proteins); 0 (TNIP1 protein, human); 0 (Tumor Necrosis Factor-alpha); 0 (Ubiquitin); EC 3.4.19.12 (TNFAIP3 protein, human); EC 3.4.19.12 (Tumor Necrosis Factor alpha-Induced Protein 3)
[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:180126
[St] Status:MEDLINE
[do] DOI:10.2177/jsci.40.442


  10 / 139316 MEDLINE  
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[PMID]:29267285
[Au] Autor:Colombo DF; Burger L; Baubec T; Schübeler D
[Ad] Endereço:Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
[Ti] Título:Binding of high mobility group A proteins to the mammalian genome occurs as a function of AT-content.
[So] Source:PLoS Genet;13(12):e1007102, 2017 12.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genomic location can inform on potential function and recruitment signals for chromatin-associated proteins. High mobility group (Hmg) proteins are of similar size as histones with Hmga1 and Hmga2 being particularly abundant in replicating normal tissues and in cancerous cells. While several roles for Hmga proteins have been proposed we lack a comprehensive description of their genomic location as a function of chromatin, DNA sequence and functional domains. Here we report such a characterization in mouse embryonic stem cells in which we introduce biotin-tagged constructs of wild-type and DNA-binding domain mutants. Comparative analysis of the genome-wide distribution of Hmga proteins reveals pervasive binding, a feature that critically depends on a functional DNA-binding domain and which is shared by both Hmga proteins. Assessment of the underlying queues instructive for this binding modality identifies AT richness, defined as high frequency of A or T bases, as the major criterion for local binding. Additionally, we show that other chromatin states such as those linked to cis-regulatory regions have little impact on Hmga binding both in stem and differentiated cells. As a consequence, Hmga proteins are preferentially found at AT-rich regions such as constitutively heterochromatic regions but are absent from enhancers and promoters arguing for a limited role in regulating individual genes. In line with this model, we show that genetic deletion of Hmga proteins in stem cells causes limited transcriptional effects and that binding is conserved in neuronal progenitors. Overall our comparative study describing the in vivo binding modality of Hmga1 and Hmga2 identifies the proteins' preference for AT-rich DNA genome-wide and argues against a suggested function of Hmga at regulatory regions. Instead we discover pervasive binding with enrichment at regions of higher AT content irrespective of local variation in chromatin modifications.
[Mh] Termos MeSH primário: Sequência Rica em At
Proteínas de Grupo de Alta Mobilidade/genética
Proteínas de Grupo de Alta Mobilidade/metabolismo
[Mh] Termos MeSH secundário: Animais
Composição de Bases
Sequência de Bases
Cromatina/genética
Cromatina/metabolismo
DNA/química
DNA/genética
DNA/metabolismo
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Células-Tronco Embrionárias/metabolismo
Histonas/genética
Camundongos
Camundongos Endogâmicos C57BL
Regiões Promotoras Genéticas
Ligação Proteica
Sequências Reguladoras de Ácido Nucleico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chromatin); 0 (DNA-Binding Proteins); 0 (High Mobility Group Proteins); 0 (Histones); 9007-49-2 (DNA)
[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:171222
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007102



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