Base de dados : MEDLINE
Pesquisa : A11.872 [Categoria DeCS]
Referências encontradas : 52238 [refinar]
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[PMID]:28455696
[Au] Autor:Mentis AA; Dardiotis E; Grigoriadis N; Petinaki E; Hadjigeorgiou GM
[Ad] Endereço:Department of Microbiology, University Hospital of Larissa, University of Thessaly, Larissa, Greece. amentis1@jhu.edu.
[Ti] Título:Viruses and Multiple Sclerosis: From Mechanisms and Pathways to Translational Research Opportunities.
[So] Source:Mol Neurobiol;54(5):3911-3923, 2017 Jul.
[Is] ISSN:1559-1182
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Viruses are directly or indirectly implicated in multiple sclerosis (MS). Here, we review the evidence on the virus-related pathophysiology of MS, introduce common experimental models, and explore the ways in which viruses cause demyelination. By emphasizing knowledge gaps, we highlight future research directions for effective MS diagnostics and therapies: (i) identifying biomarkers for at-risk individuals, (ii) searching for direct evidence of specific causative viruses, (iii) establishing the contribution of host genetic factors and viruses, and (iv) investigating the contribution of immune regulation at extra-CNS sites. Research in these areas is likely to be facilitated by the application of high-throughput technologies, the development of systems-based bioinformatic approaches, careful selection of experimental models, and the acquisition of high-quality clinical material for tissue-based research.
[Mh] Termos MeSH primário: Esclerose Múltipla/virologia
Pesquisa Médica Translacional
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Progressão da Doença
Seres Humanos
Modelos Biológicos
Esclerose Múltipla/patologia
Esclerose Múltipla/fisiopatologia
Células-Tronco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[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:170430
[St] Status:MEDLINE
[do] DOI:10.1007/s12035-017-0530-6


  2 / 52238 MEDLINE  
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[PMID]:29282749
[Au] Autor:Hou L; Wang J; Wang Y; Hua X; Wu J
[Ad] Endereço:Renji Hospital, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), School of Medicine, Bio-X Institutes, Shanghai Jiao Tong University, Shanghai, China.
[Ti] Título:Compared proteomic analysis of 8- and 32-week-old postnatal porcine ovaries.
[So] Source:Cell Biochem Funct;36(1):34-42, 2018 Jan.
[Is] ISSN:1099-0844
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pigs share many anatomical and physiological features with humans, offering a unique and viable model for biomedical research. Tandem mass tag method followed by mass spectrometry analysis was utilized to identify peptides (47,405), proteins (14,701), and protein groups (7634) in ovaries of 8- and 32-week-old postnatal Banna miniature pigs. After annotation and analysis by Kyoto Encyclopedia of Genes and Genomes pathway and Gene Ontology, the proteins were identified as being involved in hormone metabolic pathways and maintenance, proliferation, and regulation of stem cells. In addition, we found 638 differentially expressed proteins between ovaries of 8- and 32-week-old postnatal Banna miniature pigs. We used Interactive Pathway Explorer to produce an overview of pig ovarian proteomics. Compared with those of the 8-week-old group, the proteins enriched in metabolism of steroid hormones, metabolism of lipids, and energy metabolism pathway were upregulated in the 32-week-old group, indicating physiological characteristics of sexual maturity. These findings have implications in applications of biomedicine. SIGNIFICANCE OF THE STUDY: Pigs share many anatomical and physiological features with humans, offering a unique and viable model for biomedical research. In this study, we used tandem mass tag quantitative proteomics to describe, for the first time, protein expression patterns of postnatal pig ovaries. Proteins involved in hormone metabolic pathways and maintenance, proliferation, and regulation of stem cells were identified. With further analysis by Interactive Pathway Explorer, proteins enriched in metabolism of steroid hormones, metabolism of lipids, and energy metabolism pathway were upregulated in the 32-week-old group, indicating physiological characteristics of sexual maturity. These findings have implications in applications of biomedicine.
[Mh] Termos MeSH primário: Ovário/química
Peptídeos/análise
Proteínas/análise
Proteômica
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Cromatografia Líquida
Feminino
Espectrometria de Massas
Camundongos
Camundongos Nus
Ovário/metabolismo
Peptídeos/metabolismo
Proteínas/metabolismo
Células-Tronco/citologia
Células-Tronco/metabolismo
Suínos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peptides); 0 (Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171229
[St] Status:MEDLINE
[do] DOI:10.1002/cbf.3315


  3 / 52238 MEDLINE  
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[PMID]:29267673
[Au] Autor:Yan Y; Qi S; Gong SQ; Shang G; Zhao Y
[Ad] Endereço:Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Department of Pediatric Dentistry, Shanghai, China.
[Ti] Título:Effect of CRABP2 on the proliferation and odontoblastic differentiation of hDPSCs.
[So] Source:Braz Oral Res;31:e112, 2017 Dec 18.
[Is] ISSN:1807-3107
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Cellular retinoic acid-binding protein 2 (CRABP2) has been detected in several organs during embryonic development. Recent studies have demonstrated that CRABP2 plays important roles in the retinoic acid, ß-catenin and Notch signaling pathways, as well as in the interaction between epithelial and mesenchymal cells, which are important for human dental pulp stem cells (hDPSCs) and tooth development. In the present study, the expression of CRABP2 during mouse molar development and the role of CRABP2 in hDPSC odontoblastic differentiation were evaluated. CRABP2 was gradually decreased during the development of the first maxillary molar, which exhibited the same trend as the expression of CRABP2 during the odontoblastic induction of hDPSCs. CRABP2 knockdown inhibited the proliferative ability of hDPSCs, while it enhanced odontoblastic differentiation via promoting mineralization nodule formation and upregulating the activity of alkaline phosphatase and the expression of mineralization-related genes. The present study uncovered a novel function of CRABP2 in hDPSCs. Our data suggest that CRABP2 may act as a regulator during the proliferation and differentiation of hDPSCs.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Proliferação Celular/fisiologia
Polpa Dentária/citologia
Odontoblastos/fisiologia
Receptores do Ácido Retinoico/fisiologia
Células-Tronco/fisiologia
[Mh] Termos MeSH secundário: Fosfatase Alcalina
Análise de Variância
Animais
Antraquinonas
Western Blotting
Comunicação Celular
Células Cultivadas
Corantes
Regulação para Baixo/fisiologia
Feminino
Seres Humanos
Imuno-Histoquímica
Masculino
Camundongos Endogâmicos C57BL
Receptores do Ácido Retinoico/análise
Valores de Referência
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthraquinones); 0 (Coloring Agents); 0 (Receptors, Retinoic Acid); 0 (retinoic acid binding protein II, cellular); 60MEW57T9G (alizarin); EC 3.1.3.1 (Alkaline Phosphatase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


  4 / 52238 MEDLINE  
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[PMID]:29267658
[Au] Autor:Ferrúa CP; Centeno EGZ; Rosa LCD; Amaral CCD; Severo RF; Sarkis-Onofre R; Nascimento GG; Cordenonzi G; Bast RK; Demarco FF; Nedel F
[Ad] Endereço:Universidade Católica de Pelotas - UCPel, Program in Health and Behavior, Pelotas, RS, Brazil.
[Ti] Título:How has dental pulp stem cells isolation been conducted? A scoping review.
[So] Source:Braz Oral Res;31:e87, 2017 Dec 18.
[Is] ISSN:1807-3107
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:The objective of this study was to realize a scoping review the literature in order to identify the profile of DPSCs isolation and analyze the possible risk factors that could change the native behavior of these cells. An initial search was conducted using the following MeSH terms: "(dental pulp stem cell [MeSH])"; "(dental pulp [MeSH])" AND "(stem cell [MeSH])"; "("dental pulp stem cell" [MeSH]")". The electronic search was done without date restriction up to and including April 2014, in PubMed, Scopus, Scielo and ISI Web of Knowledge databases. Studies were submitted to inclusion and exclusion criteria and 222 articles were included. Data showed that over the past 15 years many studies have been conducted using DPSCs. However this is the first systematic review regarding the isolation of stem cell, and more specifically of dental pulp stem cells. The isolation of dental pulp stem cells showed great variability, hampering the development of standard protocols to achieve in vitro dental pulp stem cells with similar characteristics. This scoping review combined, for the first time, the methodologies used for dental pulp stem isolation, highlighting the most frequently used.
[Mh] Termos MeSH primário: Polpa Dentária/citologia
Células-Tronco/citologia
[Mh] Termos MeSH secundário: Técnicas de Cultura de Células
Colagenases
Meios de Cultura
Seres Humanos
Viés de Publicação
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Culture Media); EC 3.4.24.- (Collagenases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


  5 / 52238 MEDLINE  
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[PMID]:29382818
[Au] Autor:Sánchez-Iranzo H; Galardi-Castilla M; Minguillón C; Sanz-Morejón A; González-Rosa JM; Felker A; Ernst A; Guzmán-Martínez G; Mosimann C; Mercader N
[Ad] Endereço:Development of the Epicardium and Its Role during Regeneration Group, Centro Nacional de Investigaciones Cardiovasculares (CNIC-ISCIII), Melchor Fernández Almagro 3, 28029, Madrid, Spain.
[Ti] Título:Tbx5a lineage tracing shows cardiomyocyte plasticity during zebrafish heart regeneration.
[So] Source:Nat Commun;9(1):428, 2018 01 30.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:During development, mesodermal progenitors from the first heart field (FHF) form a primitive cardiac tube, to which progenitors from the second heart field (SHF) are added. The contribution of FHF and SHF progenitors to the adult zebrafish heart has not been studied to date. Here we find, using genetic tbx5a lineage tracing tools, that the ventricular myocardium in the adult zebrafish is mainly derived from tbx5a cells, with a small contribution from tbx5a SHF progenitors. Notably, ablation of ventricular tbx5a -derived cardiomyocytes in the embryo is compensated by expansion of SHF-derived cells. In the adult, tbx5a expression is restricted to the trabeculae and excluded from the outer cortical layer. tbx5a-lineage tracing revealed that trabecular cardiomyocytes can switch their fate and differentiate into cortical myocardium during adult heart regeneration. We conclude that a high degree of cardiomyocyte cell fate plasticity contributes to efficient regeneration.
[Mh] Termos MeSH primário: Ventrículos do Coração/citologia
Miocárdio/citologia
Miócitos Cardíacos/citologia
Regeneração/genética
Proteínas com Domínio T-Box/genética
Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Diferenciação Celular
Linhagem da Célula/genética
Rastreamento de Células
Embrião não Mamífero
Regulação da Expressão Gênica no Desenvolvimento
Genes Reporter
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Ventrículos do Coração/crescimento & desenvolvimento
Ventrículos do Coração/metabolismo
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Miocárdio/metabolismo
Miócitos Cardíacos/metabolismo
Cadeias Leves de Miosina/genética
Cadeias Leves de Miosina/metabolismo
Organogênese/genética
Células-Tronco/citologia
Células-Tronco/metabolismo
Proteínas com Domínio T-Box/deficiência
Peixe-Zebra/crescimento & desenvolvimento
Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Luminescent Proteins); 0 (Myosin Light Chains); 0 (T-Box Domain Proteins); 0 (T-box transcription factor 5); 0 (red fluorescent protein); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02650-6


  6 / 52238 MEDLINE  
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[PMID]:28464904
[Au] Autor:Bardeesi ASA; Gao J; Zhang K; Yu S; Wei M; Liu P; Huang H
[Ad] Endereço:Zhongshan Medical School, Sun Yat-sen University, Guangzhou, China.
[Ti] Título:A novel role of cellular interactions in vascular calcification.
[So] Source:J Transl Med;15(1):95, 2017 May 03.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A series of clinical trials have confirmed the correlation between vascular calcification (VC) and cardiovascular events and mortality. However, current treatments have little effects on the regression of VC. Potent and illustrative mechanisms have been proven to exist in both bone metabolism and VC, indicating that these two processes share similarities in onset and progression. Multiple osteoblast-like cells and signaling pathways are involved in the process of VC. In this review, we summarized the roles of different osteoblast-like cells and we emphasized on how they communicated and interacted with each other using different signaling pathways. Further studies are needed to uncover the underlying mechanisms and to provide novel therapies for VC.
[Mh] Termos MeSH primário: Comunicação Celular
Calcificação Vascular/patologia
[Mh] Termos MeSH secundário: Animais
Células Endoteliais/patologia
Seres Humanos
Osteoblastos/patologia
Transdução de Sinais
Células-Tronco/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[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:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12967-017-1190-z


  7 / 52238 MEDLINE  
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[PMID]:27771363
[Au] Autor:Decker RS
[Ad] Endereço:Translational Research Program in Pediatric Orthopaedics, Division of Orthopaedic Surgery, The Children's Hospital of Philadelphia, PA 19104, United States. Electronic address: RDecker@gnf.org.
[Ti] Título:Articular cartilage and joint development from embryogenesis to adulthood.
[So] Source:Semin Cell Dev Biol;62:50-56, 2017 02.
[Is] ISSN:1096-3634
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Within each synovial joint, the articular cartilage is uniquely adapted to bear dynamic compressive loads and shear forces throughout the joint's range of motion. Injury and age-related degeneration of the articular cartilage often lead to significant pain and disability, as the intrinsic repair capability of the tissue is extremely limited. Current surgical and biological treatment options have been unable to restore cartilage de novo. Before successful clinical cartilage restoration strategies can be developed, a better understanding of how the cartilage forms during normal development is essential. This review focuses on recent progress made towards addressing key questions about articular cartilage morphogenesis, including the origin of synovial joint progenitor cells, postnatal development and growth of the tissue. These advances have provided novel insight into fundamental questions about the developmental biology of articular cartilage, as well as potential cell sources that may participate in joint response to injury.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Cartilagem Articular/embriologia
Desenvolvimento Embrionário
Articulações/embriologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Morfogênese
Células-Tronco/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[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


  8 / 52238 MEDLINE  
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[PMID]:28461069
[Au] Autor:Shiryaev SA; Farhy C; Pinto A; Huang CT; Simonetti N; Elong Ngono A; Dewing A; Shresta S; Pinkerton AB; Cieplak P; Strongin AY; Terskikh AV
[Ad] Endereço:Sanford-Burnham-Prebys Medical Discovery Institute, Center for Neuroscience, Aging, and Stem Cell Research, La Jolla, CA 92037, United States.
[Ti] Título:Characterization of the Zika virus two-component NS2B-NS3 protease and structure-assisted identification of allosteric small-molecule antagonists.
[So] Source:Antiviral Res;143:218-229, 2017 07.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The recent re-emergence of Zika virus (ZIKV) , a member of the Flaviviridae family, has become a global emergency. Currently, there are no effective methods of preventing or treating ZIKV infection, which causes severe neuroimmunopathology and is particularly harmful to the developing fetuses of infected pregnant women. However, the pathology induced by ZIKV is unique among flaviviruses, and knowledge of the biology of other family members cannot easily be extrapolated to ZIKV. Thus, structure-function studies of ZIKV proteins are urgently needed to facilitate the development of effective preventative and therapeutic agents. Like other flaviviruses, ZIKV expresses an NS2B-NS3 protease, which consists of the NS2B cofactor and the NS3 protease domain and is essential for cleavage of the ZIKV polyprotein precursor and generation of fully functional viral proteins. Here, we report the enzymatic characterization of ZIKV protease, and we identify structural scaffolds for allosteric small-molecule inhibitors of this protease. Molecular modeling of the protease-inhibitor complexes suggests that these compounds bind to the druggable cavity in the NS2B-NS3 protease interface and affect productive interactions of the protease domain with its cofactor. The most potent compound demonstrated efficient inhibition of ZIKV propagation in vitro in human fetal neural progenitor cells and in vivo in SJL mice. The inhibitory scaffolds could be further developed into valuable research reagents and, ultimately, provide a roadmap for the selection of efficient inhibitors of ZIKV infection.
[Mh] Termos MeSH primário: Sítio Alostérico
Inibidores de Proteases/química
Inibidores de Proteases/farmacologia
Proteínas não Estruturais Virais/química
Zika virus/enzimologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Antivirais/antagonistas & inibidores
Antivirais/química
Sequência de Bases
Ativação Enzimática
Feminino
Flavivirus/química
Expressão Gênica
Seres Humanos
Concentração Inibidora 50
Camundongos
Modelos Moleculares
Ligação Proteica
Conformação Proteica
Domínios e Motivos de Interação entre Proteínas
RNA Helicases/química
RNA Helicases/efeitos dos fármacos
Fatores de Transcrição SOXB1/genética
Alinhamento de Sequência
Serina Endopeptidases/química
Serina Endopeptidases/efeitos dos fármacos
Células-Tronco
Proteínas não Estruturais Virais/efeitos dos fármacos
Proteínas Virais/química
Proteínas Virais/genética
Zika virus/química
Zika virus/genética
Zika virus/crescimento & desenvolvimento
Infecção pelo Zika virus/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (NS2B protein, flavivirus); 0 (NS3 protein, flavivirus); 0 (Protease Inhibitors); 0 (SOX2 protein, human); 0 (SOXB1 Transcription Factors); 0 (Viral Nonstructural Proteins); 0 (Viral Proteins); EC 3.4.21.- (Serine Endopeptidases); EC 3.6.4.13 (RNA Helicases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  9 / 52238 MEDLINE  
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[PMID]:28450738
[Au] Autor:Kim M; Costello J
[Ad] Endereço:Personalized Genomic Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Korea.
[Ti] Título:DNA methylation: an epigenetic mark of cellular memory.
[So] Source:Exp Mol Med;49(4):e322, 2017 04 28.
[Is] ISSN:2092-6413
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA methylation is a stable epigenetic mark that can be inherited through multiple cell divisions. During development and cell differentiation, DNA methylation is dynamic, but some DNA methylation patterns may be retained as a form of epigenetic memory. DNA methylation profiles can be useful for the lineage classification and quality control of stem cells such as embryonic stem cells, induced pluripotent cells and mesenchymal stem cells. During cancer initiation and progression, genome-wide and gene-specific DNA methylation changes occur as a consequence of mutated or deregulated chromatin regulators. Early aberrant DNA methylation states occurring during transformation appear to be retained during tumor evolution. Similarly, DNA methylation differences among different regions of a tumor reflect the history of cancer cells and their response to the tumor microenvironment. Therefore, DNA methylation can be a useful molecular marker for cancer diagnosis and drug treatment.
[Mh] Termos MeSH primário: Reprogramação Celular/genética
Metilação de DNA
Epigênese Genética
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Células-Tronco/citologia
Células-Tronco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180224
[Lr] Data última revisão:
180224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1038/emm.2017.10


  10 / 52238 MEDLINE  
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[PMID]:28450733
[Au] Autor:An J; Rao A; Ko M
[Ad] Endereço:Department of Biological Sciences, Chonbuk National University, Jeonju, Korea.
[Ti] Título:TET family dioxygenases and DNA demethylation in stem cells and cancers.
[So] Source:Exp Mol Med;49(4):e323, 2017 04 28.
[Is] ISSN:2092-6413
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The methylation of cytosine and subsequent oxidation constitutes a fundamental epigenetic modification in mammalian genomes, and its abnormalities are intimately coupled to various pathogenic processes including cancer development. Enzymes of the Ten-eleven translocation (TET) family catalyze the stepwise oxidation of 5-methylcytosine in DNA to 5-hydroxymethylcytosine and further oxidation products. These oxidized 5-methylcytosine derivatives represent intermediates in the reversal of cytosine methylation, and also serve as stable epigenetic modifications that exert distinctive regulatory roles. It is becoming increasingly obvious that TET proteins and their catalytic products are key regulators of embryonic development, stem cell functions and lineage specification. Over the past several years, the function of TET proteins as a barrier between normal and malignant states has been extensively investigated. Dysregulation of TET protein expression or function is commonly observed in a wide range of cancers. Notably, TET loss-of-function is causally related to the onset and progression of hematologic malignancy in vivo. In this review, we focus on recent advances in the mechanistic understanding of DNA methylation-demethylation dynamics, and their potential regulatory functions in cellular differentiation and oncogenic transformation.
[Mh] Termos MeSH primário: Metilação de DNA
Oxigenases de Função Mista/metabolismo
Neoplasias/genética
Proteínas Proto-Oncogênicas/metabolismo
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Epigênese Genética
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Oxigenases de Função Mista/genética
Neoplasias/enzimologia
Neoplasias/metabolismo
Proteínas Proto-Oncogênicas/genética
Células-Tronco/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins); EC 1.- (Mixed Function Oxygenases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180224
[Lr] Data última revisão:
180224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1038/emm.2017.5



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BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde