Base de dados : MEDLINE
Pesquisa : A11.500 [Categoria DeCS]
Referências encontradas : 4239 [refinar]
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[PMID]:28950101
[Au] Autor:Cao J; Wang J; Jackman CP; Cox AH; Trembley MA; Balowski JJ; Cox BD; De Simone A; Dickson AL; Di Talia S; Small EM; Kiehart DP; Bursac N; Poss KD
[Ad] Endereço:Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA; Regeneration Next, Duke University, Durham, NC 27710, USA.
[Ti] Título:Tension Creates an Endoreplication Wavefront that Leads Regeneration of Epicardial Tissue.
[So] Source:Dev Cell;42(6):600-615.e4, 2017 Sep 25.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mechanisms that control cell-cycle dynamics during tissue regeneration require elucidation. Here we find in zebrafish that regeneration of the epicardium, the mesothelial covering of the heart, is mediated by two phenotypically distinct epicardial cell subpopulations. These include a front of large, multinucleate leader cells, trailed by follower cells that divide to produce small, mononucleate daughters. By using live imaging of cell-cycle dynamics, we show that leader cells form by spatiotemporally regulated endoreplication, caused primarily by cytokinesis failure. Leader cells display greater velocities and mechanical tension within the epicardial tissue sheet, and experimentally induced tension anisotropy stimulates ectopic endoreplication. Unbalancing epicardial cell-cycle dynamics with chemical modulators indicated autonomous regenerative capacity in both leader and follower cells, with leaders displaying an enhanced capacity for surface coverage. Our findings provide evidence that mechanical tension can regulate cell-cycle dynamics in regenerating tissue, stratifying the source cell features to improve repair.
[Mh] Termos MeSH primário: Endorreduplicação
Pericárdio/fisiologia
Regeneração
[Mh] Termos MeSH secundário: Animais
Fenômenos Biomecânicos
Movimento Celular
Células Gigantes/patologia
Hipertrofia
Camundongos Endogâmicos C57BL
Mitose
Poliploidia
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170927
[St] Status:MEDLINE


  2 / 4239 MEDLINE  
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[PMID]:28935707
[Au] Autor:Paikari A; D Belair C; Saw D; Blelloch R
[Ad] Endereço:The Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, Center for Reproductive Sciences, University of California, San Francisco, San Francisco, CA 94143, USA.
[Ti] Título:The eutheria-specific miR-290 cluster modulates placental growth and maternal-fetal transport.
[So] Source:Development;144(20):3731-3743, 2017 10 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The vertebrate-specific ESCC microRNA family arises from two genetic loci in mammals: miR-290/miR-371 and miR-302. The miR-302 locus is found broadly among vertebrates, whereas the miR-290/miR-371 locus is unique to eutheria, suggesting a role in placental development. Here, we evaluate that role. A knock-in reporter for the mouse miR-290 cluster is expressed throughout the embryo until gastrulation, when it becomes specifically expressed in extraembryonic tissues and the germline. In the placenta, expression is limited to the trophoblast lineage, where it remains highly expressed until birth. Deletion of the miR-290 cluster gene ( ) results in reduced trophoblast progenitor cell proliferation and a reduced DNA content in endoreduplicating trophoblast giant cells. The resulting placenta is reduced in size. In addition, the vascular labyrinth is disorganized, with thickening of the maternal-fetal blood barrier and an associated reduction in diffusion. Multiple mRNA targets of the miR-290 cluster microRNAs are upregulated. These data uncover a crucial function for the miR-290 cluster in the regulation of a network of genes required for placental development, suggesting a central role for these microRNAs in the evolution of placental mammals.
[Mh] Termos MeSH primário: MicroRNAs/genética
MicroRNAs/fisiologia
Placenta/fisiologia
[Mh] Termos MeSH secundário: Animais
Linhagem da Célula
Proliferação Celular
Feminino
Perfilação da Expressão Gênica
Genótipo
Células Gigantes/citologia
Troca Materno-Fetal
Camundongos
Camundongos Knockout
Família Multigênica
Gravidez
Análise de Sequência de RNA
Trofoblastos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (MIRN290 microRNA, mouse); 0 (MicroRNAs)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1242/dev.151654


  3 / 4239 MEDLINE  
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[PMID]:28910710
[Au] Autor:Wang W; Yang L; Huang X; Fu W; Pan D; Cai L; Ye J; Liu J; Xia N; Cheng T; Zhu H
[Ad] Endereço:State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, National Institute of Diagnostics and Vaccine Development in Infectious Diseases, School of Public Health, Xiamen University, Xiamen 361102, PR China.
[Ti] Título:Outer nuclear membrane fusion of adjacent nuclei in varicella-zoster virus-induced syncytia.
[So] Source:Virology;512:34-38, 2017 Dec.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Syncytia formation has been considered important for cell-to-cell spread and pathogenesis of many viruses. As a syncytium forms, individual nuclei often congregate together, allowing close contact of nuclear membranes and possibly fusion to occur. However, there is currently no reported evidence of nuclear membrane fusion between adjacent nuclei in wild-type virus-induced syncytia. Varicella-zoster virus (VZV) is one typical syncytia-inducing virus that causes chickenpox and shingles in humans. Here, we report, for the first time, an interesting observation of apparent fusion of the outer nuclear membranes from juxtaposed nuclei that comprise VZV syncytia both in ARPE-19 human epithelial cells in vitro and in human skin xenografts in the SCID-hu mouse model in vivo. This work reveals a novel aspect of VZV-related cytopathic effect in the context of multinucleated syncytia. Additionally, the information provided by this study could be helpful for future studies on interactions of viruses with host cell nuclei.
[Mh] Termos MeSH primário: Células Epiteliais/patologia
Células Epiteliais/virologia
Células Gigantes/virologia
Herpesvirus Humano 3/fisiologia
Membrana Nuclear/patologia
[Mh] Termos MeSH secundário: Fusão Celular
Linhagem Celular
Seres Humanos
Membrana Nuclear/virologia
Pele/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE


  4 / 4239 MEDLINE  
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[PMID]:28854178
[Au] Autor:Vujic A; Bassaneze V; Lee RT
[Ad] Endereço:Department of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts, USA.
[Ti] Título:Genetic insights into mammalian heart regeneration.
[So] Source:Nat Genet;49(9):1292-1293, 2017 Aug 30.
[Is] ISSN:1546-1718
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genetic and functional analyses of 120 mouse strains have identified a heart regeneration candidate gene that modulates the contractile sarcomeric apparatus. This gene, Tnni3k, controls the frequency of the mononuclear, diploid cardiomyocyte population, which affects cardiomyocyte proliferative potential after injury.
[Mh] Termos MeSH primário: Coração/fisiologia
Mamíferos/fisiologia
Regeneração/genética
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/genética
Quimera
Células Gigantes/metabolismo
Seres Humanos
Mamíferos/genética
Camundongos
Camundongos Endogâmicos C57BL
Desenvolvimento Muscular/genética
Miócitos Cardíacos/fisiologia
[Pt] Tipo de publicação:NEWS
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170831
[St] Status:MEDLINE
[do] DOI:10.1038/ng.3942


  5 / 4239 MEDLINE  
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[PMID]:28822649
[Au] Autor:Pazdernik M; Netuka I; Maly J; Kettner J; Voska L; Riha H; Pirk J; Melenovsky V; Kautzner J
[Ad] Endereço:Cardiac Centre, IKEM, Prague, Czech Republic; Department of Cardiology, 2nd Medical School, Charles University Hospital Motol, Prague, Czech Republic. Electronic address: michal.pazdernik@email.cz.
[Ti] Título:A Complex Heart Team's Approach to a Patient With Giant Cell Myocarditis.
[So] Source:Can J Cardiol;33(10):1335.e5-1335.e7, 2017 Oct.
[Is] ISSN:1916-7075
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Giant cell myocarditis is known as a rare and frequently fatal type of myocarditis that is usually characterized by progressive congestive heart failure and frequent ventricular arrhythmias. We report a rare case of giant cell myocarditis in a 64-year-old previously healthy woman. The case was complicated by the rapid development of progressive acute heart failure, which required the comprehensive care of our heart team. Using a broad spectrum of therapeutic approaches, the patient successfully underwent heart transplantation.
[Mh] Termos MeSH primário: Células Gigantes/patologia
Insuficiência Cardíaca/etiologia
Miocárdio/patologia
Equipe de Assistência ao Paciente
[Mh] Termos MeSH secundário: Doença Aguda
Biópsia
Feminino
Seguimentos
Insuficiência Cardíaca/diagnóstico
Insuficiência Cardíaca/cirurgia
Transplante de Coração
Seres Humanos
Imagem Cinética por Ressonância Magnética
Meia-Idade
Miocardite/complicações
Miocardite/diagnóstico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170821
[St] Status:MEDLINE


  6 / 4239 MEDLINE  
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[PMID]:28760929
[Au] Autor:Whiteley L; Meffert T; Haug M; Weidenmaier C; Hopf V; Bitschar K; Schittek B; Kohler C; Steinmetz I; West TE; Schwarz S
[Ad] Endereço:Interfaculty Institute of Microbiology and Infection Medicine, University of Tuebingen, Tuebingen, Germany.
[Ti] Título:Entry, Intracellular Survival, and Multinucleated-Giant-Cell-Forming Activity of Burkholderia pseudomallei in Human Primary Phagocytic and Nonphagocytic Cells.
[So] Source:Infect Immun;85(10), 2017 Oct.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The human pathogen and the related species are facultative intracellular bacteria characterized by the ability to escape into the cytosol of the host cell and to stimulate the formation of multinucleated giant cells (MNGCs). MNGC formation is induced via an unknown mechanism by bacterial type VI secretion system 5 (T6SS-5), which is an essential virulence factor in both species. Despite the vital role of the intracellular life cycle in the pathogenesis of the bacteria, the range of host cell types permissive for initiation and completion of the intracellular cycle is poorly defined. In the present study, we used several different types of human primary cells to evaluate bacterial entry, intracellular survival, and MNGC formation. We report the capacity of to enter, efficiently replicate in, and mediate MNGC formation of vein endothelial and bronchial epithelial cells, indicating that the T6SS-5 is important in the host-pathogen interaction in these cells. Furthermore, we show that invades fibroblasts and keratinocytes and survives inside these cells as well as in monocyte-derived macrophages and neutrophils for at least 17 h postinfection; however, MNGC formation is not induced in these cells. In contrast, infection of mixed neutrophils and RAW264.7 macrophages with stimulated the formation of heterotypic MNGCs in a T6SS-5-dependent manner. In summary, the ability of the bacteria to enter and survive as well as induce MNGC formation in certain host cells may contribute to the pathogenesis observed in infection.
[Mh] Termos MeSH primário: Burkholderia pseudomallei/fisiologia
Células Gigantes/microbiologia
Interações Hospedeiro-Patógeno
Macrófagos/microbiologia
Fagócitos/microbiologia
[Mh] Termos MeSH secundário: Animais
Brônquios/citologia
Brônquios/microbiologia
Burkholderia pseudomallei/crescimento & desenvolvimento
Burkholderia pseudomallei/patogenicidade
Linhagem Celular
Células Cultivadas
Citosol/microbiologia
Células Endoteliais/microbiologia
Células Epiteliais/microbiologia
Fibroblastos/microbiologia
Seres Humanos
Queratinócitos/microbiologia
Camundongos
Neutrófilos/microbiologia
Sistemas de Secreção Tipo VI/metabolismo
Virulência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Type VI Secretion Systems)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE


  7 / 4239 MEDLINE  
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[PMID]:28679100
[Au] Autor:Jani SM; Nallamothu BK; Cooper LT; Smith A; Fazel R
[Ad] Endereço:From the MedStar Heart and Vascular Institute, MedStar Washington Hospital Center, Washington, DC (S.M.J.); Ann Arbor Veterans Affairs Medical Center and the Department of Internal Medicine, University of Michigan Medical School - both in Ann Arbor (B.K.N.); the Division of Cardiology, Mayo Clinic,
[Ti] Título:Beating, Fast and Slow.
[So] Source:N Engl J Med;377(1):72-78, 2017 07 06.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Angina Pectoris/diagnóstico
Eletrocardiografia
Miocardite/diagnóstico
Miócitos Cardíacos/patologia
[Mh] Termos MeSH secundário: Angina Pectoris/complicações
Angina Pectoris/tratamento farmacológico
Atenolol/efeitos adversos
Biópsia
Bradicardia/induzido quimicamente
Dor no Peito/etiologia
Diabetes Mellitus Tipo 2/complicações
Diagnóstico Diferencial
Dispneia/etiologia
Células Gigantes
Bloqueio Cardíaco/etiologia
Seres Humanos
Hipertensão/complicações
Masculino
Meia-Idade
Miocardite/complicações
Taquicardia Ventricular/etiologia
[Pt] Tipo de publicação:CASE REPORTS; CLINICAL CONFERENCE; JOURNAL ARTICLE
[Nm] Nome de substância:
50VV3VW0TI (Atenolol)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170706
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMcps1608688


  8 / 4239 MEDLINE  
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[PMID]:28646649
[Au] Autor:Ji Y; Liu T; Jia Y; Liu B; Yu Q; Cui X; Guo F; Chang H; Zhu Q
[Ad] Endereço:State Key Laboratory of Veterinary Etiological Biology, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, PR China.
[Ti] Título:Two single mutations in the fusion protein of Newcastle disease virus confer hemagglutinin-neuraminidase independent fusion promotion and attenuate the pathogenicity in chickens.
[So] Source:Virology;509:146-151, 2017 Sep.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The fusion (F) protein of Newcastle disease virus (NDV) affects viral infection and pathogenicity through mediating membrane fusion. Previously, we found NDV with increased fusogenic activity in which contained T458D or G459D mutation in the F protein. Here, we investigated the effects of these two mutations on viral infection, fusogenicity and pathogenicity. Syncytium formation assays indicated that T458D or G459D increased the F protein cleavage activity and enhanced cell fusion with or without the presence of HN protein. The T458D- or G459D-mutated NDV resulted in a decrease in virus replication or release from cells. The animal study showed that the pathogenicity of the mutated NDVs was attenuated in chickens. These results indicate that these two single mutations in F altered or diminished the requirement of HN for promoting membrane fusion. The increased fusogenic activity may disrupt the cellular machinery and consequently decrease the virus replication and pathogenicity in chickens.
[Mh] Termos MeSH primário: Proteínas Mutantes/metabolismo
Mutação de Sentido Incorreto
Doença de Newcastle/patologia
Vírus da Doença de Newcastle/fisiologia
Proteínas Virais de Fusão/metabolismo
Internalização do Vírus
[Mh] Termos MeSH secundário: Animais
Fusão Celular
Galinhas
Modelos Animais de Doenças
Células Gigantes/virologia
Proteínas Mutantes/genética
Doença de Newcastle/virologia
Vírus da Doença de Newcastle/genética
Vírus da Doença de Newcastle/patogenicidade
Proteínas Virais de Fusão/genética
Virulência
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mutant Proteins); 0 (Viral Fusion Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170721
[Lr] Data última revisão:
170721
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170625
[St] Status:MEDLINE


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[PMID]:28613142
[Au] Autor:Dubois J; Cavanagh MH; Terrier O; Hamelin MÈ; Lina B; Shi R; Rosa-Calatrava M; Boivin G
[Ad] Endereço:1​Centre de Recherche en Infectiologie of the Centre Hospitalier Universitaire de Québec and Université Laval, Québec, Canada 2​Laboratoire de Virologie et Pathologie Humaine - VirPath Team, Centre International de Recherche en Infectiologie CIRI, Inserm U1111, CNRS UMR5308, ENS Lyon, Université
[Ti] Título:Mutations in the fusion protein heptad repeat domains of human metapneumovirus impact on the formation of syncytia.
[So] Source:J Gen Virol;98(6):1174-1180, 2017 Jun.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Human metapneumovirus (HMPV) is an important cause of respiratory tract infections. The mechanism by which its fusion (F) protein is responsible for variable cytopathic effects in vitro remains unknown. We aligned the F sequences of the poorly fusogenic B2/CAN98-75 strain and the hyperfusogenic A1/C-85473 strain and identified divergent residues located in the two functional heptad repeats domains (HRA and HRB). We generated recombinant viruses by inserting the mutations N135T-G139N-T143K-K166E-E167D in HRA and/or K479R-N482S in HRB, corresponding to swapped sequences from C-85473, into CAN98-75 background and investigated their impact on in vitro phenotype and fusogenicity. We demonstrated that the five HRA mutations enhanced the fusogenicity of the recombinant rCAN98-75 virus, almost restoring the phenotype of the wild-type rC-85473 strain, whereas HRB substitutions alone had no significant effect on cell-cell fusion. Altogether, our results support the importance of the HRA domain for an HMPV-triggered fusion mechanism and identify key residues that modulate syncytium formation.
[Mh] Termos MeSH primário: Fusão Celular
Células Gigantes/virologia
Metapneumovirus/crescimento & desenvolvimento
Proteínas Mutantes/metabolismo
Mutação
Proteínas Virais de Fusão/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Análise Mutacional de DNA
Células Epiteliais/fisiologia
Células Epiteliais/virologia
Macaca mulatta
Metapneumovirus/genética
Modelos Moleculares
Proteínas Mutantes/química
Proteínas Mutantes/genética
Conformação Proteica
Domínios Proteicos
Recombinação Genética
Genética Reversa
Proteínas Virais de Fusão/química
Proteínas Virais de Fusão/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mutant Proteins); 0 (Viral Fusion Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000796


  10 / 4239 MEDLINE  
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[PMID]:28596102
[Au] Autor:Zhuang L; Trueb B
[Ad] Endereço:Department of Clinical Research, University of Bern, 3008 Bern, Switzerland.
[Ti] Título:Evolution of the fusogenic activity of the receptor FGFRL1.
[So] Source:Arch Biochem Biophys;625-626:54-64, 2017 Jul 01.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:FGFRL1 is a transmembrane receptor that can induce the fusion of CHO cells to multinucleated syncytia. This cell fusion activity has been attributed to the extracellular Ig3 domain of the receptor. We investigated how the fusogenic activity evolved during the evolution of animals. We found that the Ig3 domain from humans, mice, chicken and fish stimulates fusion of CHO cells, while the Ig3 domain from lancelet and sea urchin does not. It is therefore conceivable that the fusogenic activity of FGFRL1 developed during the evolution of vertebrates. Bony fish contain two copies of the FGFRL1 gene because they have undergone a whole-genome duplication. One of the corresponding proteins (FGFRL1a) induces cell-cell fusion, while the other (FGFRL1b) does not. Analysis of chimeric constructs and in vitro mutagenesis suggested that FGFRL1b has lost its fusogenic activity after duplication. A rescue experiment supported this conclusion. When four amino acids were changed, the Ig3 domain of FGFRL1b was converted into an active, fusogenic protein comparable to FGFRL1a. The four amino acids are located in a hydrophobic pocket of the Ig3 domain. It is likely that this hydrophobic pocket interacts with a target molecule on the membrane of adjacent cells to induce cell-cell fusion.
[Mh] Termos MeSH primário: Células Gigantes/metabolismo
Receptor Tipo 5 de Fator de Crescimento de Fibroblastos/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Células CHO
Fusão Celular
Clonagem Molecular
Cricetulus
Evolução Molecular
Células Gigantes/citologia
Seres Humanos
Domínios Proteicos
Receptor Tipo 5 de Fator de Crescimento de Fibroblastos/química
Receptor Tipo 5 de Fator de Crescimento de Fibroblastos/genética
Alinhamento de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FGFRL1 protein, human); 0 (Receptor, Fibroblast Growth Factor, Type 5)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE



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