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Pesquisa : D12.776.543.750.705.408.200.800 [Categoria DeCS]
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[PMID]:28772128
[Au] Autor:Lohneis P; Sinn M; Bischoff S; Jühling A; Pelzer U; Wislocka L; Bahra M; Sinn BV; Denkert C; Oettle H; Bläker H; Riess H; Jöhrens K; Striefler JK
[Ad] Endereço:Universitätsmedizin Charité Berlin, Institute of Pathology, Charitéplatz 1, 10117 Berlin, Germany. Electronic address: philipp.lohneis@charite.de.
[Ti] Título:Cytotoxic tumour-infiltrating T lymphocytes influence outcome in resected pancreatic ductal adenocarcinoma.
[So] Source:Eur J Cancer;83:290-301, 2017 Sep.
[Is] ISSN:1879-0852
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We studied the prognostic effect of CD3-, CD8- and CD103-positive T lymphocytes in a cohort of 165 patients with resected pancreatic ductal adenocarcinomas (PDACs) of the treatment group (adjuvant gemcitabine) and the untreated control group of the CONKO-001 study. METHODS: Immunohistochemical stainings on tissue microarrays (TMAs) against CD3, CD8 and CD103 were performed according to standard procedures. RESULTS: A high number of CD8-positive lymphocytes were significantly and independently associated with longer disease-free survival (DFS) and overall survival (OS) in the overall study population. Median DFS/OS were 7.4/18.1 months for patients with a low number of CD8-positive intratumoural lymphocytes (≤42 per 1 mm tissue core) and 12.7/25.2 months for patients with high numbers (>42 per 1-mm tissue core; p = 0.008/0.020; HR 0.62/0.65). The ratio of intraepithelial to total CD103-positive lymphocytes, but not total numbers of CD103-positive lymphocytes or CD103-positive intraepithelial lymphocytes, was associated with significantly improved DFS and OS in the overall study population (p = 0.022/0.009). Median DFS/OS was 5.9/15.7 for patients with a ratio of intraepithelial to total CD103-positive intratumoural lymphocytes higher than 0.3 and 11.6/24.7 for patients with a lower ratio. CONCLUSION: T-lymphocyte subpopulations might be prognostic in resectable PDAC but need standardization and verification by further studies.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Carcinoma Ductal Pancreático/imunologia
Linfócitos do Interstício Tumoral/imunologia
Neoplasias Pancreáticas/imunologia
Linfócitos T Citotóxicos/imunologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Antimetabólitos Antineoplásicos/uso terapêutico
Complexo CD3/metabolismo
Carcinoma Ductal Pancreático/patologia
Carcinoma Ductal Pancreático/terapia
Desoxicitidina/análogos & derivados
Desoxicitidina/uso terapêutico
Intervalo Livre de Doença
Feminino
Seres Humanos
Integrina beta4/análise
Masculino
Meia-Idade
Neoplasias Pancreáticas/patologia
Neoplasias Pancreáticas/terapia
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (CD3 Complex); 0 (Integrin beta4); 0W860991D6 (Deoxycytidine); B76N6SBZ8R (gemcitabine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE


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[PMID]:28414312
[Au] Autor:Porpiglia E; Samusik N; Van Ho AT; Cosgrove BD; Mai T; Davis KL; Jager A; Nolan GP; Bendall SC; Fantl WJ; Blau HM
[Ad] Endereço:Blau Laboratory, Stanford University School of Medicine, Stanford, California 94305, USA.
[Ti] Título:High-resolution myogenic lineage mapping by single-cell mass cytometry.
[So] Source:Nat Cell Biol;19(5):558-567, 2017 May.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Muscle regeneration is a dynamic process during which cell state and identity change over time. A major roadblock has been a lack of tools to resolve a myogenic progression in vivo. Here we capitalize on a transformative technology, single-cell mass cytometry (CyTOF), to identify in vivo skeletal muscle stem cell and previously unrecognized progenitor populations that precede differentiation. We discovered two cell surface markers, CD9 and CD104, whose combined expression enabled in vivo identification and prospective isolation of stem and progenitor cells. Data analysis using the X-shift algorithm paired with single-cell force-directed layout visualization defined a molecular signature of the activated stem cell state (CD44 /CD98 /MyoD ) and delineated a myogenic trajectory during recovery from acute muscle injury. Our studies uncover the dynamics of skeletal muscle regeneration in vivo and pave the way for the elucidation of the regulatory networks that underlie cell-state transitions in muscle diseases and ageing.
[Mh] Termos MeSH primário: Linhagem da Célula
Separação Celular/métodos
Citometria de Fluxo/métodos
Desenvolvimento Muscular
Músculo Esquelético/metabolismo
Mioblastos Esqueléticos/metabolismo
Regeneração
Análise de Célula Única/métodos
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Proliferação Celular
Células Cultivadas
Venenos Elapídicos/toxicidade
Proteína-1 Reguladora de Fusão/metabolismo
Genes Reporter
Genótipo
Ensaios de Triagem em Larga Escala
Receptores de Hialuronatos/metabolismo
Integrina beta4/metabolismo
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Desenvolvimento Muscular/efeitos dos fármacos
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/lesões
Músculo Esquelético/patologia
Proteína MyoD/metabolismo
Mioblastos Esqueléticos/efeitos dos fármacos
Mioblastos Esqueléticos/patologia
Fator de Transcrição PAX7/deficiência
Fator de Transcrição PAX7/genética
Fenótipo
Regeneração/efeitos dos fármacos
Células-Tronco/efeitos dos fármacos
Células-Tronco/patologia
Tetraspanina-29/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cd44 protein, mouse); 0 (Cd9 protein, mouse); 0 (Elapid Venoms); 0 (Fusion Regulatory Protein-1); 0 (Hyaluronan Receptors); 0 (Integrin beta4); 0 (Luminescent Proteins); 0 (MyoD Protein); 0 (MyoD1 myogenic differentiation protein); 0 (PAX7 Transcription Factor); 0 (Pax7 protein, mouse); 0 (Tetraspanin-29); 37223-96-4 (notexin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3507


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[PMID]:28300755
[Au] Autor:Garimella R; Tadikonda P; Tawfik O; Gunewardena S; Rowe P; Van Veldhuizen P
[Ad] Endereço:Division of Medical Clinical Oncology, The University of Kansas Medical Center, Kansas City, KS 66160, USA. Rama.Garimella@va.gov.
[Ti] Título:Vitamin D Impacts the Expression of Runx2 Target Genes and Modulates Inflammation, Oxidative Stress and Membrane Vesicle Biogenesis Gene Networks in 143B Osteosarcoma Cells.
[So] Source:Int J Mol Sci;18(3), 2017 Mar 16.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Osteosarcoma (OS) is an aggressive malignancy of bone affecting children, adolescents and young adults. Understanding vitamin D metabolism and vitamin D regulated genes in OS is an important aspect of vitamin D/cancer paradigm, and in evaluating vitamin D as adjuvant therapy for human OS. Vitamin D treatment of 143B OS cells induced significant and novel changes in the expression of genes that regulate: (a) inflammation and immunity; (b) formation of reactive oxygen species, metabolism of cyclic nucleotides, sterols, vitamins and mineral (calcium), quantity of gap junctions and skeletogenesis; (c) bone mineral density; and (d) cell viability of skeletal cells, aggregation of bone cancer cells and exocytosis of secretory vesicles. Ingenuity pathway analysis revealed significant reduction in Runx2 target genes such as fibroblast growth factor -1, -12 ( and ), bone morphogenetic factor-1 ( ), SWI/SNF related, matrix associated actin dependent regulator of chromatin subfamily a, member 4 ( ), Matrix extracellular phosphoglycoprotein ( ), Integrin, ß4 ( ), Matrix Metalloproteinase -1, -28 ( and ), and signal transducer and activator of transcription-4 ( ) in vitamin D treated 143B OS cells. These genes interact with the inflammation, oxidative stress and membrane vesicle biogenesis gene networks. Vitamin D not only inhibited the expression of Runx2 target genes , and kallikrein related peptidase-7 ( ), but also migration and invasion of 143B OS cells. Vitamin D regulated Runx2 target genes or their products represent potential therapeutic targets and laboratory biomarkers for applications in translational oncology.
[Mh] Termos MeSH primário: Subunidade alfa 1 de Fator de Ligação ao Core/genética
Redes Reguladoras de Genes
Osteossarcoma/metabolismo
Estresse Oxidativo
Vesículas Transportadoras/genética
Vitamina D/farmacologia
Vitaminas/farmacologia
[Mh] Termos MeSH secundário: Proteína Morfogenética Óssea 1/genética
Proteína Morfogenética Óssea 1/metabolismo
Linhagem Celular Tumoral
Subunidade alfa 1 de Fator de Ligação ao Core/metabolismo
DNA Helicases/genética
DNA Helicases/metabolismo
Proteínas da Matriz Extracelular/genética
Proteínas da Matriz Extracelular/metabolismo
Fatores de Crescimento de Fibroblastos/genética
Fatores de Crescimento de Fibroblastos/metabolismo
Glicoproteínas/genética
Glicoproteínas/metabolismo
Seres Humanos
Inflamação/genética
Integrina beta4/genética
Integrina beta4/metabolismo
Calicreínas/genética
Calicreínas/metabolismo
Metaloproteinases da Matriz/genética
Metaloproteinases da Matriz/metabolismo
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
Fosfoproteínas/genética
Fosfoproteínas/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Vesículas Transportadoras/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Core Binding Factor Alpha 1 Subunit); 0 (Extracellular Matrix Proteins); 0 (Glycoproteins); 0 (Integrin beta4); 0 (MEPE protein, human); 0 (Nuclear Proteins); 0 (Phosphoproteins); 0 (RUNX2 protein, human); 0 (Transcription Factors); 0 (Vitamins); 1406-16-2 (Vitamin D); 62031-54-3 (Fibroblast Growth Factors); EC 3.4.21.- (KLK7 protein, human); EC 3.4.21.- (Kallikreins); EC 3.4.24.- (Matrix Metalloproteinases); EC 3.4.24.19 (BMP1 protein, human); EC 3.4.24.19 (Bone Morphogenetic Protein 1); EC 3.6.1.- (SMARCA4 protein, human); EC 3.6.4.- (DNA Helicases)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170420
[Lr] Data última revisão:
170420
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170317
[St] Status:MEDLINE


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[PMID]:28287822
[Au] Autor:Sinha M; Lowell CA
[Ad] Endereço:Department of Laboratory Medicine and Program in Immunology, University of California, San Francisco, California.
[Ti] Título:Efficiency and Specificity of Gene Deletion in Lung Epithelial Doxycycline-Inducible Cre Mice.
[So] Source:Am J Respir Cell Mol Biol;57(2):248-257, 2017 Aug.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The transgenic mouse strains surfactant protein C-reverse tetracycline transactivator (SP-C-rtTA), club cell secretory protein (CCSP)-rtTA, and tetracycline operator (TetO)-Cre have been invaluable for spatiotemporally regulating gene deletion in the pulmonary epithelium. In this study, we measured the efficiency and specificity of gene deletion that can be achieved in these mice using the Rosa26-eYFP reporter. Triple-transgenic mice (tTg or rtTA/TetO-Cre/Rosa-eYFP) were bred and treated with various doxycycline (dox) regimens to induce gene deletion, which was then quantified in various cell populations by flow cytometry. In these crosses, we found that the TetO-Cre transgene must be transmitted through the female parent to avoid germline gene deletion. With dox exposure during lung development, SP-C-tTg mice deleted in ∼65-75% of alveolar epithelial type II (ATII) cells, but in only ∼45-50% of the integrin ß4 population, which consisted of club cells and distal lung progenitor cells. In contrast, CCSP-tTg mice deleted in ∼50% of ATII cells and ∼80% of integrin ß4 cells. Upon dox treatment of adults, deletion in ATII cells and integrin ß4 cells in SP-C-tTg mice dropped significantly to ∼20% and ∼6%, respectively, whereas CCSP-tTg mice deleted in ∼57% of ATII and ∼40% of integrin ß4 cells. Interestingly, untreated CCSP-tTg mice also deleted in ∼40% of integrin ß4 cells, indicating significant leakiness of CCSP-tTg in ß4 cells. In all mouse groups, minimal deletion occurred in mouse tracheal epithelial cells or in mesenchymal or hematopoietic cells. These data provide the first quantitative, side-by-side comparison of the deletion efficiency for these widely used transgenic mouse strains.
[Mh] Termos MeSH primário: Células Epiteliais Alveolares/metabolismo
Deleção de Genes
Técnicas de Inativação de Genes
Integrases/genética
Pulmão/citologia
Camundongos Transgênicos/genética
Traqueia/citologia
Transgenes
[Mh] Termos MeSH secundário: Animais
Proteínas de Bactérias/genética
Proteínas de Transporte/genética
Doxiciclina/farmacologia
Feminino
Citometria de Fluxo
Genes Reporter
Integrina beta4/análise
Proteínas Luminescentes/genética
Pulmão/embriologia
Masculino
Herança Materna
Camundongos
Camundongos Endogâmicos C57BL
Especificidade de Órgãos
Peptídeos/genética
Uteroglobina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Carrier Proteins); 0 (Integrin beta4); 0 (Luminescent Proteins); 0 (Peptides); 0 (Scgb1a1 protein, mouse); 0 (Sftpc protein, mouse); 0 (Tet O resistance protein, Bacteria); 0 (yellow fluorescent protein, Bacteria); 9060-09-7 (Uteroglobin); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases); N12000U13O (Doxycycline)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2016-0208OC


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[PMID]:28011194
[Au] Autor:Dilly AK; Tang K; Guo Y; Joshi S; Ekambaram P; Maddipati KR; Cai Y; Tucker SC; Honn KV
[Ad] Endereço:Departments of Pathology-Bioactive Lipids Research Program, Detroit, MI 48202, United States. Electronic address: akd37@pitt.edu.
[Ti] Título:Convergence of eicosanoid and integrin biology: Role of Src in 12-LOX activation.
[So] Source:Exp Cell Res;351(1):1-10, 2017 Feb 01.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:12-Lipoxygenase (12-LOX) metabolizes arachidonic acid to 12(S)-hydroxyeicosatetraenoic acid, or 12(S)-HETE, a proinflammatory bioactive lipid implicated in tumor angiogenesis, growth, and metastasis. The mechanisms underlying 12-LOX-mediated signaling in cancer progression are still ill-defined. In the present study we demonstrate that 12-LOX phosphorylation and subsequent enzymatic activity occurs after integrin ß4 stimulation and Src kinase recruitment to the integrin subunit. Inhibition of Src activity by PP2 or Src dominant-negative mutants reduced 12-LOX tyrosine phosphorylation and 12(S)-HETE production in response to integrin ß4 stimulation in A431 cells. The pertinent Src-targeted residues for 12-LOX activity were mapped to Y19 and Y614, where 12-LOX mutants Y19F and Y614F showed 70% less enzymatic activity. Furthermore, we have shown that the 12-LOX activity modulated by these residues impacts migration. To our knowledge, this is the first report that c-Src kinase activity is required for ß4-integrin-mediated phosphorylation of 12-LOX.
[Mh] Termos MeSH primário: Ácido 12-Hidroxi-5,8,10,14-Eicosatetraenoico/metabolismo
Araquidonato 12-Lipoxigenase/metabolismo
Movimento Celular
Integrina beta4/metabolismo
Quinases da Família src/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Células HEK293
Seres Humanos
Integrina beta4/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ITGB4 protein, human); 0 (Integrin beta4); 59985-28-3 (12-Hydroxy-5,8,10,14-eicosatetraenoic Acid); EC 1.13.11.31 (Arachidonate 12-Lipoxygenase); EC 2.7.10.2 (src-Family Kinases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170518
[Lr] Data última revisão:
170518
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161225
[St] Status:MEDLINE


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[PMID]:27763564
[Au] Autor:Acosta KB; Lorenzini Campos MN; Etcheverry SB; Zapata PD
[Ad] Endereço:Instituto de Biotecnología Misiones "Dra. Maria EbeReca" (InBioMis), Facultad de Ciencias Exactas, Químicas y Naturales, Universidad Nacional de Misiones, Ruta Nacional Nº12 km 7 ½, Posadas 3300, Argentina. acostakb@yahoo.com.ar.
[Ti] Título:α6ß4 Integrin Genetic Variations (A380T and R1281W) and Breast Cancer Risk in an Argentinian Population.
[So] Source:Int J Mol Sci;17(10), 2016 Oct 18.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The α6ß4 integrin is composed of the α6 and ß4 subunits that are encoded by the and the genes, respectively. The α6ß4 main function is to intervene in lamination and epithelia integrity maintenance by cell-matrix interactions. This integrin appears to have importance in breast cancer malignancy, as well as other epithelial carcinomas. The aim of this work was to investigate the potential role of (A380T) and (R1281W) genetic variations in breast cancer susceptibility, in a female population from the northeast region of Argentina (Misiones). We performed a case-control study of 85 breast cancer patients and 113 cancer-free controls. Genotyping was performed by RFLP-PCR. For (A380T) single nucleotide polymorphism, a high frequency of heterozygous genotype GA in cases compared to controls was observed, achieving values of 48% and 49%, respectively. No association between the A380T SNP and breast cancer development was found (Odds Ratio = 0.92; 95% Confidence Interval = 0.52-1.63; = 0.884). In conclusion, we did not find evidence of an association between A380T ( ) and the risk of developing breast cancer. The results represent the first report of these genetic variations in breast cancer; therefore, they are an important contribution to the literature.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Integrina alfa6/genética
Integrina beta4/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Adulto
Idoso
Argentina/epidemiologia
Mama/metabolismo
Mama/patologia
Neoplasias da Mama/epidemiologia
Neoplasias da Mama/patologia
Estudos de Casos e Controles
Feminino
Frequência do Gene
Variação Genética
Genótipo
Seres Humanos
Meia-Idade
Razão de Chances
Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ITGA6 protein, human); 0 (ITGB4 protein, human); 0 (Integrin alpha6); 0 (Integrin beta4)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE


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[PMID]:27736988
[Au] Autor:Moriyama M; Moriyama H; Uda J; Kubo H; Nakajima Y; Goto A; Akaki J; Yoshida I; Matsuoka N; Hayakawa T
[Ad] Endereço:Pharmaceutical Research and Technology Institute, Kindai University, Higashi-Osaka, Osaka, Japan.
[Ti] Título:Beneficial Effects of the Genus Aloe on Wound Healing, Cell Proliferation, and Differentiation of Epidermal Keratinocytes.
[So] Source:PLoS One;11(10):e0164799, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aloe has been used as a folk medicine because it has several important therapeutic properties. These include wound and burn healing, and Aloe is now used in a variety of commercially available topical medications for wound healing and skin care. However, its effects on epidermal keratinocytes remain largely unclear. Our data indicated that both Aloe vera gel (AVG) and Cape aloe extract (CAE) significantly improved wound healing in human primary epidermal keratinocytes (HPEKs) and a human skin equivalent model. In addition, flow cytometry analysis revealed that cell surface expressions of ß1-, α6-, ß4-integrin, and E-cadherin increased in HPEKs treated with AVG and CAE. These increases may contribute to cell migration and wound healing. Treatment with Aloe also resulted in significant changes in cell-cycle progression and in increases in cell number. Aloe increased gene expression of differentiation markers in HPEKs, suggesting roles for AVG and CAE in the improvement of keratinocyte function. Furthermore, human skin epidermal equivalents developed from HPEKs with medium containing Aloe were thicker than control equivalents, indicating the effectiveness of Aloe on enhancing epidermal development. Based on these results, both AVG and CAE have benefits in wound healing and in treatment of rough skin.
[Mh] Termos MeSH primário: Aloe/química
Diferenciação Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Extratos Vegetais/farmacologia
[Mh] Termos MeSH secundário: Aloe/metabolismo
Caderinas/genética
Caderinas/metabolismo
Linhagem Celular
Movimento Celular/efeitos dos fármacos
Proteínas Ricas em Prolina do Estrato Córneo/genética
Proteínas Ricas em Prolina do Estrato Córneo/metabolismo
Seres Humanos
Integrina alfa6/genética
Integrina alfa6/metabolismo
Integrina beta1/genética
Integrina beta1/metabolismo
Integrina beta4/genética
Integrina beta4/metabolismo
Queratinócitos/citologia
Queratinócitos/efeitos dos fármacos
Queratinócitos/metabolismo
Microscopia de Fluorescência
Modelos Biológicos
Extratos Vegetais/química
Cicatrização
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (Cornified Envelope Proline-Rich Proteins); 0 (Integrin alpha6); 0 (Integrin beta1); 0 (Integrin beta4); 0 (Plant Extracts); 0 (SPRR2A protein, human); 149686-82-8 (SPRR1B protein, human)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161014
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0164799


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[PMID]:27348469
[Au] Autor:Langlands AJ; Almet AA; Appleton PL; Newton IP; Osborne JM; Näthke IS
[Ad] Endereço:Cell and Developmental Biology, School of Life Sciences, University of Dundee, Dundee, United Kingdom.
[Ti] Título:Paneth Cell-Rich Regions Separated by a Cluster of Lgr5+ Cells Initiate Crypt Fission in the Intestinal Stem Cell Niche.
[So] Source:PLoS Biol;14(6):e1002491, 2016 Jun.
[Is] ISSN:1545-7885
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The crypts of the intestinal epithelium house the stem cells that ensure the continual renewal of the epithelial cells that line the intestinal tract. Crypt number increases by a process called crypt fission, the division of a single crypt into two daughter crypts. Fission drives normal tissue growth and maintenance. Correspondingly, it becomes less frequent in adulthood. Importantly, fission is reactivated to drive adenoma growth. The mechanisms governing fission are poorly understood. However, only by knowing how normal fission operates can cancer-associated changes be elucidated. We studied normal fission in tissue in three dimensions using high-resolution imaging and used intestinal organoids to identify underlying mechanisms. We discovered that both the number and relative position of Paneth cells and Lgr5+ cells are important for fission. Furthermore, the higher stiffness and increased adhesion of Paneth cells are involved in determining the site of fission. Formation of a cluster of Lgr5+ cells between at least two Paneth-cell-rich domains establishes the site for the upward invagination that initiates fission.
[Mh] Termos MeSH primário: Mucosa Intestinal/citologia
Celulas de Paneth/citologia
Receptores Acoplados a Proteínas-G/metabolismo
Nicho de Células-Tronco
Células-Tronco/citologia
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Adesão Celular
Contagem de Células
Divisão Celular
Proliferação Celular
Integrina beta4/metabolismo
Mucosa Intestinal/metabolismo
Intestino Delgado/citologia
Intestino Delgado/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Microscopia Confocal
Modelos Biológicos
Organoides/citologia
Organoides/metabolismo
Celulas de Paneth/metabolismo
Receptores Acoplados a Proteínas-G/genética
Células-Tronco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin beta4); 0 (Lgr5 protein, mouse); 0 (Receptors, G-Protein-Coupled)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160628
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pbio.1002491


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[PMID]:27193492
[Au] Autor:Li X; Qian H; Sogame R; Hirako Y; Tsuruta D; Ishii N; Koga H; Tsuchisaka A; Jin Z; Tsubota K; Fukumoto A; Sotozono C; Kinoshita S; Hashimoto T
[Ad] Endereço:Department of Dermatology, Kurume University School of Medicine, and Kurume University Institute of Cutaneous Cell Biology, Kurume, Fukuoka.
[Ti] Título:Integrin ß4 is a major target antigen in pure ocular mucous membrane pemphigoid.
[So] Source:Eur J Dermatol;26(3):247-53, 2016 Jun 01.
[Is] ISSN:1952-4013
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Previous studies of ocular mucous membrane pemphigoid (OMMP) have identified several components of the basement membrane zone to be autoantigens, including integrin ß4. However, there are no extensive or definitive reported studies that address this, particularly in pure OMMP. To clarify the major autoantigens in pure OMMP. In this study, we examined sera from 43 pure OMMP patients for both IgG and IgA antibodies using newly developed immunoblotting analyses with a hemidesmosome-rich fraction and various recombinant proteins of integrin α6ß4, in addition to our routine immune-serological tests. Using a hemidesmosome-rich fraction, sera from patients with pure OMMP demonstrated reactivity of IgG and/or IgA antibodies to integrin ß4, BP180 and laminin-332. The reactivity of pure OMMP sera to integrin ß4 was further confirmed by immunoblotting using integrin ß4 recombinant proteins. Using concentrated supernatant of HaCaT cells, only one serum sample showed positive IgG and IgA reactivity to LAD-1, the ectodomain of BP180. None of the pure OMMP sera reacted with any autoantigens on immunoblotting using normal human epidermal or dermal extracts, or purified human laminin-332. Integrin ß4 was considered to be the major and specific autoantigen for pure OMMP. The new methods established in this study are useful for detection of various autoantigens, particularly integrin ß4.
[Mh] Termos MeSH primário: Imunoglobulina A/sangue
Imunoglobulina G/sangue
Integrina beta4/imunologia
Penfigoide Mucomembranoso Benigno/sangue
[Mh] Termos MeSH secundário: Autoanticorpos/sangue
Autoantígenos/imunologia
Estudos de Casos e Controles
Moléculas de Adesão Celular/imunologia
Técnica Indireta de Fluorescência para Anticorpo
Hemidesmossomos
Seres Humanos
Immunoblotting/métodos
Colágenos não Fibrilares/imunologia
Penfigoide Mucomembranoso Benigno/imunologia
Proteínas Recombinantes/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Autoantigens); 0 (Cell Adhesion Molecules); 0 (Immunoglobulin A); 0 (Immunoglobulin G); 0 (Integrin beta4); 0 (Non-Fibrillar Collagens); 0 (Recombinant Proteins); 0 (collagen type XVII); 0 (kalinin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170623
[Lr] Data última revisão:
170623
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160520
[St] Status:MEDLINE
[do] DOI:10.1684/ejd.2016.2772


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[PMID]:27178753
[Au] Autor:Tai YL; Lai IR; Peng YJ; Ding ST; Shen TL
[Ad] Endereço:Department of Plant Pathology and Microbiology, National Taiwan University, Taipei, Taiwan.
[Ti] Título:Activation of focal adhesion kinase through an interaction with ß4 integrin contributes to tumorigenicity of colon cancer.
[So] Source:FEBS Lett;590(12):1826-37, 2016 06.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:High expression of either ß4 integrin or focal adhesion kinase (FAK) has been reported in human colon cancer. However, it remains unclear how ß4 integrin together with FAK contributes to the tumorigenicity of colon cancer. Here, we demonstrate that the co-overexpression of ß4 integrin and FAK positively correlates with advanced stages of human colon cancer. Activated ß4 integrin interacts with FAK and subsequently induces FAK phosphorylation at Tyr397. Furthermore, ablation of the ß4 integrin/FAK complex and/or FAK activation impair colon cancer cell proliferation, anchorage-independent growth, and tumorigenicity. Our data indicate that the ß4 integrin/FAK complex and subsequent FAK activation are essential regulators during the tumorigenicity of colon cancer, and we suggest an alternative strategy for colon cancer therapy.
[Mh] Termos MeSH primário: Neoplasias do Colo/metabolismo
Quinase 1 de Adesão Focal/metabolismo
Integrina beta4/metabolismo
Proteínas de Neoplasias/metabolismo
[Mh] Termos MeSH secundário: Neoplasias do Colo/genética
Neoplasias do Colo/patologia
Feminino
Quinase 1 de Adesão Focal/genética
Seres Humanos
Integrina beta4/genética
Masculino
Proteínas de Neoplasias/genética
Fosforilação/genética
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ITGB4 protein, human); 0 (Integrin beta4); 0 (Neoplasm Proteins); EC 2.7.10.2 (Focal Adhesion Kinase 1); EC 2.7.10.2 (PTK2 protein, human)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160515
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12215



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