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Pesquisa : D12.644.276.930.500 [Categoria DeCS]
Referências encontradas : 1056 [refinar]
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  1 / 1056 MEDLINE  
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[PMID]:29194448
[Au] Autor:Nagata Y; Kiyono T; Okamura K; Goto YI; Matsuo M; Ikemoto-Uezumi M; Hashimoto N
[Ad] Endereço:Department of Regenerative Medicine, National Center for Geriatrics and Gerontology, Morioka, Oobu, Aichi, Japan.
[Ti] Título:Interleukin-1beta (IL-1ß)-induced Notch ligand Jagged1 suppresses mitogenic action of IL-1ß on human dystrophic myogenic cells.
[So] Source:PLoS One;12(12):e0188821, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Duchenne muscular dystrophy (DMD) is a severe X-linked recessive muscle disorder caused by mutations in the dystrophin gene. Nonetheless, secondary processes involving perturbation of muscle regeneration probably exacerbate disease progression, resulting in the fatal loss of muscle in DMD patients. A dysfunction of undifferentiated myogenic cells is the most likely cause for the reduction of regenerative capacity of muscle. To clarify molecular mechanisms in perturbation of the regenerative capacity of DMD muscle, we have established several NCAM (CD56)-positive immortalized human dystrophic and non-dystrophic myogenic cell lines from DMD and healthy muscles. A pro-inflammatory cytokine, IL-1ß, promoted cell cycle progression of non-dystrophic myogenic cells but not DMD myogenic cells. In contrast, IL-1ß upregulated the Notch ligand Jagged1 gene in DMD myogenic cells but not in non-dystrophic myogenic cells. Knockdown of Jagged1 in DMD myogenic cells restored the IL-1ß-promoted cell cycle progression. Conversely, enforced expression of Jagged1-blocked IL-1ß promoted proliferation of non-dystrophic myogenic cells. In addition, IL-1ß prevented myogenic differentiation of DMD myogenic cells depending on Jagged1 but not of non-dystrophic myogenic cells. These results demonstrate that Jagged1 induced by IL-1ß in DMD myogenic cells modified the action of IL-1ß and reduced the ability to proliferate and differentiate. IL-1ß induced Jagged1 gene expression may be a feedback response to excess stimulation with this cytokine because high IL-1ß (200-1000 pg/ml) induced Jagged1 gene expression even in non-dystrophic myogenic cells. DMD myogenic cells are likely to acquire the susceptibility of the Jagged1 gene to IL-1ß under the microcircumstances in DMD muscles. The present results suggest that Jagged1 induced by IL-1ß plays a crucial role in the loss of muscle regeneration capacity of DMD muscles. The IL-1ß/Jagged1 pathway may be a new therapeutic target to ameliorate exacerbation of muscular dystrophy in a dystrophin-independent manner.
[Mh] Termos MeSH primário: Interleucina-1beta/metabolismo
Proteína Jagged-1/metabolismo
Distrofia Muscular de Duchenne/metabolismo
Receptor Notch3/metabolismo
[Mh] Termos MeSH secundário: Diferenciação Celular
Células Cultivadas
Seres Humanos
Desenvolvimento Muscular
Distrofia Muscular de Duchenne/patologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Jagged-1 Protein); 0 (NOTCH3 protein, human); 0 (Receptor, Notch3)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188821


  2 / 1056 MEDLINE  
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[PMID]:29232552
[Au] Autor:Zheng H; Bae Y; Kasimir-Bauer S; Tang R; Chen J; Ren G; Yuan M; Esposito M; Li W; Wei Y; Shen M; Zhang L; Tupitsyn N; Pantel K; King C; Sun J; Moriguchi J; Jun HT; Coxon A; Lee B; Kang Y
[Ad] Endereço:Department of Molecular Biology, Princeton University, Washington Road, LTL 255, Princeton, NJ 08544, USA.
[Ti] Título:Therapeutic Antibody Targeting Tumor- and Osteoblastic Niche-Derived Jagged1 Sensitizes Bone Metastasis to Chemotherapy.
[So] Source:Cancer Cell;32(6):731-747.e6, 2017 Dec 11.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone metastasis is a major health threat to breast cancer patients. Tumor-derived Jagged1 represents a central node in mediating tumor-stromal interactions that promote osteolytic bone metastasis. Here, we report the development of a highly effective fully human monoclonal antibody against Jagged1 (clone 15D11). In addition to its inhibitory effect on bone metastasis of Jagged1-expressing tumor cells, 15D11 dramatically sensitizes bone metastasis to chemotherapy, which induces Jagged1 expression in osteoblasts to provide a survival niche for cancer cells. We further confirm the bone metastasis-promoting function of osteoblast-derived Jagged1 using osteoblast-specific Jagged1 transgenic mouse model. These findings establish 15D11 as a potential therapeutic agent for the prevention or treatment of bone metastasis.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Antineoplásicos/farmacologia
Neoplasias Ósseas/tratamento farmacológico
Neoplasias Ósseas/secundário
Proteína Jagged-1/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Camundongos
Camundongos Transgênicos
Osteoblastos/efeitos dos fármacos
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antineoplastic Agents); 0 (Jagged-1 Protein)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE


  3 / 1056 MEDLINE  
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[PMID]:29073173
[Au] Autor:Sanghez V; Luzzi A; Clarke D; Kee D; Beuder S; Rux D; Osawa M; Madrenas J; Chou TF; Kyba M; Iacovino M
[Ad] Endereço:Division of Medical Genetics, Department of Pediatrics, Harbor-UCLA Medical Center, Torrance, CA, United States of America.
[Ti] Título:Notch activation is required for downregulation of HoxA3-dependent endothelial cell phenotype during blood formation.
[So] Source:PLoS One;12(10):e0186818, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hemogenic endothelium (HE) undergoes endothelial-to-hematopoietic transition (EHT) to generate blood, a process that requires progressive down-regulation of endothelial genes and induction of hematopoietic ones. Previously, we have shown that the transcription factor HoxA3 prevents blood formation by inhibiting Runx1 expression, maintaining endothelial gene expression and thus blocking EHT. In the present study, we show that HoxA3 also prevents blood formation by inhibiting Notch pathway. HoxA3 induced upregulation of Jag1 ligand in endothelial cells, which led to cis-inhibition of the Notch pathway, rendering the HE nonresponsive to Notch signals. While Notch activation alone was insufficient to promote blood formation in the presence of HoxA3, activation of Notch or downregulation of Jag1 resulted in a loss of the endothelial phenotype which is a prerequisite for EHT. Taken together, these results demonstrate that Notch pathway activation is necessary to downregulate endothelial markers during EHT.
[Mh] Termos MeSH primário: Células Endoteliais/metabolismo
Hematopoese/fisiologia
Proteínas de Homeodomínio/metabolismo
Receptores Notch/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Animais
Regulação para Baixo/fisiologia
Células Endoteliais/citologia
Proteínas de Homeodomínio/genética
Proteína Jagged-1/biossíntese
Proteína Jagged-1/genética
Camundongos
Receptores Notch/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Homeodomain Proteins); 0 (Hoxa3 protein, mouse); 0 (Jag1 protein, mouse); 0 (Jagged-1 Protein); 0 (Receptors, Notch)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171027
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186818


  4 / 1056 MEDLINE  
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[PMID]:28904063
[Au] Autor:Sierra RA; Trillo-Tinoco J; Mohamed E; Yu L; Achyut BR; Arbab A; Bradford JW; Osborne BA; Miele L; Rodriguez PC
[Ad] Endereço:H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.
[Ti] Título:Anti-Jagged Immunotherapy Inhibits MDSCs and Overcomes Tumor-Induced Tolerance.
[So] Source:Cancer Res;77(20):5628-5638, 2017 Oct 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Myeloid-derived suppressor cells (MDSC) are a major obstacle to promising forms of cancer immunotherapy, but tools to broadly limit their immunoregulatory effects remain lacking. In this study, we assessed the therapeutic effect of the humanized anti-Jagged1/2-blocking antibody CTX014 on MDSC-mediated T-cell suppression in tumor-bearing mice. CTX014 decreased tumor growth, affected the accumulation and tolerogenic activity of MDSCs in tumors, and inhibited the expression of immunosuppressive factors arginase I and iNOS. Consequently, anti-Jagged therapy overcame tumor-induced T-cell tolerance, increased the infiltration of reactive CD8 T cells into tumors, and enhanced the efficacy of T-cell-based immunotherapy. Depletion of MDSC-like cells restored tumor growth in mice treated with anti-Jagged, whereas coinjection of MDSC-like cells from anti-Jagged-treated mice with cancer cells delayed tumor growth. Jagged1/2 was induced in MDSCs by tumor-derived factors via NFkB-p65 signaling, and conditional deletion of NFkB-p65 blocked MDSC function. Collectively, our results offer a preclinical proof of concept for the use of anti-Jagged1/2 to reprogram MDSC-mediated T-cell suppression in tumors, with implications to broadly improve the efficacy of cancer therapy. .
[Mh] Termos MeSH primário: Imunoterapia/métodos
Proteína Jagged-1/antagonistas & inibidores
Proteína Jagged-1/imunologia
Células Supressoras Mieloides/imunologia
Neoplasias Experimentais/imunologia
Neoplasias Experimentais/terapia
[Mh] Termos MeSH secundário: Animais
Anticorpos/imunologia
Anticorpos/farmacologia
Carcinoma Pulmonar de Lewis/imunologia
Carcinoma Pulmonar de Lewis/terapia
Feminino
Seres Humanos
Imunoterapia Adotiva/métodos
Melanoma Experimental/imunologia
Melanoma Experimental/terapia
Camundongos
Camundongos Endogâmicos C57BL
Transdução de Sinais
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Jagged-1 Protein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-17-0357


  5 / 1056 MEDLINE  
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[PMID]:28863329
[Au] Autor:Zhu G; Wang X; Xiao H; Liu X; Fang Y; Zhai B; Xu R; Han G; Chen G; Hou C; Shen B; Li Y; Ma N; Wu H; Liu G; Wang R
[Ad] Endereço:Laboratory of Immunology, Institute of Basic Medical Sciences, Beijing 100850, China; Joint National Laboratory for Antibody Drug Engineering, Henan University, Kaifeng, Henan 475004, China.
[Ti] Título:Both Notch1 and its ligands in B cells promote antibody production.
[So] Source:Mol Immunol;91:17-23, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Notch1 signaling regulates B and T lymphocyte development and also in vitro promotes antibody secretion upon B cell activation. However, it is still unclear about the role of Notch1 in antibody production upon in vitro and in vivo mixture lymphocytes activation. We first showed that Notch1 expressed in LPS-activated CD19 B cells and CD19 mediated Notch1 knock-down in LPS-activated B cells. Furthermore, we demonstrated that Notch1 knock-down in B cells reduced antibody production in LPS-stimulated B cells but did not affect antibody production in LPS-stimulated splenocytes and in experimental allergic encephalomyelitis (EAE) mice. Importantly, Notch1 ligands Dll1 and Jag1 expressed in B cells and pre-coated Notch1 protein promotes Notch1-knocked down B cells to produce antibody in LPS-stimulated B cells suggesting that Notch1 in other cells may promote antibody production by binding its ligands Dll1 and Jag1 in B cells. Together, our results suggest that both Notch1 and its ligands in B cells play an important role in antibody production.
[Mh] Termos MeSH primário: Formação de Anticorpos
Linfócitos B/imunologia
Regulação da Expressão Gênica/imunologia
Peptídeos e Proteínas de Sinalização Intercelular/imunologia
Proteína Jagged-1/imunologia
Receptor Notch1/imunologia
[Mh] Termos MeSH secundário: Animais
Encefalomielite Autoimune Experimental/induzido quimicamente
Encefalomielite Autoimune Experimental/imunologia
Encefalomielite Autoimune Experimental/patologia
Técnicas de Silenciamento de Genes
Peptídeos e Proteínas de Sinalização Intercelular/genética
Proteína Jagged-1/genética
Lipopolissacarídeos/toxicidade
Camundongos
Camundongos Transgênicos
Receptor Notch1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dlk1 protein, mouse); 0 (Intercellular Signaling Peptides and Proteins); 0 (Jag1 protein, mouse); 0 (Jagged-1 Protein); 0 (Lipopolysaccharides); 0 (Notch1 protein, mouse); 0 (Receptor, Notch1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE


  6 / 1056 MEDLINE  
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[PMID]:28714968
[Au] Autor:Pitulescu ME; Schmidt I; Giaimo BD; Antoine T; Berkenfeld F; Ferrante F; Park H; Ehling M; Biljes D; Rocha SF; Langen UH; Stehling M; Nagasawa T; Ferrara N; Borggrefe T; Adams RH
[Ad] Endereço:Max Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, and University of Münster, Faculty of Medicine, Röntgenstrasse 20, D-48149 Münster, Germany.
[Ti] Título:Dll4 and Notch signalling couples sprouting angiogenesis and artery formation.
[So] Source:Nat Cell Biol;19(8):915-927, 2017 Aug.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Endothelial sprouting and proliferation are tightly coordinated processes mediating the formation of new blood vessels during physiological and pathological angiogenesis. Endothelial tip cells lead sprouts and are thought to suppress tip-like behaviour in adjacent stalk endothelial cells by activating Notch. Here, we show with genetic experiments in postnatal mice that the level of active Notch signalling is more important than the direct Dll4-mediated cell-cell communication between endothelial cells. We identify endothelial expression of VEGF-A and of the chemokine receptor CXCR4 as key processes controlling Notch-dependent vessel growth. Surprisingly, genetic experiments targeting endothelial tip cells in vivo reveal that they retain their function without Dll4 and are also not replaced by adjacent, Dll4-positive cells. Instead, activation of Notch directs tip-derived endothelial cells into developing arteries and thereby establishes that Dll4-Notch signalling couples sprouting angiogenesis and artery formation.
[Mh] Termos MeSH primário: Células Endoteliais/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Proteínas de Membrana/metabolismo
Neovascularização Fisiológica
Receptor Notch1/metabolismo
Artéria Retiniana/metabolismo
[Mh] Termos MeSH secundário: Animais
Comunicação Celular
Diferenciação Celular
Linhagem da Célula
Movimento Celular
Proliferação Celular
Células Cultivadas
Feminino
Regulação da Expressão Gênica
Genótipo
Peptídeos e Proteínas de Sinalização Intracelular/genética
Proteína Jagged-1/genética
Proteína Jagged-1/metabolismo
Masculino
Proteínas de Membrana/genética
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Fenótipo
Receptor Notch1/genética
Receptores CXCR4/genética
Receptores CXCR4/metabolismo
Artéria Retiniana/citologia
Transdução de Sinais
Fatores de Tempo
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCR4 protein, mouse); 0 (DLL4 protein, mouse); 0 (Intracellular Signaling Peptides and Proteins); 0 (Jag1 protein, mouse); 0 (Jagged-1 Protein); 0 (Membrane Proteins); 0 (Notch1 protein, mouse); 0 (Receptor, Notch1); 0 (Receptors, CXCR4); 0 (Vascular Endothelial Growth Factor A); 0 (vascular endothelial growth factor A, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3555


  7 / 1056 MEDLINE  
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[PMID]:28688656
[Au] Autor:Zagory JA; Dietz W; Park A; Fenlon M; Xu J; Utley S; Mavila N; Wang KS
[Ad] Endereço:Department of Surgery, Children's Hospital Los Angeles, Los Angeles, California.
[Ti] Título:Notch signaling promotes ductular reactions in biliary atresia.
[So] Source:J Surg Res;215:250-256, 2017 Jul.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Biliary atresia (BA) is a congenital, progressive, fibro-obliterative disease of the extrahepatic biliary tree and the most common cause of end-stage liver disease in children. BA is characterized by extensive intrahepatic proliferating ductular reactions that may contribute to biliary fibrosis. Lineage tracing during experimental cholestasis indicates that cells within ductular reactions derive from PROM1-expressing hepatic progenitor cells. Given the role of Notch signaling in normal biliary development, we hypothesize that activated Notch signaling promotes the formation of ductular reactions in BA. METHODS: Liver samples collected from BA infants at Kasai portoenterostomy and age-matched controls, as well as from wild-type and Prom1 knockout mice with 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-induced experimental cholestasis were analyzed histologically using immunofluorescence and by quantitative polymerase chain reaction. RESULTS: Increased expression of genes encoding Notch ligand JAG1 and its receptor NOTCH2 was observed in BA livers compared with control by quantitative polymerase chain reaction analyses. Livers of DDC-treated mice, which exhibit cytokeratin-19-positive ductular reactions typical of BA livers, demonstrated significant increases in the expression level of the gene encoding Notch2, as well as downstream Notch target gene Hes1 compared with control. Prom1 knockout mice exhibit diminished ductular reactions and decreased levels of Jag1 and Hes1 compared with littermate controls. CONCLUSIONS: Human BA and cholestasis induced by DDC are associated with Notch signaling activation. Null mutation of Prom1 is associated with decreased ductular reactions and decreased Notch signaling activation during DDC treatment. These data are consistent with Notch signaling promoting ductular reactions of Prom1 expressing progenitor cells in BA.
[Mh] Termos MeSH primário: Atresia Biliar/metabolismo
Atresia Biliar/patologia
Receptor Notch2/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Antígeno AC133/genética
Antígeno AC133/metabolismo
Animais
Biomarcadores/metabolismo
Estudos de Casos e Controles
Seres Humanos
Imuno-Histoquímica
Proteína Jagged-1/metabolismo
Camundongos
Camundongos Knockout
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fatores de Transcrição HES-1/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (Biomarkers); 0 (Hes1 protein, mouse); 0 (JAG1 protein, human); 0 (Jag1 protein, mouse); 0 (Jagged-1 Protein); 0 (NOTCH2 protein, human); 0 (Notch2 protein, mouse); 0 (Prom1 protein, mouse); 0 (Receptor, Notch2); 0 (Transcription Factor HES-1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170710
[St] Status:MEDLINE


  8 / 1056 MEDLINE  
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[PMID]:28645563
[Au] Autor:Cheng Z; Yuan X; Qu Y; Li X; Wu G; Li C; Zu X; Yang N; Ke X; Zhou J; Xie N; Xu X; Liu S; Shen Y; Li H; Zhang W
[Ad] Endereço:Department of Phytochemistry, School of Pharmacy, Second Military Medical University, Shanghai 200433, China.
[Ti] Título:Bruceine D inhibits hepatocellular carcinoma growth by targeting ß-catenin/jagged1 pathways.
[So] Source:Cancer Lett;403:195-205, 2017 Sep 10.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Hepatocellular carcinoma (HCC) is known for high mortality and limited available treatments. Aberrant activation of the Wnt and Notch signaling pathways is critical to liver carcinogenesis and progression. Here, we identified a small molecule, bruceine D (BD), as a Notch inhibitor, using an RBP-Jκ-dependent luciferase-reporter system. BD significantly inhibited liver tumor growth and enhanced the therapeutic effects of sorafenib in various murine HCC models. Mechanistically, BD promotes proteasomal degradation of ß-catenin and the depletion of its nuclear accumulation, which in turn disrupts the Wnt/ß-catenin-dependent transcription of the Notch ligand Jagged1 in HCC. Our findings provide important information about a novel Wnt/Notch crosstalk inhibitor that is synergistic with sorafenib for treatment of HCC, and therefore have high clinical impact.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Carcinoma Hepatocelular/tratamento farmacológico
Proliferação Celular/efeitos dos fármacos
Proteína Jagged-1/metabolismo
Neoplasias Hepáticas/tratamento farmacológico
Quassinas/farmacologia
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Animais
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Apoptose/efeitos dos fármacos
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/patologia
Linhagem Celular Tumoral
Relação Dose-Resposta a Droga
Regulação para Baixo
Sinergismo Farmacológico
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Proteína Jagged-1/genética
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Masculino
Camundongos Endogâmicos BALB C
Camundongos Nus
Niacinamida/análogos & derivados
Niacinamida/farmacologia
Compostos de Fenilureia/farmacologia
Complexo de Endopeptidases do Proteassoma/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Proteólise
Fatores de Tempo
Transcrição Genética
Transfecção
Carga Tumoral/efeitos dos fármacos
Via de Sinalização Wnt/efeitos dos fármacos
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (CTNNB1 protein, human); 0 (JAG1 protein, human); 0 (Jagged-1 Protein); 0 (Phenylurea Compounds); 0 (Protein Kinase Inhibitors); 0 (Quassins); 0 (beta Catenin); 21499-66-1 (bruceine D); 25X51I8RD4 (Niacinamide); 9ZOQ3TZI87 (sorafenib); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170625
[St] Status:MEDLINE


  9 / 1056 MEDLINE  
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[PMID]:28636968
[Au] Autor:Maryanovich M; Frenette PS
[Ad] Endereço:Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine, New York, NY 10461, USA; Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York, NY 10461, USA.
[Ti] Título:T-Regulating Hair Follicle Stem Cells.
[So] Source:Immunity;46(6):979-981, 2017 Jun 20.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regulatory T (Treg) cells are well known to modulate inflammatory responses. In a recent issue of Cell, Ali et al. (2017) reveal a function for Treg cells in stem cell maintenance by showing that skin-resident Foxp3 Treg cells preferentially localize to the hair follicle stem cell (HFSC) niche to control HFSC-mediated hair regeneration.
[Mh] Termos MeSH primário: Células-Tronco Adultas/imunologia
Folículo Piloso/imunologia
Tolerância Imunológica
Nicho de Células-Tronco/imunologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Fatores de Transcrição Forkhead/metabolismo
Seres Humanos
Proteína Jagged-1/genética
Proteína Jagged-1/metabolismo
Camundongos
Camundongos Knockout
Receptores Notch/metabolismo
Regeneração
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Jag1 protein, mouse); 0 (Jagged-1 Protein); 0 (Receptors, Notch)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE


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[PMID]:28625320
[Au] Autor:Xue S; He L; Zhang X; Zhou J; Li F; Wang X
[Ad] Endereço:Department of Dermatology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
[Ti] Título:Expression of Jagged1/Notch3 Signaling Pathway and their Relationship with the Tumor Angiogenesis in TNBC.
[So] Source:Arch Med Res;48(2):169-179, 2017 Feb.
[Is] ISSN:1873-5487
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: Jagged1/Notch3 signaling pathway plays a key role in angiogenesis of breast cancer, but little is known in TNBC. This study was designed to investigate the expression of Jagged1/Notch3 mRNA and protein in TNBC, analyze their correlations with clinicopathological characteristics and prognosis. Moreover, the interrelationship among Jagged1/Notch3 and VEGF was initially evaluated. METHODS: Jagged1/Notch3 mRNA and protein expression levels were determined by Q-RT-PCR and Western blotting. Additionally, Immunohistochemistry for Jagged1/Notch3 was detected by Ventana platform, VEGF and CD34 was performed using the EnVision/HRP technique. RESULTS: mRNA transcriptionof Jagged1/Notch3 was in accord with protein expression. TNBC patients with positive Jagged1 expression had poorer DFS (p = 0.008) and OS (p = 0.004). Jagged1 expression was independent predictors of OS (p = 0.038). The expression of VEGF was positively correlative to MVD (p = 0.018), MVD was significantly associated with Jagged1 (p <0.0001) and Notch3 (p <0.0001). The expression of Jagged1/Notch3 has no correlation with VEGF, only in positive VEGF expression of TNBC patients Jagged1/Notch3 had influence on DFS and OS (p <0.05). CONCLUSION: Jagged1/Notch3 was -expressed at both the mRNA and protein levels, Jagged1 served as an independent predictor of poor prognosis. We speculate that there is a cross-talk between Jagged1/Notch3 and VEGF in TNBC angiogenesis. Jagged1/Notch3 is expected to be an important signaling pathway for TNBC progression and a potential target for TNBC neovascularization therapy.
[Mh] Termos MeSH primário: Proteína Jagged-1/metabolismo
Neovascularização Patológica/metabolismo
Receptor Notch3/metabolismo
Neoplasias de Mama Triplo Negativas/metabolismo
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Proteína Jagged-1/genética
Neovascularização Patológica/genética
Prognóstico
RNA Mensageiro/metabolismo
Transdução de Sinais
Neoplasias de Mama Triplo Negativas/irrigação sanguínea
Neoplasias de Mama Triplo Negativas/diagnóstico
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Jagged-1 Protein); 0 (RNA, Messenger); 0 (Receptor, Notch3); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE



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