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[PMID]:29229388
[Au] Autor:Zhou S; Yu L; Xiong M; Dai G
[Ad] Endereço:Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei, PR China.
[Ti] Título:LncRNA SNHG12 promotes tumorigenesis and metastasis in osteosarcoma by upregulating Notch2 by sponging miR-195-5p.
[So] Source:Biochem Biophys Res Commun;495(2):1822-1832, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Osteosarcoma is the most common primary malignant bone tumor and has a high fatality rate in children and adolescents. Recently, an increasing amount of evidence has demonstrated that lncRNAs have crucial roles in regulating biological characteristics in malignant tumors. Therefore, this research was carried out to uncover the biological function and the potential molecular mechanism of SNHG12 in osteosarcoma. In this study, we found that SNHG12 was significantly upregulated in both osteosarcoma tissues and cell lines and osteosarcoma patients with high levels of SNHG12 tended to have a poor prognosis. We evaluated the biological function of SNHG12 in 143B and U2OS cells and show that the downregulation of SNHG12 suppressed cell proliferation by blocking cell cycle progression at the G0/G1 phase and weakened cell invasion and migration abilities. Dual-luciferase reporter and RIP assays were conducted to confirm that SNHG12 functioned as a ceRNA, modulating the expression of Notch2 by sponging miR-195-5p in osteosarcoma. We further demonstrate that Notch2 played a crucial role in activating the Notch signaling pathway. In conclusion, SNHG12 might serve as a valuable biomarker and prognosis factor in osteosarcoma patients. The SNHG12/miR-195-5p/Notch2-Notch signaling pathway axis might become a novel therapeutic for osteosarcoma.
[Mh] Termos MeSH primário: Neoplasias Ósseas/genética
MicroRNAs/genética
Osteossarcoma/genética
RNA Longo não Codificante/genética
Receptor Notch2/genética
[Mh] Termos MeSH secundário: Neoplasias Ósseas/etiologia
Neoplasias Ósseas/patologia
Carcinogênese/genética
Pontos de Checagem do Ciclo Celular/genética
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Feminino
Técnicas de Silenciamento de Genes
Seres Humanos
Masculino
Modelos Biológicos
Invasividade Neoplásica/genética
Metástase Neoplásica/genética
Osteossarcoma/etiologia
Osteossarcoma/patologia
RNA Longo não Codificante/antagonistas & inibidores
Transdução de Sinais
Regulação para Cima
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MIRN195 microRNA, human); 0 (MicroRNAs); 0 (NOTCH2 protein, human); 0 (RNA, Long Noncoding); 0 (Receptor, Notch2); 0 (SNHG12 long non-coding RNA, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE


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[PMID]:27776108
[Au] Autor:Hombrink P; Helbig C; Backer RA; Piet B; Oja AE; Stark R; Brasser G; Jongejan A; Jonkers RE; Nota B; Basak O; Clevers HC; Moerland PD; Amsen D; van Lier RA
[Ad] Endereço:Department of Hematopoiesis, Sanquin Research and Landsteiner Laboratory, Amsterdam, the Netherlands.
[Ti] Título:Programs for the persistence, vigilance and control of human CD8 lung-resident memory T cells.
[So] Source:Nat Immunol;17(12):1467-1478, 2016 Dec.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tissue-resident memory T cells (T cells) in the airways mediate protection against respiratory infection. We characterized T cells expressing integrin α (CD103) that reside within the epithelial barrier of human lungs. These cells had specialized profiles of chemokine receptors and adhesion molecules, consistent with their unique localization. Lung T cells were poised for rapid responsiveness by constitutive expression of deployment-ready mRNA encoding effector molecules, but they also expressed many inhibitory regulators, suggestive of programmed restraint. A distinct set of transcription factors was active in CD103 T cells, including Notch. Genetic and pharmacological experiments with mice revealed that Notch activity was required for the maintenance of CD103 T cells. We have thus identified specialized programs underlying the residence, persistence, vigilance and tight control of human lung T cells.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/fisiologia
Memória Imunológica
Vírus da Influenza A Subtipo H3N2/imunologia
Pulmão/imunologia
Infecções por Orthomyxoviridae/imunologia
Receptor Notch1/metabolismo
Receptor Notch2/metabolismo
Infecções Respiratórias/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD/metabolismo
Células Cultivadas
Feminino
Seres Humanos
Cadeias alfa de Integrinas/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Meia-Idade
Receptor Notch1/genética
Receptor Notch2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Integrin alpha Chains); 0 (Notch1 protein, mouse); 0 (Notch2 protein, mouse); 0 (Receptor, Notch1); 0 (Receptor, Notch2); 0 (alpha E integrins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161101
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3589


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[PMID]:28820917
[Au] Autor:Sant DW; Tao W; Field MG; Pelaez D; Jin K; Capobianco A; Dubovy SR; Tse DT; Wang G
[Ad] Endereço:John P. Hussman Institute for Human Genomics, Dr. John T. Macdonald Foundation Department of Human Genetics, University of Miami Miller School of Medicine, Miami, Florida, United States.
[Ti] Título:Whole Exome Sequencing of Lacrimal Gland Adenoid Cystic Carcinoma.
[So] Source:Invest Ophthalmol Vis Sci;58(6):BIO240-BIO246, 2017 May 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: To identify genomic mutations in lacrimal gland adenoid cystic carcinoma (LGACC) samples from patients. Methods: Genomic DNA was extracted from LGACC specimens. Whole exome sequencing (exome-seq) was conducted to screen for mutations. Capillary sequencing was performed to verify mutations in genes shared by multiple samples. Luciferase assays were used to evaluate functional consequences of NOTCH1 mutations. Results: The mutation profile of LGACC was complicated. The most frequently mutated gene observed (28.6%) was bromodomain PHD finger transcription factor (BPTF). No mutation was identified in common cancer genes such as TP53, KRAS, and BRAF. However, mutations predicted to be functionally severe were accumulated in the Notch signaling pathway including NOTCH1 and NOTCH2, of which mutations have been reported in head/neck adenoid cystic carcinoma (ACC). Of 14 LGACC samples, five samples carry mutations in Notch pathway genes. Capillary sequencing verified all the mutations in the two NOTCH genes identified by exome-seq. Compared to the wild-type NOTCH1, three frame shifting mutations and two missense mutations (C387W and L1600Q) increased luciferase activity approximately 10- to 25-fold. Conclusions: Major genomic mutation profiles in LGACC were uncovered by exome-seq. Although preliminary in nature, the Notch pathway could be a potential therapeutic target for LGACC.
[Mh] Termos MeSH primário: Carcinoma Adenoide Cístico/genética
Exoma/genética
Neoplasias Oculares/genética
Genes Neoplásicos/genética
Doenças do Aparelho Lacrimal/genética
Receptor Notch1/genética
Receptor Notch2/genética
[Mh] Termos MeSH secundário: Western Blotting
DNA de Neoplasias/genética
Mutação da Fase de Leitura
Genes Reporter
Seres Humanos
Mutação de Sentido Incorreto
Plasmídeos
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Neoplasm); 0 (NOTCH1 protein, human); 0 (NOTCH2 protein, human); 0 (Receptor, Notch1); 0 (Receptor, Notch2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170826
[Lr] Data última revisão:
170826
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170819
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.16-21097


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[PMID]:28733035
[Au] Autor:Geng H; Guan J
[Ad] Endereço:Qingdao University, Qingdao, Shandong, 266000, China; Maternal and Child Health Hospital of Zibo City, Shandong, 255022, China.
[Ti] Título:MiR-18a-5p inhibits endothelial-mesenchymal transition and cardiac fibrosis through the Notch2 pathway.
[So] Source:Biochem Biophys Res Commun;491(2):329-336, 2017 Sep 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hyperglycemia plays a crucial role in the pathogenesis of diabetic complications; however, the mechanisms underlying diabetic cardiac fibrosis remain unclear. Endothelial cells are known to contribute to cardiac fibrosis through endothelial-mesenchymal transition (EndMT) under high glucose stimulation. Here we investigated the expression of miR-18a-5p and examined its functional role in human aortic valvular endothelial cells (HAVECs). Using HAVECs, we revealed that miR-18a-5p regulated high glucose-induced EndMT. Moreover, high glucose levels induced Notch2 expression, which promoted EndMT, resulting in the downregulation of vascular endothelial cadherin and CD31 and upregulation of fibroblast-specific protein-1, α-smooth muscle actin, fibronectin, and vimentin. Furthermore, Notch2 was identified as a target of miR-18a-5p. Our data showed that the overexpression of miR-18a-5p could downregulate Notch2 expression and subsequently suppress EndMT. In conclusion, our findings demonstrated that miR-18a-5p/Notch2 signaling pathway participates in the regulation of high glucose-induced EndMT, and may act as a novel promising target for myocardial fibrosis in diabetic cardiomyopathy.
[Mh] Termos MeSH primário: Dependovirus/genética
Cardiomiopatias Diabéticas/genética
Fibrose Endomiocárdica/genética
Transição Epitelial-Mesenquimal
MicroRNAs/genética
Receptor Notch2/genética
[Mh] Termos MeSH secundário: Actinas/genética
Actinas/metabolismo
Animais
Valva Aórtica/citologia
Valva Aórtica/efeitos dos fármacos
Valva Aórtica/metabolismo
Caderinas/genética
Caderinas/metabolismo
Proteínas de Ligação ao Cálcio/genética
Proteínas de Ligação ao Cálcio/metabolismo
Linhagem Celular
Dependovirus/metabolismo
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/genética
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Experimental/patologia
Cardiomiopatias Diabéticas/induzido quimicamente
Cardiomiopatias Diabéticas/patologia
Cardiomiopatias Diabéticas/prevenção & controle
Fibrose Endomiocárdica/induzido quimicamente
Fibrose Endomiocárdica/patologia
Fibrose Endomiocárdica/prevenção & controle
Células Endoteliais/citologia
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/metabolismo
Fibronectinas/genética
Fibronectinas/metabolismo
Regulação da Expressão Gênica
Vetores Genéticos/administração & dosagem
Vetores Genéticos/química
Vetores Genéticos/metabolismo
Glucose/farmacologia
Ventrículos do Coração/metabolismo
Ventrículos do Coração/patologia
Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
MicroRNAs/metabolismo
Molécula-1 de Adesão Celular Endotelial de Plaquetas/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Receptor Notch2/metabolismo
Transdução de Sinais
Estreptozocina
Vimentina/genética
Vimentina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (Cadherins); 0 (Calcium-Binding Proteins); 0 (FSP1 protein, human); 0 (Fibronectins); 0 (MIRN18A microRNA, human); 0 (MicroRNAs); 0 (NOTCH2 protein, human); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Receptor, Notch2); 0 (Vimentin); 5W494URQ81 (Streptozocin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170723
[St] Status:MEDLINE


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[PMID]:28705113
[Au] Autor:Wang J; Liu Q; Gao H; Wan D; Li C; Li Z; Zhang Y
[Ad] Endereço:1 Beijing Neurosurgical Institute, Capital Medical University, Beijing, China.
[Ti] Título:EGFL7 participates in regulating biological behavior of growth hormone-secreting pituitary adenomas via Notch2/DLL3 signaling pathway.
[So] Source:Tumour Biol;39(7):1010428317706203, 2017 Jul.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Growth hormone-secreting pituitary adenoma accounts for about 20% of the third most common intracranial neoplasm-pituitary adenomas-which makes up 15% of all intracranial tumors. The growth hormone-secreting pituitary adenoma invasion is a key risk factor associated with the operation results and highly correlated with the clinical prognosis. The epidermal growth factor-like domain multiple 7 protein, a unique 29 kDa secreted angiogenic factor, can result in pathologic angiogenesis and enhance the tumor migration and invasion. In this study, for the first time we found that epidermal growth factor-like domain multiple 7 protein expression was markedly higher in invasive growth hormone-secreting pituitary adenoma than non-invasive growth hormone-secreting pituitary adenoma. The tumor volume, histologic subtypes, invasiveness and recurrence of growth hormone-secreting pituitary adenoma were significantly associated with epidermal growth factor-like domain multiple 7 protein expression. Furthermore, we discovered that the histological classification methods of growth hormone-secreting pituitary adenoma according to electron microscopic examination and biological marker classification methods according to epidermal growth factor-like domain multiple 7 protein expression are more valuable in clinical application than the traditional classification methods based on Knosp and Hardy-Wilson grades. In summary, our results indicated epidermal growth factor-like domain multiple 7 protein participates in growth hormone-secreting pituitary adenoma proliferation and invasion regulation via Notch2/DLL3 signaling pathway. These findings raised the possibility that epidermal growth factor-like domain multiple 7 protein might serve as a useful biomarker to assess growth hormone-secreting pituitary adenoma invasion and prognosis or a potential therapeutic target for growth hormone-secreting pituitary adenoma treatment.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Neoplasias Encefálicas/genética
Fatores de Crescimento Endotelial/genética
Adenoma Hipofisário Secretor de Hormônio do Crescimento/genética
Peptídeos e Proteínas de Sinalização Intracelular/genética
Proteínas de Membrana/genética
Receptor Notch2/genética
[Mh] Termos MeSH secundário: Adulto
Neoplasias Encefálicas/patologia
Fatores de Crescimento Endotelial/biossíntese
Feminino
Regulação Neoplásica da Expressão Gênica
Adenoma Hipofisário Secretor de Hormônio do Crescimento/patologia
Seres Humanos
Masculino
Meia-Idade
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Recidiva Local de Neoplasia/genética
Recidiva Local de Neoplasia/patologia
Prognóstico
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (DLL3 protein, human); 0 (EGFL7 protein, human); 0 (Endothelial Growth Factors); 0 (Intracellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (NOTCH2 protein, human); 0 (Receptor, Notch2)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170728
[Lr] Data última revisão:
170728
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317706203


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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


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[PMID]:28592489
[Au] Autor:Zanotti S; Yu J; Sanjay A; Schilling L; Schoenherr C; Economides AN; Canalis E
[Ad] Endereço:From the Departments of Orthopaedic Surgery and.
[Ti] Título:Sustained Notch2 signaling in osteoblasts, but not in osteoclasts, is linked to osteopenia in a mouse model of Hajdu-Cheney syndrome.
[So] Source:J Biol Chem;292(29):12232-12244, 2017 Jul 21.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Individuals with Hajdu-Cheney syndrome (HCS) present with osteoporosis, and HCS is associated with mutations causing deletions of the proline-, glutamic acid-, serine-, and threonine-rich (PEST) domain that are predicted to enhance NOTCH2 stability and cause gain-of-function. Previously, we demonstrated that mice harboring mutations analogous to those in HCS ( ) are severely osteopenic because of enhanced bone resorption. We attributed this phenotype to osteoclastic sensitization to the receptor activator of nuclear factor-κB ligand and increased osteoblastic tumor necrosis factor superfamily member 11 ( ) expression. Here, to determine the individual contributions of osteoclasts and osteoblasts to HCS osteopenia, we created a conditional-by-inversion ( ) model in which Cre recombination generates a allele expressing a Notch2 mutant lacking the PEST domain. Germ line inversion phenocopied the mutant, validating the model. To activate Notch2 in osteoclasts or osteoblasts, mice were bred with mice expressing Cre from the or the promoter, respectively. These crosses created experimental mice harboring a allele in Cre-expressing cells and control littermates expressing a wild-type transcript. inversion in -expressing cells had no skeletal consequences and did not affect the capacity of bone marrow macrophages to form osteoclasts In contrast, inversion in osteoblasts led to generalized osteopenia associated with enhanced bone resorption in the cancellous bone compartment and with suppressed endocortical mineral apposition rate. Accordingly, activation in osteoblast-enriched cultures from mice induced expression. In conclusion, introduction of the HCS mutation in osteoblasts, but not in osteoclasts, causes osteopenia.
[Mh] Termos MeSH primário: Doenças Ósseas Metabólicas/etiologia
Síndrome de Hajdu-Cheney/fisiopatologia
Mutação
Osteoblastos/metabolismo
Receptor Notch2/genética
Transdução de Sinais
[Mh] Termos MeSH secundário: Alelos
Animais
Células da Medula Óssea/imunologia
Células da Medula Óssea/metabolismo
Células da Medula Óssea/patologia
Células Cultivadas
Cruzamentos Genéticos
Feminino
Deleção de Genes
Síndrome de Hajdu-Cheney/imunologia
Síndrome de Hajdu-Cheney/metabolismo
Síndrome de Hajdu-Cheney/patologia
Seres Humanos
Macrófagos/imunologia
Macrófagos/metabolismo
Macrófagos/patologia
Masculino
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Osteoblastos/patologia
Osteoclastos/metabolismo
Osteoclastos/patologia
Domínios e Motivos de Interação entre Proteínas
Receptor Notch2/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (NOTCH2 protein, human); 0 (Notch2 protein, mouse); 0 (Receptor, Notch2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.786129


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[PMID]:28581486
[Au] Autor:Wu N; Nguyen Q; Wan Y; Zhou T; Venter J; Frampton GA; DeMorrow S; Pan D; Meng F; Glaser S; Alpini G; Bai H
[Ad] Endereço:Department of Medicine, Texas A&M Health Science Center, College of Medicine, Temple, TX, USA.
[Ti] Título:The Hippo signaling functions through the Notch signaling to regulate intrahepatic bile duct development in mammals.
[So] Source:Lab Invest;97(7):843-853, 2017 Jul.
[Is] ISSN:1530-0307
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Hippo signaling pathway and the Notch signaling pathway are evolutionary conserved signaling cascades that have important roles in embryonic development of many organs. In murine liver, disruption of either pathway impairs intrahepatic bile duct development. Recent studies suggested that the Notch signaling receptor Notch2 is a direct transcriptional target of the Hippo signaling pathway effector YAP, and the Notch signaling is a major mediator of the Hippo signaling in maintaining biliary cell characteristics in adult mice. However, it remains to be determined whether the Hippo signaling pathway functions through the Notch signaling in intrahepatic bile duct development. We found that loss of the Hippo signaling pathway tumor suppressor Nf2 resulted in increased expression levels of the Notch signaling pathway receptor Notch2 in cholangiocytes but not in hepatocytes. When knocking down Notch2 on the background of Nf2 deficiency in mouse livers, the excessive bile duct development induced by Nf2 deficiency was suppressed by heterozygous and homozygous deletion of Notch2 in a dose-dependent manner. These results implicated that Notch signaling is one of the downstream effectors of the Hippo signaling pathway in regulating intrahepatic bile duct development.
[Mh] Termos MeSH primário: Ductos Biliares Intra-Hepáticos/crescimento & desenvolvimento
Neurofibromatose 2/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Receptor Notch2/metabolismo
[Mh] Termos MeSH secundário: Animais
Ductos Biliares Intra-Hepáticos/metabolismo
Ductos Biliares Intra-Hepáticos/patologia
Feminino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Neurofibromatose 2/genética
Proteínas Serina-Treonina Quinases/genética
Receptor Notch2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Notch2 protein, mouse); 0 (Receptor, Notch2); EC 2.7.11.1 (Hippo protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.1038/labinvest.2017.29


  9 / 577 MEDLINE  
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[PMID]:28572448
[Au] Autor:Suckling RJ; Korona B; Whiteman P; Chillakuri C; Holt L; Handford PA; Lea SM
[Ad] Endereço:Sir William Dunn School of Pathology, University of Oxford, Oxford, UK.
[Ti] Título:Structural and functional dissection of the interplay between lipid and Notch binding by human Notch ligands.
[So] Source:EMBO J;36(15):2204-2215, 2017 Aug 01.
[Is] ISSN:1460-2075
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Recent data have expanded our understanding of Notch signalling by identifying a C2 domain at the N-terminus of Notch ligands, which has both lipid- and receptor-binding properties. We present novel structures of human ligands Jagged2 and Delta-like4 and human Notch2, together with functional assays, which suggest that ligand-mediated coupling of membrane recognition and Notch binding is likely to be critical in establishing the optimal context for Notch signalling. Comparisons between the Jagged and Delta family show a huge diversity in the structures of the loops at the apex of the C2 domain implicated in membrane recognition and Jagged1 missense mutations, which affect these loops and are associated with extrahepatic biliary atresia, lead to a loss of membrane recognition, but do not alter Notch binding. Taken together, these data suggest that C2 domain binding to membranes is an important element in tuning ligand-dependent Notch signalling in different physiological contexts.
[Mh] Termos MeSH primário: Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Proteína Jagged-2/metabolismo
Metabolismo dos Lipídeos
Proteínas de Membrana/metabolismo
Receptor Notch1/metabolismo
Receptor Notch2/metabolismo
[Mh] Termos MeSH secundário: Cristalografia por Raios X
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/química
Proteína Jagged-2/química
Proteínas de Membrana/química
Modelos Moleculares
Ligação Proteica
Conformação Proteica
Domínios Proteicos
Receptor Notch2/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Intracellular Signaling Peptides and Proteins); 0 (Jagged-2 Protein); 0 (Membrane Proteins); 0 (NOTCH1 protein, human); 0 (NOTCH2 protein, human); 0 (Receptor, Notch1); 0 (Receptor, Notch2); 0 (delta protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.15252/embj.201796632


  10 / 577 MEDLINE  
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[PMID]:28495268
[Au] Autor:Torres-Ortiz MC; Gutiérrez-Ospina G; Gómez-Chavarín M; Murcia C; Alonso-Morales RA; Perera-Marín G
[Ad] Endereço:Departamento de Reproducción, Facultad de Medicina Veterinaria y Zootecnia, Universidad Nacional Autónoma de México, Mexico; Departamento de Biología Celular y Fisiología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Mexico.
[Ti] Título:The presence of VEGF and Notch2 during preantral-antral follicular transition in infantile rats: Anatomical evidence and its implications.
[So] Source:Gen Comp Endocrinol;249:82-92, 2017 Aug 01.
[Is] ISSN:1095-6840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Folliculogenesis is a process that depends on angiogenesis, in which VEGF and Notch signaling pathway members are involved. Although this pathway is present in preantral and antral follicular structures during the second stage of folliculogenesis, this association has not been described. Therefore, this study aimed to identify VEGF and Notch2 in ovary structures of infantile rats after induction of follicular development with a gonadotropin stimulus. In order to explore this possibility we analyzed rat ovary morphology from days 10-25 after birth; subsequently, the transition from preantral follicle to an antral stage was analyzed by the induction of follicular development with equine chorionic gonadotropin (eCG) and VEGF and Notch were identified in the rat ovary by fluorescence. The histological analysis revealed that the ovary of a 10-day-old rat has the highest percentage of preantral follicles and based on this a 10IU eCG dose promoted an increase in the number of antral follicles, as well as a decrease in the number of preantral follicles, related to which there was an increase in ovary weight and size. In addition, a higher concentration of circulating estradiol was observed, proliferation of granulosa cells in both follicle groups was stimulated, and the accumulation of VEGF in granulosa and theca cells and in the antral follicle oocyte was increased (p<0.05), whereas the presence of Notch2 was limited to mural granulosa cells, in granulosa cells that formed the cumulus oophorus and in the oocyte of both groups of follicles. The multiple correspondence analysis allowed us to support an association between VEGF and Notch2 during the transition from preantral to antral follicles in the ovary of an infantile rat.
[Mh] Termos MeSH primário: Folículo Ovariano/anatomia & histologia
Folículo Ovariano/metabolismo
Receptor Notch2/metabolismo
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Mh] Termos MeSH secundário: Animais
Contagem de Células
Proliferação Celular/efeitos dos fármacos
Gonadotropina Coriônica/farmacologia
Estradiol/sangue
Estradiol/metabolismo
Feminino
Células da Granulosa/citologia
Células da Granulosa/efeitos dos fármacos
Células da Granulosa/metabolismo
Cavalos
Folículo Ovariano/embriologia
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chorionic Gonadotropin); 0 (Notch2 protein, rat); 0 (Receptor, Notch2); 0 (Vascular Endothelial Growth Factor A); 4TI98Z838E (Estradiol)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170513
[St] Status:MEDLINE



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