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[PMID]:28455376
[Au] Autor:Tavares ALP; Cox TC; Maxson RM; Ford HL; Clouthier DE
[Ad] Endereço:Department of Craniofacial Biology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
[Ti] Título:Negative regulation of endothelin signaling by SIX1 is required for proper maxillary development.
[So] Source:Development;144(11):2021-2031, 2017 06 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Jaw morphogenesis is a complex event mediated by inductive signals that establish and maintain the distinct developmental domains required for formation of hinged jaws, the defining feature of gnathostomes. The mandibular portion of pharyngeal arch 1 is patterned dorsally by Jagged-Notch signaling and ventrally by endothelin receptor A (EDNRA) signaling. Loss of EDNRA signaling disrupts normal ventral gene expression, the result of which is homeotic transformation of the mandible into a maxilla-like structure. However, loss of Jagged-Notch signaling does not result in significant changes in maxillary development. Here we show in mouse that the transcription factor SIX1 regulates dorsal arch development not only by inducing dorsal expression but also by inhibiting endothelin 1 ( ) expression in the pharyngeal endoderm of the dorsal arch, thus preventing dorsal EDNRA signaling. In the absence of SIX1, but not JAG1, aberrant EDNRA signaling in the dorsal domain results in partial duplication of the mandible. Together, our results illustrate that SIX1 is the central mediator of dorsal mandibular arch identity, thus ensuring separation of bone development between the upper and lower jaws.
[Mh] Termos MeSH primário: Endotelina-1/metabolismo
Proteínas de Homeodomínio/metabolismo
Maxila/embriologia
Maxila/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Padronização Corporal/genética
Região Branquial/metabolismo
Anormalidades Craniofaciais/embriologia
Anormalidades Craniofaciais/genética
Anormalidades Craniofaciais/patologia
Embrião de Mamíferos/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Integrases/metabolismo
Camundongos
Modelos Biológicos
Crista Neural/metabolismo
Receptor de Endotelina A/metabolismo
Receptores Notch/metabolismo
Proteínas Serrate-Jagged/metabolismo
Fator de Transcrição Sp7
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Regulação para Cima/genética
Zigoma/embriologia
Zigoma/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Homeodomain Proteins); 0 (Receptor, Endothelin A); 0 (Receptors, Notch); 0 (Serrate-Jagged Proteins); 0 (Six1 protein, mouse); 0 (Sp7 Transcription Factor); 0 (Sp7 protein, mouse); 0 (Transcription Factors); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1242/dev.145144


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[PMID]:28734865
[Au] Autor:Tveitarås MK; Reigstad I; Leiss L; Reed RK; Stuhr L
[Ad] Endereço:Department of Biomedicine, University of Bergen, 5009 Bergen, Norway; Matrix Biology group, Haukeland University Hospital, Norway; Center for Cancer Biomarkers (CCBIO), University of Bergen, Norway.
[Ti] Título:Single factors alone can induce mesenchymal-like morphology, but not promote full EMT in breast cancer cell lines with different hormone statuses.
[So] Source:Exp Cell Res;359(1):257-265, 2017 Oct 01.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Epithelial to mesenchymal transition (EMT) is considered to be important for cancer invasion and metastasis. Tumour hypoxia, in addition to Transforming Growth Factor-ß (TGF-ß) and Notch, amongst others, have been suggested to be involved in EMT. We therefore investigated if hypoxia, TGF-ß1 and the Notch ligand Jagged-1 alone induced morphological changes with corresponding EMT signatures in different epithelial breast cancer cell lines in vitro. Furthermore, we also studied whether or not TGF-ß1, or Jagged-1 in combination with hypoxia added any effect on EMT. METHODS: The cells were exposed to normoxia or hypoxia alone or in combination with TGF-ß1 or Jagged-1. Morphological responses to treatment were investigated by light microscopy, and changes in markers for EMT and hypoxia were evaluated by western blot analysis and immunofluorescence studies. RESULTS: One of the four cell lines (MCF7) became elongated and highly multipolar, indicative of EMT, following hypoxia, TGF-ß1 and Jagged-1 treatment per se with the most distinct morphological shift seen with Jagged-1 treatment in combination with hypoxia. Also, when regarding hypoxia, MCF7 cells showed the greatest change in EMT-markers of the four cell lines tested, but these changes were not consistent with a typical EMT pattern. The morphology of BT474 cells was not altered following Jagged-1 treatment, however, Jagged-1 increased E-cadherin levels. Morphology was changed following TGF-ß1 treatment of BT474 cells, but it did not affect E-cadherin levels. Neither Jagged-1 nor TGF-ß1 altered the levels of Vimentin in the BT474 cell line. The E-cadherin responses to hypoxia varied with end-point in both MCF7 and BT474 cells, and in most cases were not consistent with EMT. CONCLUSION: Our results using four different breast cancer cell lines in vitro do not provide evidence that EMT is induced by hypoxia alone or in combination with TGF-ß1 or the Notch ligand Jagged-1. The inconsistency in morphological appearance and EMT-markers, as well as the time dependent variation in E-cadherin responses could not support EMT. Importantly, there was not one single common response pattern to the stimuli used, suggesting that cell lines with different hormone statuses display individual traits that respond differently to the stimuli applied. Thus, based on the present results, common statements that single factors by themselves can induce EMT seem questionable.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Transição Epitelial-Mesenquimal
Hormônios/metabolismo
Mesoderma/patologia
[Mh] Termos MeSH secundário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Western Blotting
Hipóxia Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Feminino
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Ligantes
Mesoderma/efeitos dos fármacos
Receptores Notch/metabolismo
Proteínas Serrate-Jagged/metabolismo
Fator de Crescimento Transformador beta1/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (HIF1A protein, human); 0 (Hormones); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Ligands); 0 (Receptors, Notch); 0 (Serrate-Jagged Proteins); 0 (Transforming Growth Factor beta1); 0 (endothelial PAS domain-containing protein 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170724
[St] Status:MEDLINE


  3 / 1136 MEDLINE  
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[PMID]:28478502
[Au] Autor:Rapp JB; Bellah RD; Maya C; Pawel BR; Anupindi SA
[Ad] Endereço:Department of Radiology, Temple University Hospital, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA.
[Ti] Título:Frequency and pathogenesis of central liver nodules in Alagille syndrome patients: Reply to Libbrecht and Cassiman.
[So] Source:Pediatr Radiol;47(8):1025, 2017 07.
[Is] ISSN:1432-1998
[Cp] País de publicação:Germany
[La] Idioma:eng
[Mh] Termos MeSH primário: Síndrome de Alagille
Neoplasias Hepáticas
[Mh] Termos MeSH secundário: Seres Humanos
Proteínas Serrate-Jagged
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
0 (Serrate-Jagged Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170508
[St] Status:MEDLINE
[do] DOI:10.1007/s00247-017-3881-2


  4 / 1136 MEDLINE  
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[PMID]:28474254
[Au] Autor:Libbrecht L; Cassiman D
[Ad] Endereço:Liver Research Unit, University of Leuven, Leuven, Belgium. louis.libbrecht@uclouvain.be.
[Ti] Título:Frequency and pathogenesis of central liver nodules in Alagille syndrome patients.
[So] Source:Pediatr Radiol;47(8):1023-1024, 2017 07.
[Is] ISSN:1432-1998
[Cp] País de publicação:Germany
[La] Idioma:eng
[Mh] Termos MeSH primário: Síndrome de Alagille
Neoplasias Hepáticas
[Mh] Termos MeSH secundário: Seres Humanos
Proteínas Serrate-Jagged
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
0 (Serrate-Jagged Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE
[do] DOI:10.1007/s00247-017-3880-3


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[PMID]:28394891
[Au] Autor:Lee TV; Pandey A; Jafar-Nejad H
[Ad] Endereço:Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, United States of America.
[Ti] Título:Xylosylation of the Notch receptor preserves the balance between its activation by trans-Delta and inhibition by cis-ligands in Drosophila.
[So] Source:PLoS Genet;13(4):e1006723, 2017 Apr.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Drosophila glucoside xylosyltransferase Shams xylosylates Notch and inhibits Notch signaling in specific contexts including wing vein development. However, the molecular mechanisms underlying context-specificity of the shams phenotype is not known. Considering the role of Delta-Notch signaling in wing vein formation, we hypothesized that Shams might affect Delta-mediated Notch signaling in Drosophila. Using genetic interaction studies, we find that altering the gene dosage of Delta affects the wing vein and head bristle phenotypes caused by loss of Shams or by mutations in the Notch xylosylation sites. Clonal analysis suggests that loss of shams promotes Delta-mediated Notch activation. Further, Notch trans-activation by ectopically overexpressed Delta shows a dramatic increase upon loss of shams. In agreement with the above in vivo observations, cell aggregation and ligand-receptor binding assays show that shams knock-down in Notch-expressing cells enhances the binding between Notch and trans-Delta without affecting the binding between Notch and trans-Serrate and cell surface levels of Notch. Loss of Shams does not impair the cis-inhibition of Notch by ectopic overexpression of ligands in vivo or the interaction of Notch and cis-ligands in S2 cells. Nevertheless, removing one copy of endogenous ligands mimics the effects of loss shams on Notch trans-activation by ectopic Delta. This favors the notion that trans-activation of Notch by Delta overcomes the cis-inhibition of Notch by endogenous ligands upon loss of shams. Taken together, our data suggest that xylosylation selectively impedes the binding of Notch with trans-Delta without affecting its binding with cis-ligands and thereby assists in determining the balance of Notch receptor's response to cis-ligands vs. trans-Delta during Drosophila development.
[Mh] Termos MeSH primário: Proteínas de Homeodomínio/genética
Discos Imaginais/crescimento & desenvolvimento
Receptores Notch/genética
Proteínas Serrate-Jagged/genética
Fatores de Transcrição/genética
Asas de Animais/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Animais
Drosophila melanogaster/genética
Drosophila melanogaster/crescimento & desenvolvimento
Regulação da Expressão Gênica no Desenvolvimento/genética
Proteínas de Homeodomínio/metabolismo
Discos Imaginais/metabolismo
Ligantes
Mutação
Fenótipo
Ligação Proteica
Receptores Notch/metabolismo
Proteínas Serrate-Jagged/metabolismo
Transdução de Sinais
Fatores de Transcrição/metabolismo
Asas de Animais/metabolismo
Xilose/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Homeodomain Proteins); 0 (Ligands); 0 (Receptors, Notch); 0 (Serrate-Jagged Proteins); 0 (Transcription Factors); 0 (distal-less protein, insect); A1TA934AKO (Xylose)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170602
[Lr] Data última revisão:
170602
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006723


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[PMID]:27487663
[Au] Autor:Golubtzova NN; Vasiliyeva OV; Petrov VV; Gunin AG
[Ti] Título:[CHANGES OF THE CONTENT OF DLL4 AND Jag-1 ANGIOGENESIS REGULATORS IN HUMAN DERMIS IN ONTOGENESIS].
[So] Source:Morfologiia;149(1):48-52, 2016.
[Is] ISSN:1026-3543
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The goal of this study was to examine the contents of D114 and Jag-1 angiogenesis regulators in human dermis at different age periods. D114 and Jag-1 were demonstrated by indirect immunohistochemistry in skin sections of fetuses of 20-40 gestational weeks and in persons aged from birth to 85 years. D114 was studied in 150 skin samples of 72 females and 78 males, while Jag-1 was examined in 120 samples of 58 females and 62 males. It is found that the immunoreactivity was mainly expressed by the endothelial cells. Vessels, which gave a positive reaction to D114 and Jag-1, were found throughout the entire thickness of the dermis, both in fetuses, and people of all age groups. Expression of D114 in the vessels of dermal microvasculature was shown to increase from 20 weeks of gestation to 20 years. With the further age increase, the intensity of the reaction of blood vessels for D114 was decreased. Expression of Jag-1 in dermal microvessels was enhanced from 20 weeks of gestation to 85 years. The results are discussed in connection with the role of D114 and Jag-1 in angiogenesis in human dermis during ontogeny.
[Mh] Termos MeSH primário: Proteínas de Ligação ao Cálcio/biossíntese
Derme
Células Endoteliais/metabolismo
Regulação da Expressão Gênica/fisiologia
Peptídeos e Proteínas de Sinalização Intercelular/biossíntese
Proteínas de Membrana/biossíntese
Envelhecimento da Pele/fisiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Criança
Pré-Escolar
Derme/irrigação sanguínea
Derme/citologia
Derme/metabolismo
Células Endoteliais/citologia
Feminino
Seres Humanos
Lactente
Recém-Nascido
Masculino
Meia-Idade
Proteínas Serrate-Jagged
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Calcium-Binding Proteins); 0 (DLL4 protein, human); 0 (Intercellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (Serrate-Jagged Proteins)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160805
[St] Status:MEDLINE


  7 / 1136 MEDLINE  
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[PMID]:26971877
[Au] Autor:Kerr BA; West XZ; Kim YW; Zhao Y; Tischenko M; Cull RM; Phares TW; Peng XD; Bernier-Latmani J; Petrova TV; Adams RH; Hay N; Naga Prasad SV; Byzova TV
[Ad] Endereço:Department of Molecular Cardiology, Joseph J. Jacobs Center for Thrombosis and Vascular Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA.
[Ti] Título:Stability and function of adult vasculature is sustained by Akt/Jagged1 signalling axis in endothelium.
[So] Source:Nat Commun;7:10960, 2016 Mar 14.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The signalling pathways operational in quiescent, post-development vasculature remain enigmatic. Here we show that unlike neovascularization, endothelial Akt signalling in established vasculature is crucial not for endothelial cell (EC) survival, but for sustained interactions with pericytes and vascular smooth muscle cells (VSMCs) regulating vascular stability and function. Inducible endothelial-specific Akt1 deletion in adult global Akt2KO mice triggers progressive VSMC apoptosis. In hearts, this causes a loss of arteries and arterioles and, despite a high capillary density, diminished vascular patency and severe cardiac dysfunction. Similarly, endothelial Akt deletion induces retinal VSMC loss and basement membrane deterioration resulting in vascular regression and retinal atrophy. Mechanistically, the Akt/mTOR axis controls endothelial Jagged1 expression and, thereby, Notch signalling regulating VSMC maintenance. Jagged1 peptide treatment of Akt1ΔEC;Akt2KO mice and Jagged1 re-expression in Akt-deficient endothelium restores VSMC coverage. Thus, sustained endothelial Akt1/2 signalling is critical in maintaining vascular stability and homeostasis, thereby preserving tissue and organ function.
[Mh] Termos MeSH primário: Vasos Sanguíneos/metabolismo
Proteínas de Ligação ao Cálcio/genética
Células Endoteliais/metabolismo
Endotélio/metabolismo
Homeostase/genética
Peptídeos e Proteínas de Sinalização Intercelular/genética
Proteínas de Membrana/genética
Proteínas Proto-Oncogênicas c-akt/genética
[Mh] Termos MeSH secundário: Angiografia
Animais
Materiais Biocompatíveis
Barreira Hematoencefálica/metabolismo
Proteínas de Ligação ao Cálcio/metabolismo
Colágeno
Vasos Coronários/metabolismo
Combinação de Medicamentos
Ecocardiografia
Olho/irrigação sanguínea
Imunofluorescência
Regulação da Expressão Gênica
Coração
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Immunoblotting
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Proteína Jagged-1
Laminina
Pulmão/irrigação sanguínea
Proteínas de Membrana/metabolismo
Camundongos
Camundongos Knockout
Músculo Liso Vascular/citologia
Miócitos de Músculo Liso
Pericitos
Proteoglicanas
Proteínas Proto-Oncogênicas c-akt/metabolismo
Retina
Vasos Retinianos/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Proteínas Serrate-Jagged
Transdução de Sinais/genética
Microtomografia por Raio-X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biocompatible Materials); 0 (Calcium-Binding Proteins); 0 (Drug Combinations); 0 (Intercellular Signaling Peptides and Proteins); 0 (JAG1 protein, human); 0 (Jag1 protein, mouse); 0 (Jagged-1 Protein); 0 (Laminin); 0 (Membrane Proteins); 0 (Proteoglycans); 0 (Serrate-Jagged Proteins); 119978-18-6 (matrigel); 9007-34-5 (Collagen); EC 2.7.11.1 (Akt1 protein, mouse); EC 2.7.11.1 (Akt2 protein, mouse); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160315
[St] Status:MEDLINE
[do] DOI:10.1038/ncomms10960


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[PMID]:26965898
[Au] Autor:Tattersall IW; Du J; Cong Z; Cho BS; Klein AM; Dieck CL; Chaudhri RA; Cuervo H; Herts JH; Kitajewski J
[Ad] Endereço:Obstetrics/Gynecology, Columbia University, New York, NY, USA.
[Ti] Título:In vitro modeling of endothelial interaction with macrophages and pericytes demonstrates Notch signaling function in the vascular microenvironment.
[So] Source:Angiogenesis;19(2):201-15, 2016 Apr.
[Is] ISSN:1573-7209
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Angiogenesis is regulated by complex interactions between endothelial cells and support cells of the vascular microenvironment, such as tissue myeloid cells and vascular mural cells. Multicellular interactions during angiogenesis are difficult to study in animals and challenging in a reductive setting. We incorporated stromal cells into an established bead-based capillary sprouting assay to develop assays that faithfully reproduce major steps of vessel sprouting and maturation. We observed that macrophages enhance angiogenesis, increasing the number and length of endothelial sprouts, a property we have dubbed "angiotrophism." We found that polarizing macrophages toward a pro-inflammatory profile further increased their angiotrophic stimulation of vessel sprouting, and this increase was dependent on macrophage Notch signaling. To study endothelial/pericyte interactions, we added vascular pericytes directly to the bead-bound endothelial monolayer. These pericytes formed close associations with the endothelial sprouts, causing increased sprout number and vessel caliber. We found that Jagged1 expression and Notch signaling are essential for the growth of both endothelial cells and pericytes and may function in their interaction. We observed that combining endothelial cells with both macrophages and pericytes in the same sprouting assay has multiplicative effects on sprouting. These results significantly improve bead-capillary sprouting assays and provide an enhanced method for modeling interactions between the endothelium and the vascular microenvironment. Achieving this in a reductive in vitro setting represents a significant step toward a better understanding of the cellular elements that contribute to the formation of mature vasculature.
[Mh] Termos MeSH primário: Comunicação Celular
Microambiente Celular
Células Endoteliais da Veia Umbilical Humana/citologia
Macrófagos/citologia
Modelos Biológicos
Neovascularização Fisiológica
Pericitos/citologia
Receptores Notch/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Polaridade Celular
Sobrevivência Celular
Técnicas de Cocultura
Técnicas de Silenciamento de Genes
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Inflamação/patologia
Mediadores da Inflamação/metabolismo
Macrófagos/metabolismo
Camundongos
Células Mieloides/citologia
Células Mieloides/metabolismo
Pericitos/metabolismo
Proteínas Serrate-Jagged/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Inflammation Mediators); 0 (Receptors, Notch); 0 (Serrate-Jagged Proteins)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160312
[St] Status:MEDLINE
[do] DOI:10.1007/s10456-016-9501-1


  9 / 1136 MEDLINE  
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[PMID]:26939553
[Au] Autor:Wang W; Jossin Y; Chai G; Lien WH; Tissir F; Goffinet AM
[Ad] Endereço:Université catholique de Louvain, Institute of Neuroscience, 73 Avenue Mounier, Box B1.7316, 1200 Brussels, Belgium.
[Ti] Título:Feedback regulation of apical progenitor fate by immature neurons through Wnt7-Celsr3-Fzd3 signalling.
[So] Source:Nat Commun;7:10936, 2016 Mar 04.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Sequential generation of neurons and glial cells during development is critical for the wiring and function of the cerebral cortex. This process requires accurate coordination of neural progenitor cell (NPC) fate decisions, by NPC-autonomous mechanisms as well as by negative feedback from neurons. Here, we show that neurogenesis is protracted and gliogenesis decreased in mice with mutations of genes Celsr3 and Fzd3. This phenotype is not due to gene inactivation in progenitors, but rather in immature cortical neurons. Mutant neurons are unable to upregulate expression of Jag1 in response to cortical Wnt7, resulting in blunted activation of Notch signalling in NPC. Thus, Celsr3 and Fzd3 enable immature neurons to respond to Wnt7, upregulate Jag1 and thereby facilitate feedback signals that tune the timing of NPC fate decisions via Notch activation.
[Mh] Termos MeSH primário: Caderinas/metabolismo
Receptores Frizzled/metabolismo
Regulação da Expressão Gênica/fisiologia
Proteínas Proto-Oncogênicas/metabolismo
Receptores de Superfície Celular/metabolismo
Transdução de Sinais/fisiologia
Proteínas Wnt/metabolismo
[Mh] Termos MeSH secundário: Animais
Bromodesoxiuridina
Caderinas/genética
Proteínas de Ligação ao Cálcio/genética
Proteínas de Ligação ao Cálcio/metabolismo
Córtex Cerebral/citologia
Córtex Cerebral/embriologia
Feminino
Receptores Frizzled/genética
Peptídeos e Proteínas de Sinalização Intercelular/genética
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Proteína Jagged-1
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Camundongos
Mutação
Neurogênese/fisiologia
Gravidez
Proteínas Proto-Oncogênicas/genética
Receptores de Superfície Celular/genética
Receptores Notch/genética
Receptores Notch/metabolismo
Proteínas Serrate-Jagged
Coloração e Rotulagem
Proteínas Wnt/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cadherins); 0 (Calcium-Binding Proteins); 0 (Celsr3 protein, mouse); 0 (Frizzled Receptors); 0 (Fzd3 protein, mouse); 0 (Intercellular Signaling Peptides and Proteins); 0 (Jag1 protein, mouse); 0 (Jagged-1 Protein); 0 (Membrane Proteins); 0 (Proto-Oncogene Proteins); 0 (Receptors, Cell Surface); 0 (Receptors, Notch); 0 (Serrate-Jagged Proteins); 0 (Wnt Proteins); 0 (Wnt7a protein, mouse); 0 (Wnt7b protein, mouse); G34N38R2N1 (Bromodeoxyuridine)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160305
[St] Status:MEDLINE
[do] DOI:10.1038/ncomms10936


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[PMID]:26930648
[Au] Autor:Chang WH; Ho BC; Hsiao YJ; Chen JS; Yeh CH; Chen HY; Chang GC; Su KY; Yu SL
[Ad] Endereço:Institute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
[Ti] Título:JAG1 Is Associated with Poor Survival through Inducing Metastasis in Lung Cancer.
[So] Source:PLoS One;11(3):e0150355, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:JAG1 is a Notch ligand that plays a critical role in multiple signaling pathways. However, the functionality of JAG1 in non-small cell lung cancer (NSCLC) has not been investigated thoroughly. By comparison of gene transcripted RNA profiles in the cell line pair with differential invasion ability, we identified JAG1 as a potential metastasis enhancer in lung cancer. Ectopic expression of JAG1 on lung cancer cells enhanced cell migration and invasion as well as metastasis in vitro and in vivo. Conversely, knockdown of JAG1 with siRNA in highly invasive cancer cells led to the reduction of migration and invasion. In clinical analysis, JAG1 mRNA expression was higher in tumors than in adjacent normal tissues in 14 of 20 patients with squamous cell carcinoma (SCC). SCC patients with higher JAG1 transcription had poor overall survival than those with low-transcripted JAG1. Microarray analysis indicated that the enforced JAG1 transcription was associated with an elevated HSPA2 RNA transcription, which played a role in promoting cancer cell migration and invasion. In conclusion, this is the first study that demonstrated that JAG1 might act as a potential prognostic marker and JAG1/HSPA2 axis mediates lung cancer malignancy at least partly.
[Mh] Termos MeSH primário: Proteínas de Ligação ao Cálcio/genética
Peptídeos e Proteínas de Sinalização Intercelular/genética
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Proteínas de Membrana/genética
Metástase Neoplásica/genética
[Mh] Termos MeSH secundário: Animais
Biomarcadores Tumorais/genética
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Carcinoma de Células Escamosas/genética
Carcinoma de Células Escamosas/patologia
Linhagem Celular Tumoral
Movimento Celular/genética
Proteínas de Choque Térmico HSP70/genética
Seres Humanos
Proteína Jagged-1
Camundongos
Camundongos SCID
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Metástase Neoplásica/patologia
Prognóstico
Proteínas Serrate-Jagged
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Calcium-Binding Proteins); 0 (HSP70 Heat-Shock Proteins); 0 (HSPA2 protein, human); 0 (Intercellular Signaling Peptides and Proteins); 0 (JAG1 protein, human); 0 (Jag1 protein, mouse); 0 (Jagged-1 Protein); 0 (Membrane Proteins); 0 (Serrate-Jagged Proteins)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160302
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0150355



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