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  1. Article: Notch signaling in development and cancer.

    Bolós, Victoria / Grego-Bessa, Joaquín / de la Pompa, José Luis

    Endocrine reviews

    2007  Volume 28, Issue 3, Page(s) 339–363

    Abstract: Notch is an evolutionarily conserved local cell signaling mechanism that participates in a variety of cellular processes: cell fate specification, differentiation, proliferation, apoptosis, adhesion, epithelial-mesenchymal transition, migration, and ... ...

    Abstract Notch is an evolutionarily conserved local cell signaling mechanism that participates in a variety of cellular processes: cell fate specification, differentiation, proliferation, apoptosis, adhesion, epithelial-mesenchymal transition, migration, and angiogenesis. These processes can be subverted in Notch-mediated pathological situations. In the first part of this review, we will discuss the role of Notch in vertebrate central nervous system development, somitogenesis, cardiovascular and endocrine development, with attention to the mechanisms by which Notch regulates cell fate specification and patterning in these tissues. In the second part, we will review the molecular aspects of Notch-mediated neoplasias, where Notch can act as an oncogene or as a tumor suppressor. From all these studies, it becomes evident that the outcome of Notch signaling is strictly context-dependent and differences in the strength, timing, cell type, and context of the signal may affect the final outcome. It is essential to understand how Notch integrates inputs from other signaling pathways and how specificity is achieved, because this knowledge may be relevant for future therapeutic applications.
    MeSH term(s) Animals ; Bone Development/physiology ; Cardiovascular System/embryology ; Cardiovascular System/metabolism ; Central Nervous System/embryology ; Central Nervous System/metabolism ; Endocrine System/embryology ; Endocrine System/metabolism ; Gastrointestinal Tract/embryology ; Gastrointestinal Tract/metabolism ; Humans ; Neoplasms/metabolism ; Neoplasms/physiopathology ; Receptors, Notch/metabolism ; Signal Transduction/physiology
    Chemical Substances Receptors, Notch
    Language English
    Publishing date 2007-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 603096-8
    ISSN 1945-7189 ; 0163-769X
    ISSN (online) 1945-7189
    ISSN 0163-769X
    DOI 10.1210/er.2006-0046
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1562: Show issues Location:
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  2. Article ; Online: Notch and epithelial-mesenchyme transition in development and tumor progression: another turn of the screw.

    Grego-Bessa, Joaquín / Díez, Juan / Timmerman, Luika / de la Pompa, José Luis

    Cell cycle (Georgetown, Tex.)

    2004  Volume 3, Issue 6, Page(s) 718–721

    Abstract: Notch is an ancient cell signaling system that regulates cell fate specification, stem cell maintenance and initiation of differentiation in embryonic and postnatal tissues.(1) Alteration of these functions in the adult have been associated to various ... ...

    Abstract Notch is an ancient cell signaling system that regulates cell fate specification, stem cell maintenance and initiation of differentiation in embryonic and postnatal tissues.(1) Alteration of these functions in the adult have been associated to various types of cancer in which Notch may act as an oncogene or as a tumor suppressor. As occurs during development, Notch cooperates with other signaling pathways in the transformation process. Notch has recently been shown to promote epithelial-to-mesenchymal transition (EMT) during cardiac valve formation, via snail induction and subsequent cadherin downregulation. One implication of this work is that Notch acting through a similar mechanism, may also be involved in the EMT process that occurs during tumor progression and converts polarized epithelial cells into motile, invasive cells.
    MeSH term(s) Animals ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/pathology ; Epithelial Cells/pathology ; Humans ; Mesoderm/pathology ; Neoplasms/genetics ; Neoplasms/pathology ; Proto-Oncogene Proteins/physiology ; Receptor, Notch1 ; Receptor, Notch2 ; Receptor, Notch4 ; Receptors, Cell Surface/physiology ; Receptors, Notch ; Signal Transduction/physiology ; Transcription Factors/physiology
    Chemical Substances NOTCH1 protein, human ; NOTCH2 protein, human ; NOTCH4 protein, human ; Proto-Oncogene Proteins ; Receptor, Notch1 ; Receptor, Notch2 ; Receptor, Notch4 ; Receptors, Cell Surface ; Receptors, Notch ; Transcription Factors
    Language English
    Publishing date 2004-06-28
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Notch promotes epithelial-mesenchymal transition during cardiac development and oncogenic transformation.

    Timmerman, Luika A / Grego-Bessa, Joaquín / Raya, Angel / Bertrán, Esther / Pérez-Pomares, José María / Díez, Juan / Aranda, Sergi / Palomo, Sergio / McCormick, Frank / Izpisúa-Belmonte, Juan Carlos / de la Pompa, José Luis

    Genes & development

    2004  Volume 18, Issue 1, Page(s) 99–115

    Abstract: Epithelial-to-mesenchymal transition (EMT) is fundamental to both embryogenesis and tumor metastasis. The Notch intercellular signaling pathway regulates cell fate determination throughout metazoan evolution, and overexpression of activating alleles is ... ...

    Abstract Epithelial-to-mesenchymal transition (EMT) is fundamental to both embryogenesis and tumor metastasis. The Notch intercellular signaling pathway regulates cell fate determination throughout metazoan evolution, and overexpression of activating alleles is oncogenic in mammals. Here we demonstrate that Notch activity promotes EMT during both cardiac development and oncogenic transformation via transcriptional induction of the Snail repressor, a potent and evolutionarily conserved mediator of EMT in many tissues and tumor types. In the embryonic heart, Notch functions via lateral induction to promote a selective transforming growth factor-beta (TGFbeta)-mediated EMT that leads to cellularization of developing cardiac valvular primordia. Embryos that lack Notch signaling elements exhibit severely attenuated cardiac snail expression, abnormal maintenance of intercellular endocardial adhesion complexes, and abortive endocardial EMT in vivo and in vitro. Accordingly, transient ectopic expression of activated Notch1 (N1IC) in zebrafish embryos leads to hypercellular cardiac valves, whereas Notch inhibition prevents valve development. Overexpression of N1IC in immortalized endothelial cells in vitro induces EMT accompanied by oncogenic transformation, with corresponding induction of snail and repression of VE-cadherin expression. Notch is expressed in embryonic regions where EMT occurs, suggesting an intimate and fundamental role for Notch, which may be reactivated during tumor metastasis.
    MeSH term(s) Animals ; Cell Transformation, Neoplastic/genetics ; Embryo, Nonmammalian/physiology ; Embryonic and Fetal Development ; Epithelial Cells/cytology ; Gene Expression Regulation, Developmental/genetics ; Heart/embryology ; Membrane Proteins/genetics ; Mesoderm/cytology ; Mice ; Organ Culture Techniques ; Rats ; Receptors, Cell Surface/genetics ; Receptors, Notch ; Reverse Transcriptase Polymerase Chain Reaction ; Zebrafish/embryology
    Chemical Substances Membrane Proteins ; Receptors, Cell Surface ; Receptors, Notch
    Language English
    Publishing date 2004-01-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 806684-x
    ISSN 1549-5477 ; 0890-9369
    ISSN (online) 1549-5477
    ISSN 0890-9369
    DOI 10.1101/gad.276304
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Notch signaling is essential for ventricular chamber development.

    Grego-Bessa, Joaquín / Luna-Zurita, Luis / del Monte, Gonzalo / Bolós, Victoria / Melgar, Pedro / Arandilla, Alejandro / Garratt, Alistair N / Zang, Heesuk / Mukouyama, Yoh-Suke / Chen, Hanying / Shou, Weinian / Ballestar, Esteban / Esteller, Manel / Rojas, Ana / Pérez-Pomares, José María / de la Pompa, José Luis

    Developmental cell

    2007  Volume 12, Issue 3, Page(s) 415–429

    Abstract: Ventricular chamber morphogenesis, first manifested by trabeculae formation, is crucial for cardiac function and embryonic viability and depends on cellular interactions between the endocardium and myocardium. We show that ventricular Notch1 activity is ... ...

    Abstract Ventricular chamber morphogenesis, first manifested by trabeculae formation, is crucial for cardiac function and embryonic viability and depends on cellular interactions between the endocardium and myocardium. We show that ventricular Notch1 activity is highest at presumptive trabecular endocardium. RBPJk and Notch1 mutants show impaired trabeculation and marker expression, attenuated EphrinB2, NRG1, and BMP10 expression and signaling, and decreased myocardial proliferation. Functional and molecular analyses show that Notch inhibition prevents EphrinB2 expression, and that EphrinB2 is a direct Notch target acting upstream of NRG1 in the ventricles. However, BMP10 levels are found to be independent of both EphrinB2 and NRG1 during trabeculation. Accordingly, exogenous BMP10 rescues the myocardial proliferative defect of in vitro-cultured RBPJk mutants, while exogenous NRG1 rescues differentiation in parallel. We suggest that during trabeculation Notch independently regulates cardiomyocyte proliferation and differentiation, two exquisitely balanced processes whose perturbation may result in congenital heart disease.
    MeSH term(s) Animals ; Bone Morphogenetic Proteins/genetics ; Bone Morphogenetic Proteins/metabolism ; Cell Differentiation/physiology ; Cell Proliferation ; Ephrin-B2/genetics ; Ephrin-B2/metabolism ; Gene Expression Regulation, Developmental/physiology ; Heart/embryology ; Heart Ventricles/cytology ; Heart Ventricles/embryology ; Heart Ventricles/metabolism ; Mice ; Mutation/genetics ; Myoblasts, Cardiac/cytology ; Myoblasts, Cardiac/metabolism ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/metabolism ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Neuregulin-1 ; Receptor, Notch1/genetics ; Receptor, Notch1/metabolism ; Receptors, Notch/genetics ; Receptors, Notch/metabolism ; Signal Transduction/physiology
    Chemical Substances Bmp10 protein, mouse ; Bone Morphogenetic Proteins ; Ephrin-B2 ; Nerve Tissue Proteins ; Neuregulin-1 ; Notch1 protein, mouse ; Nrg1 protein, mouse ; Receptor, Notch1 ; Receptors, Notch
    Language English
    Publishing date 2007-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2006.12.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Notch activity induces Nodal expression and mediates the establishment of left-right asymmetry in vertebrate embryos.

    Raya, Angel / Kawakami, Yasuhiko / Rodriguez-Esteban, Concepcion / Buscher, Dirk / Koth, Christopher M / Itoh, Tohru / Morita, Masanobu / Raya, R Marina / Dubova, Ilir / Bessa, Joaquin Grego / de la Pompa, Jose Luis / Izpisua Belmonte, Juan Carlos

    Genes & development

    2003  Volume 17, Issue 10, Page(s) 1213–1218

    Abstract: Left-sided expression of Nodal in the lateral plate mesoderm is a conserved feature necessary for the establishment of normal left-right asymmetry during vertebrate embryogenesis. By using gain- and loss-of-function experiments in zebrafish and mouse, we ...

    Abstract Left-sided expression of Nodal in the lateral plate mesoderm is a conserved feature necessary for the establishment of normal left-right asymmetry during vertebrate embryogenesis. By using gain- and loss-of-function experiments in zebrafish and mouse, we show that the activity of the Notch pathway is necessary and sufficient for Nodal expression around the node, and for proper left-right determination. We identify Notch-responsive elements in the Nodal promoter, and unveil a direct relationship between Notch activity and Nodal expression around the node. Our findings provide evidence for a mechanism involving Notch activity that translates an initial symmetry-breaking event into asymmetric gene expression.
    MeSH term(s) Animals ; Body Patterning/physiology ; Enhancer Elements, Genetic ; Gene Expression Regulation/physiology ; Hedgehog Proteins ; Membrane Proteins/physiology ; Mice ; Nodal Protein ; Organizers, Embryonic/physiology ; Promoter Regions, Genetic ; Receptors, Notch ; Signal Transduction/physiology ; Situs Inversus/embryology ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism ; Zebrafish/embryology ; Zebrafish/genetics
    Chemical Substances Hedgehog Proteins ; Membrane Proteins ; Nodal Protein ; Nodal protein, mouse ; Receptors, Notch ; Trans-Activators ; Transforming Growth Factor beta
    Language English
    Publishing date 2003-05-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 806684-x
    ISSN 1549-5477 ; 0890-9369
    ISSN (online) 1549-5477
    ISSN 0890-9369
    DOI 10.1101/gad.1084403
    Database MEDical Literature Analysis and Retrieval System OnLINE

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