Journal ArticleDOI
Notch Signaling: Cell Fate Control and Signal Integration in Development
TLDR
Notch signaling defines an evolutionarily ancient cell interaction mechanism, which plays a fundamental role in metazoan development, providing a general developmental tool to influence organ formation and morphogenesis.Abstract:
Notch signaling defines an evolutionarily ancient cell interaction mechanism, which plays a fundamental role in metazoan development. Signals exchanged between neighboring cells through the Notch receptor can amplify and consolidate molecular differences, which eventually dictate cell fates. Thus, Notch signals control how cells respond to intrinsic or extrinsic developmental cues that are necessary to unfold specific developmental programs. Notch activity affects the implementation of differentiation, proliferation, and apoptotic programs, providing a general developmental tool to influence organ formation and morphogenesis.read more
Citations
More filters
Journal ArticleDOI
The Capsaspora genome reveals a complex unicellular prehistory of animals
Hiroshi Suga,Zehua Chen,Alex de Mendoza,Arnau Sebé-Pedrós,Matthew Brown,Eric Kramer,Martin Carr,Pierre Kerner,Michel Vervoort,Núria Sánchez-Pons,Guifré Torruella,Romain Derelle,Gerard Manning,B. Franz Lang,Carsten Russ,Brian J. Haas,Andrew J. Roger,Chad Nusbaum,Iñaki Ruiz-Trillo,Iñaki Ruiz-Trillo,Iñaki Ruiz-Trillo +20 more
TL;DR: It is proposed that the acquisition of these metazoan-specific developmental systems and the co-option of pre-existing genes drove the evolutionary transition from unicellular protists to metazoans.
Journal ArticleDOI
Retinal cell fate determination and bHLH factors.
TL;DR: It is likely that homeodomain factors regulate the layer specificity but not the neuronal fate while bHLH activators determine the neuron fate within the homedomain factor-specified layers.
Journal ArticleDOI
Functional Interaction between the Mouse Notch1 Intracellular Region and Histone Acetyltransferases PCAF and GCN5
Hisanori Kurooka,Tasuku Honjo +1 more
TL;DR: It is suggested that HATs including PCAF and GCN5 play an important role in the RBP-J-mediated transactivation by RAMIC, which is repressed by two HAT inhibitor proteins, E1A and Twist.
Journal ArticleDOI
Characterization of Notch3‐deficient mice: Normal embryonic development and absence of genetic interactions with a Notch1 mutation
Luke T. Krebs,Yingzi Xue,Christine R. Norton,John P. Sundberg,Paul Beatus,Urban Lendahl,Anne Joutel,Thomas Gridley +7 more
TL;DR: The data demonstrate that the Notch3 gene is not essential for embryonic development or fertility in mice, and does not have a redundant function with the NotCh1 gene during early embryogenesis.
Journal ArticleDOI
Notch1 signaling promotes primary melanoma progression by activating mitogen-activated protein kinase/phosphatidylinositol 3-kinase-Akt pathways and up-regulating N-cadherin expression.
Zhao-Jun Liu,Min Xiao,Klara Balint,Klara Balint,Keiran S.M. Smalley,Patricia Brafford,Ruihua Qiu,Chelsea C. Pinnix,Xueli Li,Meenhard Herlyn +9 more
TL;DR: It is shown that Notch1 signaling drives the vertical growth phase (VGP) of primary melanoma toward a more aggressive phenotype and regulation of MAPK/PI3K-Akt pathway activities and expression of N-cadherin by the Notch pathway provides a mechanistic basis for Notch signaling in the promotion ofPrimary melanoma progression.
References
More filters
Journal ArticleDOI
Notch3 mutations in CADASIL, a hereditary adult-onset condition causing stroke and dementia
Anne Joutel,Christophe Corpechot,Anne Ducros,Katayoun Vahedi,Hugues Chabriat,Philippe Mouton,Sonia Alamowitch,Valérie Domenga,Michaelle Cécillion,Emmanuelle Maréchal,Jacqueline Maciazek,Céline Vayssière,Corinne Cruaud,E. A. Cabanis,Marie Madeleine Ruchoux,Jean Weissenbach,Jean Francois Bach,Marie-Germaine Bousser,Elisabeth Tournier-Lasserve +18 more
TL;DR: The characterization of the human Notch3 gene, which was previously mapped to the CADASIL critical region, is reported, indicating that Notch 3 could be the defective protein in CADASil patients.
Journal ArticleDOI
Notch-1 signalling requires ligand-induced proteolytic release of intracellular domain.
TL;DR: It is shown that signalling by a constitutively active membrane-bound Notch-1 protein requires the proteolytic release of the Notch intracellular domain (NICD), which interacts preferentially with CSL.
Journal ArticleDOI
Signalling downstream of activated mammalian Notch.
Sophie Jarriault,Christel Brou,Frédérique Logeat,Eric H. Schroeter,Raphael Kopan,Alain Israël +5 more
TL;DR: It is shown that activated forms of mNotch associate with the human analogue of Su(H), KBF2/RBP-JK and act as transcriptional activators through theKBF2-binding sites of the HES-1 promoter and block MyoD-induced myogenesis5-7.
Journal Article
Notch signaling : Signal transduction
TL;DR: The Notch/Lin-12/Glp-1 receptor family mediates the specification of numerous cell fates during development in Drosophila and Caenorhabditis elegans and putative components of the signaling cascade are identified, including a conserved family of extracellular ligands and two cellular factors that may associate with the Notch Intracellular domain.
Journal ArticleDOI
Alagille syndrome is caused by mutations in human Jagged1, which encodes a ligand for Notch1
Linheng Li,Ian D. Krantz,Yu Deng,Yu Deng,Anna Genin,Amy B. Banta,Colin Collins,Ming Qi,Barbara J. Trask,Wen Lin Kuo,Joanne Cochran,Teresa Costa,Mary Ella M Pierpont,Elizabeth B. Rand,David A. Piccoli,Leroy Hood,Nancy B. Spinner +16 more
TL;DR: Four distinct coding mutations in JAG1 are demonstrated, providing evidence that it is the causal gene for Alagille syndrome, and supporting the hypothesis that haploinsufficiency for this gene is one of the mechanisms causing the Alagile syndrome phenotype.