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
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Journal ArticleDOI
HERP, a Novel Heterodimer Partner of HES/E(spl) in Notch Signaling
Tatsuya Iso,Vittorio Sartorelli,Coralie Poizat,Simona Iezzi,Hung-Yi Wu,Gene Chung,Larry Kedes,Yasuo Hamamori +7 more
TL;DR: It is shown that HERP has intrinsic transcriptional repression activity, which means that Notch signaling relies on cooperation between HES and HERP, two transcriptional repressors with distinctive repression mechanisms which, either as homo- or as heterodimers, regulate target gene expression.
Journal ArticleDOI
Default repression and Notch signaling: Hairless acts as an adaptor to recruit the corepressors Groucho and dCtBP to Suppressor of Hairless.
TL;DR: It is shown that, in vitro, H directly binds two corepressor proteins, Groucho (Gro) and dCtBP, which indicate that "default repression" of N pathway target genes by an unusual adaptor/corepressor complex is essential for proper cell fate specification during Drosophila peripheral nervous system development.
Journal ArticleDOI
Notch Activation Induces Endothelial Cell Cycle Arrest and Participates in Contact Inhibition: Role of p21Cip1 Repression
Michela Noseda,Linda Chang,Graeme W. McLean,Jonathan E. Grim,Bruce E. Clurman,Laura Smith,Aly Karsan +6 more
TL;DR: It is suggested that Notch activation contributes to contact inhibition of endothelial cells, in part through repression of p21Cip1 expression, through activation of the Notch pathway by the ligand Jagged1.
Journal ArticleDOI
Arterial versus venous endothelial cells.
TL;DR: Vascular endothelial cells (ECs) form the inner lining of all blood vessels from the largest artery and veins, viz., the aorta and venae cavae, respectively, to the capillaries that connect the arterial and venous systems.
Journal ArticleDOI
A common enzyme connects Notch signaling and Alzheimer's disease
Raphael Kopan,Alison Goate +1 more
TL;DR: Several studies published recently by developmental biologists, neuroscientists, and researchers who are interested in the identification of therapeutic targets and treatments for Alzheimer’s disease have tied together diverse fields of science.
References
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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.