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
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Journal ArticleDOI
Notch1 functions to suppress cone-photoreceptor fate specification in the developing mouse retina.
TL;DR: An unexpected role of Notch signaling in directly controlling neuronal cell-type composition is revealed, and a model by which, during normal retinogenesis, Notch1 functions to suppress cone-photoreceptor fate, allowing for the specification of the diversity of retinal cell types is suggested.
Journal ArticleDOI
Overexpression of activated murine Notch1 and Notch3 in transgenic mice blocks mammary gland development and induces mammary tumors.
Chunyan Hu,Anne Dievart,Mathieu Lupien,Ezequiel Calvo,Gilles Bernard Tremblay,Paul Jolicoeur,Paul Jolicoeur,Paul Jolicoeur +7 more
TL;DR: The mouse mammary tumor virus was found to target the Notch1 gene, producing insertional mutations in mammary tumors of MMTV/neu transgenic (Tg) mice, confirming the oncogenic potential of Notch 1(intra) in vivo.
Journal ArticleDOI
Increased expression of the adult stem cell marker Musashi‐1 in endometriosis and endometrial carcinoma
Martin Götte,M. Wolf,Annette Staebler,O. Buchweitz,Reinhard Kelsch,Andreas N. Schüring,Ludwig Kiesel +6 more
TL;DR: The results emphasize the role of Musashi‐1‐expressing endometrial progenitor cells in proliferating endometrium, endometriosis and endometRIoid uterine carcinoma, and support the concept of a stem cell origin of endometiosis andendometrial carcinoma.
Journal ArticleDOI
Separation of Notch1 Promoted Lineage Commitment and Expansion/Transformation in Developing T Cells
David Allman,Fredrick G. Karnell,Jennifer A. Punt,Sonia Bakkour,Lanwei Xu,Peggy Myung,Gary A. Koretzky,John C. Pui,Jon C. Aster,Warren S. Pear +9 more
TL;DR: It is demonstrated that Notch signaling directs T lineage commitment from multipotent progenitor cells; however, both expansion and leukemic transformation of this population are dependent on T cell–specific signals associated with development of DP thymocytes.
Journal ArticleDOI
Notch activation stimulates transient and selective binding of Su(H)/CSL to target enhancers
Alena Krejci,Sarah J. Bray +1 more
TL;DR: Unexpectedly, Su(H) occupancy was significantly and transiently increased following Notch activation, suggesting a more dynamic interaction with targets than hitherto proposed.
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.