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
Notch1 and Jagged1 are expressed after CNS demyelination, but are not a major rate-determining factor during remyelination.
Mark F. Stidworthy,Stephane Genoud,Wen-Wu Li,Dino P. Leone,Ned Mantei,Ueli Suter,Robin J.M. Franklin +6 more
TL;DR: It is shown that Notch1 is expressed on adult OPCs and that there are multiple cellular sources of its ligand Jagged1 in a rodent model of remyelination, and that OPC-targeted NotCh1 ablation in cuprizone-treated Plp-creER Notch 1(lox/lox) transgenic mice yielded no significant differences in remyELination parameters.
Journal ArticleDOI
Rhamnetin and Cirsiliol Induce Radiosensitization and Inhibition of Epithelial-Mesenchymal Transition (EMT) by miR-34a-mediated Suppression of Notch-1 Expression in Non-small Cell Lung Cancer Cell Lines
JiHoon Kang,Eun Gi Kim,Wanyeon Kim,Ki Moon Seong,HyeSook Youn,Jung Woo Kim,Joon Kim,BuHyun Youn +7 more
TL;DR: Evidence is provided that rhamnetin and cirsiliol can act as promising radiosensitizers that enhance the radiotherapeutic efficacy by inhibiting radiation-induced Notch-1 signaling associated with radioresistance possibly via miR-34a-mediated pathways.
Journal ArticleDOI
Notch Ligand Delta-Like 1 Is Essential for Postnatal Arteriogenesis
Anne Limbourg,Merlin Ploom,Diana Elligsen,Inga Sörensen,Tibor Ziegelhoeffer,Achim Gossler,Helmut Drexler,Florian P. Limbourg +7 more
TL;DR: Dll1-mediated Notch activation regulates ephrin-B2 expression and postnatal arteriogenesis in mice and in heterozygous Dll1 mutant mice endothelial mice.
Journal ArticleDOI
Notch and NF-kB signaling pathways regulate miR-223/FBXW7 axis in T-cell acute lymphoblastic leukemia
Vinod Kumar,Rocco Palermo,Claudio Talora,Antonio Francesco Campese,Saula Checquolo,Diana Bellavia,Luca Tottone,G Testa,Evelina Miele,Stefano Indraccolo,Alberto Amadori,Elisabetta Ferretti,Alberto Gulino,Alberto Gulino,Alessandra Vacca,Isabella Screpanti,Isabella Screpanti +16 more
TL;DR: Notch signaling deregulation is linked to the onset of several tumors including T-cell acute lymphoblastic leukemia (T-ALL) and miRNAs regulated by Notch pathway are identified, including miR-223, whose putative promoter analysis revealed a conserved RBPjk binding site, which was nested to an NF-kB consensus.
Journal ArticleDOI
Blockade of Notch1 Signaling Alleviates Murine Lupus via Blunting Macrophage Activation and M2b Polarization
TL;DR: In the SLE murine model generated by immunization with activated lymphocyte-derived DNA, infiltrated macrophages in the nephritic tissues were found to exhibit activation and M2b functional polarization, implying that Notch1 signaling-dependent macrophage M2B polarization might play a pivotal role in the pathogenesis of SLE.
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.