Interactions between Fibroblast Growth Factors and Notch Regulate Neuronal Differentiation

Faux, Clare; Turnley, Ann M.; Epa, Ruwan; Cappai, Roberto; Bartlett, Perry F.

doi:10.1523/jneurosci.21-15-05587.2001

Cited by 102 publications

(88 citation statements)

References 55 publications

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“…Studies in other mammalian systems provide further evidence for interaction between Notch and cranial suture pathways. In mouse neuroepithelial precursor cells data suggests the inhibitory action of growth factors, such as FGF1 and 2, is mediated via the Notch pathway [Faux et al, 2001]. FGF signalling is also thought to regulate the Notch pathway in mouse dental epithelium to determine stem cell fate [Harada et al, 1999].…”

Section: Discussionmentioning

confidence: 99%

Craniosynostosis in Alagille syndrome

et al. 2002

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Alagille syndrome is a multisystem developmental disorder with primary involvement of the liver, heart, skeleton, eyes and facial structures, and demonstrates highly variable expressivity with respect to all of the involved systems. Alagille syndrome is caused by mutations in the Jagged1 gene. Jagged1 is a ligand in the Notch signaling pathway that has been shown to regulate early cell fate determination. Mutations in Jagged1 have been identified in approximately 80% of patients with Alagille syndrome. We have recently identified two patients with mutation proven Alagille syndrome who also had unilateral coronal craniosynostosis. Both individuals were screened for mutations in fibroblast growth factor receptor 1, 2, 3 and TWIST genes, all associated with various types of craniosynostosis and no mutations were identified. The finding of a conserved form of craniosynostosis in two unrelated patients with Alagille syndrome and mutations in Jagged1 may indicate that Jagged1 plays a role in cranial suture formation. © 2002 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Craniosynostosis in Alagille syndrome

et al. 2002

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“…After all, STAT3-Ser phosphorylation is downstream of several pathways known to promote b-cell proliferation in various developmental stages of the pancreas, including FGF signaling (84,85), which has been shown to intercept Notch signaling components and to regulate cell proliferation and self-renewal in both NSC and pancreatic systems (58,86), several cell surface receptors, Akt, and mTOR. It is possible that Hes3 may be a mediator of some of the functions of these molecules.…”

Section: Notch Signaling In Neural Developmentmentioning

confidence: 99%

Endocrine Pancreas Development and Regeneration: Noncanonical Ideas From Neural Stem Cell Biology

et al. 2016

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Loss of insulin-producing pancreatic islet β-cells is a hallmark of type 1 diabetes. Several experimental paradigms demonstrate that these cells can, in principle, be regenerated from multiple endogenous sources using signaling pathways that are also used during pancreas development. A thorough understanding of these pathways will provide improved opportunities for therapeutic intervention. It is now appreciated that signaling pathways should not be seen as “on” or “off” but that the degree of activity may result in wildly different cellular outcomes. In addition to the degree of operation of a signaling pathway, noncanonical branches also play important roles. Thus, a pathway, once considered as “off” or “low” may actually be highly operational but may be using noncanonical branches. Such branches are only now revealing themselves as new tools to assay them are being generated. A formidable source of noncanonical signal transduction concepts is neural stem cells because these cells appear to have acquired unusual signaling interpretations to allow them to maintain their unique dual properties (self-renewal and multipotency). We discuss how such findings from the neural field can provide a blueprint for the identification of new molecular mechanisms regulating pancreatic biology, with a focus on Notch, Hes/Hey, and hedgehog pathways.

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“…Notch1 and Notch2 are presumably required to modulate interactions of cells involved in somite condensation (Gridley, 1997). Notch3 has a more recent phylogenetic origin and has been identified only in mammals (Faux et al, 2001). Notch4 also has been shown only in mammals: since it diverges in many aspects from the others, its exclusion from the Notch family has been proposed (Lardelli et al, 1995;Shirayoshi et al, 1997).…”

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confidence: 99%

Physiology and pathology of notch signalling system

Bianchi

Dotti

Federico

2005

Journal Cellular Physiology

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Notch proteins encode a family of transmembrane receptors that are part of a signalling transduction system known as Notch signalling, an extremely conserved and widely used mechanism regulating programs governing growth, apoptosis and differentiation in metazoans. Notch signalling begins when the Notch receptor binds ligands and ends when the Notch intracellular domain enters the nucleus and activates transcription of target genes. This core pathway is subjected to a wide array of regulatory influences and protein-protein interactions and is correlated with other signalling pathway. This review will sumarize recent findings concerning the physiology and pathology of Notch signalling in vascular development and homeostasis. Moreover, the clinical phenotypes of Notch3 signalling system pathology will be described, with particular regard to CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy) for which the most recent pathogenetic hypotheses are reported.

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Interactions between Fibroblast Growth Factors and Notch Regulate Neuronal Differentiation

Cited by 102 publications

References 55 publications

Craniosynostosis in Alagille syndrome

Craniosynostosis in Alagille syndrome

Endocrine Pancreas Development and Regeneration: Noncanonical Ideas From Neural Stem Cell Biology

Physiology and pathology of notch signalling system

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