Autonomous and non-autonomous regulation of mammalian neurite development by Notch1 and Delta1

Franklin, James L.; Berechid, Bridget E.; Cutting, Frank B.; Presente, Asaf; Chambers, Christopher B.; Foltz, Daniel R.; Ferreira, Adriana; Nye, Jeffrey S.

doi:10.1016/s0960-9822(00)80114-1

Cited by 138 publications

(114 citation statements)

References 55 publications

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“…Furthermore, enforced expression of i.c. Notch-1 inhibits the differentiation process (Franklin et al, 1999;Grynfeld et al, 2000). Based on these results we postulate that precise temporal regulation of the Notch signalling cascade is an integral part of NB cell differentiation from highly proliferative neuroblasts into terminally differentiated neuronal cells.…”

mentioning

confidence: 62%

Effects of the histone deacetylase inhibitor valproic acid on Notch signalling in human neuroblastoma cells

et al. 2005

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Neuroblastoma (NB), a sympathetically derived childhood tumour, shows characteristics of neuronal precursor cells, suggesting a halted differentiation process. We have previously shown that the Notch signalling cascade, a key player during normal neurogenesis, also might be involved in NB differentiation. Valproic acid (VPA), a well-tolerated antiepileptic drug, has been shown to induce differentiation and cell death of NB cells, possibly associated with its recently described HDAC inhibiting activity. Stimulation of NB cells with VPA led to increased cell death and phenotypic changes associated with differentiation, that is, neurite extension and upregulation of neuronal markers. VPA treatment also led to an activated Notch signalling cascade as shown by increased levels of intracellular Notch-1 and Hes-1, mimicking the initial phase of induced differentiation. These results reinforce that VPA potentially could be used in differentiation therapy of NB and that the effects in part could be a consequence of interference with the Notch signalling cascade.

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confidence: 62%

Effects of the histone deacetylase inhibitor valproic acid on Notch signalling in human neuroblastoma cells

et al. 2005

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“…The inhibition of CBF1-luciferase by AID was dosedependent ( Fig. 4F) and correlated with the ability of AID molecules to interact with Nbl, such that AID 39 -55 and AID [12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28] did not inhibit CBF1-luciferase activation by NICD (Fig. 4G).…”

Section: Difluorophenacetyl)-l-alanyl]-s-phenylglycine T-butylmentioning

confidence: 99%

“…The functionally active NICD translocates to the nucleus where it interacts with the CBF1-SuHLag1 (CSL ) family of transcription factors and activates the transcription of genes that regulate the ability of cells to respond to various proliferation, differentiation, or apoptotic cues (18,23). In the nervous system, NICD has been implicated in a variety of processes, including inhibition of neuronal differentiation and neurite growth, and regulation of neuronal cell death (23)(24)(25)(26)(27)(28). The apparent similarities in proteolytic activation and signal transduction of APP and Notch raises the possibility that signals from these two receptors interact.…”

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confidence: 99%

The γ-secretase-generated intracellular domain of β-amyloid precursor protein binds Numb and inhibits Notch signaling

Roncarati

Šestan

Scheinfeld

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

191

139

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“…In mammals, Notch regulates arborization of cortical neurons in vivo (5,6) and in tissue culture (7,8). In Drosophila, the Notch pathway is required for the elaboration of processes in the CNS in the developing third-instar larva (9) and in the embryo (10,11).…”

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confidence: 99%

Notch is required for long-term memory in Drosophila

Presente

Boyles

Serway

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

126

102

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A role for Notch in the elaboration of existing neural processes is emerging that is distinct from the increasingly well understood function of this gene in binary cell-fate decisions. Several research groups, by using a variety of organisms, have shown that Notch is important in the development of neural ultrastructure. Simultaneously, Presenilin (Psn) was identified both as a key mediator of Notch signaling and as a site of genetic lesions that cause earlyonset Alzheimer's disease. Here we demonstrate that Notch loss of function produces memory deficits in Drosophila melanogaster. The effects are specific to long-term memory, which is thought to depend on ultrastructural remodeling. We propose that Notch plays an important role in the neural plasticity underlying consolidated memory.W hereas the Notch protein plays an important role in binary cell-fate decisions during development (1), it is also present in the adult brain (2, 3). This finding is particularly interesting in adult Drosophila because the CNS is established by eclosion (4). Given that Notch is not needed for cell-fate decisions in the adult brain, its role in this tissue is unclear.Several groups have shown that Notch is important in the arborization of neuritic processes in development. In mammals, Notch regulates arborization of cortical neurons in vivo (5, 6) and in tissue culture (7,8). In Drosophila, the Notch pathway is required for the elaboration of processes in the CNS in the developing third-instar larva (9) and in the embryo (10, 11). Recently, this work has been extended to the analysis of the developing neuromuscular junction, a structure that serves as an accessible model for CNS plasticity. In addition, a Psn-mediated role for Notch is required in the development of neural projections mediating learned thermotaxis in Caenorhabditis elegans (12). Recently (3), we demonstrated that prolonged disruptions in Notch function produced an early lethality and an impairment in the coordinated neuromuscular activity of flight. Accordingly, because Notch clearly is involved in the regulation of neural ultrastructure during development, we investigated the possibility that Notch is also required for memory consolidation, a process believed to require remodeling of existing neurons in adults (13).Drosophila is an ideal organism for studying genes influencing behavioral phenotypes. Advances in our understanding of learning and memory mechanisms have been achieved through genetic, transgenic, and genomic studies in the fly (14). To investigate Notch function in adults, it is necessary to use conditional reagents to avoid developmental phenotypes that may kill the fly or compromise behavior. We used a Notch temperature-sensitive allele (N ts1 ) (15) and RNA interference (RNAi) derived from an inducible transgene (16), in combination with two independent behavioral assays for memory. We show that short-term memory is not impaired by conditional manipulations of Notch, but that Notch is required in adults for long-term memory. MethodsDrosophila Strai...

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Autonomous and non-autonomous regulation of mammalian neurite development by Notch1 and Delta1

Cited by 138 publications

References 55 publications

Effects of the histone deacetylase inhibitor valproic acid on Notch signalling in human neuroblastoma cells

Effects of the histone deacetylase inhibitor valproic acid on Notch signalling in human neuroblastoma cells

The γ-secretase-generated intracellular domain of β-amyloid precursor protein binds Numb and inhibits Notch signaling

Notch is required for long-term memory in Drosophila

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