Transient Notch activation initiates an irreversible switch from neurogenesis to gliogenesis by neural crest stem cells.

By S. Morrison, S. E. Perez, Zhou Qiao, J. Verdi, C. Hicks, G. Weinmaster, David J. Anderson. Cell, 2000

771 citations recorded by the source corpus.

Subfields: Developmental Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/9cd1032f841710fdfc7503946a7a00154685db9a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Developmental Neuroscience

1. K. Nave
2. N. Gaiano
3. Fred H. Gage
4. Irving L. Weissman
5. Raphael Kopan
6. M. Wicha
7. G. Dontu
8. Kyle W. Jackson

In Molecular Biology

1. Elaine Fuchs
2. M. Wicha
3. Irving L. Weissman
4. Fred H. Gage
5. N. Gaiano
6. D. Anderson
7. G. Dontu
8. Raphael Kopan

Citations in the corpus

• Stem and progenitor cells: origins, phenotypes, lineage commitments, and transdifferentiations. (2001, background): “Instructive differentiation factors for each of these differentiated derivatives have been identified: GMP2 for autonomic neurons, TGFβ for smooth muscle cells, and Nrg-1 and Notch for Schwann cells (Shah et al. 1994, 1996; Shah & Anderson 1997; Morrison et al. 2000).”
• The transcription factor Sox10 is a key regulator of peripheral glial development. (2001, background): “In vitro, transient activation of Notch signaling suffices to suppress the neurogenic differentiation of neural crest cells and accelerates glial differentiation (Morrison et al. 2000; Wakamatsu et al. 2000).”
• HES and HERP families: Multiple effectors of the notch signaling pathway (2003, background): “In the nucleus, NICD associates with a transcriptional factor, RBP-Jk (also known as CSL for CBF1/Su(H)/Lag-1) (Egan et al., 1998; Greenwald, 1998; Weinmaster, 1998; Artavanis-Tsakonas et al., 1999; Mumm and Kopan, 2000), and activates transcription from the RBP-Jk binding DNA site.”
• Notch promotes epithelial-mesenchymal transition during cardiac development and oncogenic transformation. (2004, background): “Notch signaling also can positively regulate cell fate choices, as it is able to promote the glial fate in rat neural stem cells (Morrison et al. 2000) and to regulate the T/B cell fate choice in lymphoid progenitors (Robey 1999).”
• The origin and development of glial cells in peripheral nerves (2005, background): “This is because the most obvious functions of these signals in the neural crest are to suppress glial development, or to suppress or activate neuronal developmen”
• Biological Physics of the Developing Embryo (2005, neutral): “This system is used in a wide variety of embryonic contexts to set up cell patterns, including, as we have seen previously, neurogenesis in the neural plate (Tiedemann, 1998; see also the discussion of the Kerszberg-Changeux model in Chapter 5) and in the peripheral nervous system (Wakamatsu et al.,”
• Hypoxia-inducible factors in stem cells and cancer (2009, neutral): “It is important to remember, however, that Notch effects can be complex and context dependent, as overexpression of Notch components rather promotes terminal differentiation in epidermal keratinocytes and certain neural stem and progenitor cells [62, 64, 65].”
• Role of Notch signaling in cell-fate determination of human mammary stem/progenitor cells (2004, methodology): “A synthetic peptide derived from the DSL (Delta-SerrateLAG 2) domain conserved in all Notch ligands [9] and a previously described recombinant Delta 1 ligand fused to the immunoglobulin Fc fragment (used in combination with an anti-human Fc antibody, for ligand clustering) [20] were utilized as agon”
• Vertebrate neural cell-fate determination: Lessons from the retina (2001, background): “Transient Notch signalling instructs neural crest progenitors to switch their competence from neurogenesis to gliogenesi”