Notch signalling in vertebrate neural development
By A. Louvi, S. Artavanis-Tsakonas. Nature Reviews Neuroscience, 2006
855 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/9e8066cf5e1b7956665bd01337fe83f99ce1e3e0
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Citations in the corpus
- Notch signalling: a simple pathway becomes complex (2006, background): “For example, Notch first regulates the number of cells that acquire neural potential (lateral inhibition; Box 2 ), and subsequently it determines whether progeny will adopt neural or glial fate”
- EphB signaling controls lineage plasticity of adult neural stem cell niche cells (2010, background): “To address this issue, we first examined EphB2 expression in ependymal cells after genetic deletion of Rbpj (also known as CSL, CBF1, Suppressor of Hairless, and Lag-1), a key mediator of canonical signaling by all Notch receptors (Louvi and Artavanis-Tsakonas, 2006).”
- Quiescent and active hippocampal neural stem cells with distinct morphologies respond selectively to physiological and pathological stimuli and aging. (2010, background): “Canonical Notch signaling represses proneural gene expression via Hes proteins (Louvi and Artavanis-Tsakonas, 2006), and Hes5::GFP and Mash1 expression in the DG are largely complementary.”
- Astrocytes and disease: a neurodevelopmental perspective. (2012, background): “A classic example is the notch pathway (Louvi and Artavanis-Tsakonas 2006; Pierfelice et al. 2011), which affects progenitor number but, on balance, has never been definitively shown to promote astrocytogenesis in an instructive manner (Ross et al.”
- The disintegrin/metalloproteinase ADAM10 is essential for the establishment of the brain cortex (2010, background): “Notch signals govern the decision between neuronal (in an inhibitory fashion) and glial lineages (promoting this fate), modulate the fate of terminally differentiated neurons, and affect neuronal migration and even learning and memory (Yu et al., 2001; Costa et al., 2003; Saura et al., 2004; Wang et”
- Amyloid Precursor Protein Processing and Alzheimer’s Disease (2011, background): “Notch proteolysis is triggered by binding to a member of the Delta, Serrate, Lag2 (DSL) family of ligands (Louvi & Artavanis-Tsakonas 2006), which causes Notch to be cleaved by many of the same secretases as APP, releasing a soluble ectodomain and an intracellular domain (NICD) that regulates…”