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Interaction between Reelin and Notch signaling regulates neuronal migration in the cerebral cortex.
Hashimoto-Torii K, Torii M, Sarkisian MR, Bartley CM, Shen J, Radtke F, Gridley T, Sestan N, Rakic P. Hashimoto-Torii K, et al. Neuron. 2008 Oct 23;60(2):273-84. doi: 10.1016/j.neuron.2008.09.026. Neuron. 2008. PMID: 18957219 Free PMC article.
Here we show that regulation of Notch activity plays an important part in Reelin-signal-dependent neuronal migration. ...Finally, our in vitro biochemical studies show that Reelin signaling inhibits Notch ICD degradat …
Here we show that regulation of Notch activity plays an important part in Reelin-signal-dependent neuronal
Strange bedfellows: Reelin and Notch signaling interact to regulate cell migration in the developing neocortex.
Gaiano N. Gaiano N. Neuron. 2008 Oct 23;60(2):189-91. doi: 10.1016/j.neuron.2008.10.009. Neuron. 2008. PMID: 18957210 Free article. Review.
Neuronal cell migration in the developing neocortex relies on the Reelin signaling cascade to establish the characteristic "inside out" lamination pattern. In this issue of Neuron, Rakic and colleagues report that Notch signaling,
Neuronal cell migration in the developing neocortex relies on the Reelin signaling cascade to establish the char
Reelin and Notch1 cooperate in the development of the dentate gyrus.
Sibbe M, Förster E, Basak O, Taylor V, Frotscher M. Sibbe M, et al. J Neurosci. 2009 Jul 1;29(26):8578-85. doi: 10.1523/JNEUROSCI.0958-09.2009. J Neurosci. 2009. PMID: 19571148 Free PMC article.
The extracellular matrix molecule Reelin is necessary both for normal development of the dentate gyrus radial glia and neuronal migration. ...Disabled1, a component of the Reelin-signaling pathway colocalizes with Notch1, thus indicating a direc …
The extracellular matrix molecule Reelin is necessary both for normal development of the dentate gyrus radial glia and neuronal
Presenilin-1 deficiency leads to loss of Cajal-Retzius neurons and cortical dysplasia similar to human type 2 lissencephaly.
Hartmann D, De Strooper B, Saftig P. Hartmann D, et al. Curr Biol. 1999 Jul 15;9(14):719-27. doi: 10.1016/s0960-9822(99)80331-5. Curr Biol. 1999. PMID: 10421573 Free article.
Missense mutations of PS1 that modify gamma-secretase function, leading to a pathologic processing of amyloid precursor protein, are an important cause of familial Alzheimer's disease. Physiologically, the presenilins are involved in the Notch and Wnt-beta-catenin …
Missense mutations of PS1 that modify gamma-secretase function, leading to a pathologic processing of amyloid precursor protein, are an impo …
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