J. Nye

Publications83
h-index38
Citations7,379
Highly Influential Citations368
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Radial Glial Identity Is Promoted by Notch1 Signaling in the Murine Forebrain
The intracellular domain of mouse Notch: a constitutively activated repressor of myogenesis directed at the basic helix-loop-helix region of MyoD.
TLDR
It is shown that ectopic expression of the intracellular domain of mNotch (mNotchIC) functions as a constitutively activated repressor of myogenesis both in cultured cells and in frog embryos.
Notch pathway molecules are essential for the maintenance, but not the generation, of mammalian neural stem cells.
TLDR
Both neuronal and glial differentiation in vitro were enhanced by attenuation of Notch signaling and suppressed by expressing an active form of NotCh1, consistent with a role for NotCh signaling in the maintenance of the neural stem cell, and inconsistent with a roles in a neuronal/glial fate switch.
aph-1 and pen-2 Are Required for Notch Pathway Signaling, γ-Secretase Cleavage of βAPP, and Presenilin Protein Accumulation
aph-1 and pen-2 are required for Notch pathway signaling, gamma-secretase cleavage of betaAPP, and presenilin protein accumulation.
TLDR
RNAi-mediated inactivation of aph-1, pen-2, or nicastrin in cultured Drosophila cells reduces gamma-secretase cleavage of betaAPP and Notch substrates and reduces the levels of processed presenilin.
Signal transduction by activated mNotch: importance of proteolytic processing and its regulation by the extracellular domain.
TLDR
It is demonstrated that a mNotch1 mutant protein that lacks its extracellular domain but retains its membrane-spanning region becomes proteolytically processed on its intracellular surface and, as a result, the activated intrACEllular domain (mNotchIC) is released and can move to the nucleus.
Glycogen Synthase Kinase-3β Modulates Notch Signaling and Stability
An activated Notch suppresses neurogenesis and myogenesis but not gliogenesis in mammalian cells.
TLDR
It is demonstrated that a dominant gain-of-function mutant of mNotch suppresses neurogenesis, as well as myogenesis in P19 cells, and suggests that m notch may play a similar role in the choice of fate in the developing mammalian embryo.
Porphyrins are endogenous ligands for the mitochondrial (peripheral-type) benzodiazepine receptor.
TLDR
Porphyrins appear to be endogenous ligands for mitochondrial benzodiazepine receptors, and all of the inhibitory activity in extracts of several tissues can be accounted for by their porphyrIn and metalloporphyrin content.
Autonomous and non-autonomous regulation of mammalian neurite development by Notch1 and Delta1
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