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Guy diSibio

Researcher at University of California, Los Angeles

Publications -  13
Citations -  2167

Guy diSibio is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Notch signaling pathway & Ligand (biochemistry). The author has an hindex of 8, co-authored 13 publications receiving 2070 citations. Previous affiliations of Guy diSibio include UCLA Medical Center & University of California, Berkeley.

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Notch Receptor Activation Inhibits Oligodendrocyte Differentiation

TL;DR: It is shown that oligodendrocytes and their precursors in the developing rat optic nerve express Notch1 receptors and, at the same time, retinal ganglion cells express Jagged1, a ligand of the NotCh1 receptor, along their axons.
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Metastatic Patterns of Cancers: Results From a Large Autopsy Study

TL;DR: Not surprisingly, different primary cancers tended to metastasize, with differing frequencies, to different sites, which might be helpful in deducing the origins of cancers whose primary sites are unclear at presentation.
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Expression patterns of Jagged, Delta1, Notch1, Notch2, and Notch3 genes identify ligand-receptor pairs that may function in neural development.

TL;DR: Notch genes encode receptors for a signaling pathway that regulates neurogenesis and DSL genes encode ligands that bind and activate Notch, suggesting that different DSL-Notch combinations may direct the development of distinct neural subtypes.
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Fringe differentially modulates Jagged1 and Delta1 signalling through Notch1 and Notch2.

TL;DR: In this article, the Lunatic fringe (Lfng) was found to inhibit Jagged1-mediated signalling and potentiate Delta1-medicated signalling through Notch1, and Lfng-dependent modulation of Notch signalling requires both expression of Lg and Notch extracellular domain.
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Ligand-Induced Signaling in the Absence of Furin Processing of Notch1

TL;DR: The results suggest a novel paradigm in signal transduction, one in which two isoforms of the same cell-surface receptor could mediate two distinct signaling pathways in response to ligand, and support a CSL-independent Notch signaling pathway.