Journal
PLOS ONE
Volume 4, Issue 8, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0006728
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Funding
- Intramural NIH HHS [Z01 NS002608] Funding Source: Medline
- NCI NIH HHS [R01 CA098402, CA098402] Funding Source: Medline
- NIGMS NIH HHS [R01 GM062931, GM62931] Funding Source: Medline
- NINDS NIH HHS [NS10735, F32 NS010735] Funding Source: Medline
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A ligand-independent cleavage (S1) in the extracellular domain of the mammalian Notch receptor results in what is considered to be the canonical heterodimeric form of Notch on the cell surface. The in vivo consequences and significance of this cleavage on Drosophila Notch signaling remain unclear and contradictory. We determined the cleavage site in Drosophila and examined its in vivo function by a transgenic analysis of receptors that cannot be cleaved. Our results demonstrate a correlation between loss of cleavage and loss of in vivo function of the Notch receptor, supporting the notion that S1 cleavage is an in vivo mechanism of Notch signal control.
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