|Citation||Wesley, C.S., Mok, L.P. (2003). Regulation of Notch signaling by a novel mechanism involving suppressor of hairless stability and carboxyl terminus-truncated Notch. Mol. Cell. Biol. 23(16): 5581--5593. (Export to RIS)|
|Publication Type||Research paper|
|PubMed Abstract||Different amounts of Suppressor of Hairless (SuH)-dependent Notch (N) signaling is often used during animal development to produce two different tissues from a population of equipotent cells. During Drosophila melanogaster embryogenesis, cells with high amounts of this signaling differentiate the larval epidermis whereas cells with low amounts, or none, differentiate the central nervous system (CNS). The mechanism by which SuH-dependent N signaling is increased or decreased in these different cells is obscure. The developing epidermis is known to get enriched for the full-length N (NFull) and the developing CNS for the carboxyl terminus-truncated N (NdeltaCterm). Results described here indicate that this differential accumulation of N receptors is part of a mechanism that would promote SuH-dependent N signaling in the developing epidermis but suppress it in the developing CNS. This mechanism involves SuH-dependent stability of NFull, NFull-dependent accumulation of SuH, stage specific stability of SuH, and NdeltaCterm-dependent loss of SuH and NFull.|
What does this section display?
What does this section not display?
This section does not currently display links that were removed or gene model changes.
|All updates||Click here to see a list of all updates to this record from FB2010_08 and on.|
|Language of Publication||English|
|Additional Languages of Abstract|
|Also Published As|
|Abbreviation||Mol. Cell. Biol.|
|Title||Molecular and Cellular Biology|
|Data from Reference|
|Natural transposons (1)|