Experimental evidence suggests there is. In Notch mutants, extra neurons have been detected, resulting from a transformation of sheath cells into neurons. Thus Notch function is required not only to specify the sheath cell but also to express ttk in this daughter cell of an asymmetric division. In a reciprocal experiment, overexpression of Notch turns on ttk expression in cells that normally do not express ttk . Both maternal and zygotic forms have multiple PEST sequences, correlating with rapid protein turnover.
Numb protein has an N-terminal phosphotyrosine binding domain.
Asymmetric localization but not membrane localization of both Prospero and Numb in Drosophila embryos is inhibited by latrunculin A, an inhibitor of actin assembly. Fusion of the first 76 or the first 119 aa of Numb to beta-galactosidase results in a fusion protein that localizes to the cell membrane, but fails to localize asymmetrically during mitosis. The Numb protein is involved in cell fate determination during Drosophila neural development. In Shc, this domain interacts with specific phosphotyrosine containing motifs on receptor tyrosine kinases and other signaling molecules. Residues N-terminal to the phosphotyrosine are also crucial for phosphopeptide binding to the Shc PTB domain.