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Asymmetric cortical localization of prospero in neuroblasts requires entry into mitosis; it does not depend on numb function.
Numb function in the immune system has been partially explored.
Functional studies in sponges would be necessary to state whether another protein replaces Numb function.
Overall, our data reveal important keys in the Numb function regulation, where Numb function is exquisitely regulated through its own subcellular distribution to balance alternative pathways at different stages of development.
In neuroblasts, loss of numb function results in overproliferation and tumor formation (Lee et al., 2006a; Wang et al., 2006).
Notably, Numb PTB peptides have been used to block Mdm2 function and consequently to stabilize p53-mimicking Numb function.
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This makes it difficult to understand which pathways are regulated by Numb and raises the possibility that these different roles are mediated by diverse Numb functions.
Moreover, Numb functions as a tumour suppressor in larval brains and supernumerary neuroblasts form in numb-deficient neuroblasts [ 21, 27, 28].
Recent data describe the presence of Numb in the nuclear compartment, besides its known cytoplasmic localization, raising the possibility that different Numb functions could be regulated by its differential subcellular localization.
Taken together, these data show that Numb nuclear function is dependent on the PTB domain.
All these data suggest that Numb nuclear function during T-cell development is finely regulated by its localization.
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