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Because myelin proteins might be involved in forming the niche for NPCs in vivo, they could be involved in mediating the fate decision of NPCs.
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However it is possible that ribonucleoproteins, that mediate the fate of RNAs within the cells, could be involved.
Thus it may be possible for the interaction between Nogo-66 and NgR to occur in injured CNS and mediate the fate decision of NPCs.
Some outgrowth factors such as EGF, bFGF, LIF and BMPs as exogenous factors could mediate the fate decision of NPCs [8], [9], [10].
Iridovirus-encoded LITAF and Bcl-2 could mediate the fate of host cells by regulating apoptosis [ 47, 48].
To identify the transcriptional factors that can mediate the fate specification of SE cells, we re-surveyed the expression profiles of the DNA microarrays (Figs. S4, S5).
These phosphoproteins function as clathrin adaptor molecules and have been implicated in mediating the sorting fates of a number of different permeases; and, one, Aly2, has recently been reported to be an Npr1 substrate (Lin et al. 2008; Nikko et al. 2008; Nikko and Pelham 2009; O'Donnell et al. 2010).
We have hypothesized that these axon inhibitory myelin proteins could mediate the NPCs fate decision.
IGF2BP1 encodes the IGF2 mRNA binding protein 1 (IGF2BP1) which mediates the cytoplasmic fate of specific target mRNAs including ACTB and CD44.
These expression data suggest the possibility that Grhl3 mediates the SE fate specification of uncommitted progenitor cells via canonical Wnt signaling in coordination with the dorsal midline epithelial fusion of neural folds.
Our observations identify a new role for syndecan-1 in mediating the cellular interactions and fate of positively charged submicrometer amorphous silica particles in the alveolar type II epithelial cell, a target cell for inhaled particles.
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