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The molecular details of how the Wnt pathway mediates this fate diversification were later elucidated.
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A recent paper on ASE in human cell lines, suggested that up to 68% of variants expected to result in nonsense mediated decay escape this fate via unidentified mechanisms [ 30].
To identify molecular mechanisms mediating this cell-fate decision process, we applied different perturbations to pathways activated by these growth factors.
However it is possible that ribonucleoproteins, that mediate the fate of RNAs within the cells, could be involved.
Some outgrowth factors such as EGF, bFGF, LIF and BMPs as exogenous factors could mediate the fate decision of NPCs [8], [9], [10].
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.
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.
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).
This fate change is potentially mediated through BMP-induced upregulation of Id1/3 and Hes5, which in turn inhibit Ascl1 activity (Nakashima et al., 2001).
Did Judas deserve this fate?
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