In particular, we believe that HIP/RPL29 expression is required to maintain proliferation of chondrocytes and avoid skeletal shortening.
Emerging evidence suggests that Erk1/2 activity is essential to maintain proliferation of NSC/NPCs during normal neurogenesis (Satoh et al., 2011; Vithayathil et al., 2015).
As a consequence, there is mutual activation of NOTCH signalling which maintains proliferation of this pool of uncommitted progenitors.
Thus, we conclude that NOTCH signalling is required to maintain proliferation of caudal spinal cord NP cells.
Therefore, PAX6 may maintain proliferation of a subpopulation of cells which continually provide new neural precursors which maintains the rostral fate seen within the NT2N population.
Among the various developmental roles, Tbx1 is thought to maintain proliferation of mesodermally-derived cardiac progenitors of the second heart field (SHF) [14], a migratory cell population that enters the heart in a relatively late stage of its development [15].
These major conclusions are based on the following evidences: I, Activation of NOTCH signalling in the PNTZ, presumably through Hes5, inhibits neuronal generation and is required to maintain proliferation of NP cells.
Although this might be due to the fact that the expected increase (around a 10% of TUJ1 positive cells in the control, Fig. 4G) is in the range of the experimental error of the determination of BrdU labelled cells, these results raise the question of whether NOTCH signalling is required to maintain proliferation of these cells.
Taken together, it is clear that certain unidentified factors, secreted by embryonic fibroblasts, are required for maintaining proliferation of the derived vole cell lines, whereas the presence of vole LIF is a crucial factor only during the initial stages of vole TS-like cells derivation.
Moreover, enforced expression of normal and activated forms of MYB can suppress differentiation and maintain proliferation of hematopoietic cells [ 4- 6].
