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Certainly, the data we present in this study show that the Prdm family interacts with the Notch-Hes pathway during neurogenesis, may control nervous system patterning, and may modulate neuronal progenitor cell proliferation and differentiation.
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Neuron-like morphological changes of F11 neuronal progenitor cells after the overexpression of miR-124a complied with the Tα1 promoter-driven RFP reporter gene expression visualizing the neuronal differentiation of these cells [53].
Within the telencephalon we find that Prdm16 marks neuronal progenitor cells and Prdm8 postmitotic neurons.
Thus, S1P induces proliferation in neuronal progenitor cells but apoptosis in hippocampal neurons.
93 GLP-1 analogs have been demonstrated to exert neuroprotective and aniapoptotic effects, reduce Aβ plaque accumulation, modulate long-term potentiation and synaptic plasticity, and promote the differentiation of neuronal progenitor cells.
Although neuronal progenitor cells offer hope to replace dead or damaged neurons, very little is known about the effects of heavy ion radiation on them.
Moreover, neuronal progenitor cells differentiated from the rescued MiPSCs also demonstrated normal metabolic profiles.
These results emphasize the importance of determining how human neuronal progenitor cells respond to high linear energy transfer heavy ion radiation.
Thus, we utilized a cloned line of human neuronal progenitor (NT2) cells as a model and measured their responses to irradiation with 1 GeV/nucleon 56Fe26+ ions.
Moreover, Epotris affected the number of persistent basal dendrites exhibited by neuronal progenitor cells.
Furthermore, TET1 can negatively modulate neuronal differentiation independent of its catalytic activity and through srGAP3.
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