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| Hauptseite > Publikationsdatenbank > Inhibition of BCL-2 leads to increased apoptosis and delayed neuronal differentiation in human ReNcell VM cells in vitro > print |
| Hauptseite > Publikationsdatenbank > Inhibition of BCL-2 leads to increased apoptosis and delayed neuronal differentiation in human ReNcell VM cells in vitro > print |
| 001 | 811943 | ||
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| 100 | 1 | _ | |a Fröhlich, Michael |0 P:(DE-HGF)0 |b 0 |
| 245 | _ | _ | |a Inhibition of BCL-2 leads to increased apoptosis and delayed neuronal differentiation in human ReNcell VM cells in vitro |
| 260 | _ | _ | |a Oxford [u.a.] |c 2016 |b Pergamon Press |
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| 520 | _ | _ | |a BCL-2 is a multifunctional protein involved in the regulation of apoptosis, cell cycle progression and neural developmental processes. Its function in the latter process is not well understood and needs further elucidation. Therefore, we characterized the protein expression kinetics of BCL-2 and associated regulatory proteins of the intrinsic apoptosis pathway during the process of neuronal differentiation in ReNcell VM cells with and without functional inhibition of BCL-2 by its competitive ligand HA14-1. Inhibition of BCL-2 caused a diminished BCL-2 expression and higher levels of cleaved BAX, activated Caspase-3 and cleaved PARP, all pro-apoptotic markers, when compared with untreated differentiating cells. In parallel, flow cytometric analysis of HA14-1-treated cells revealed a delayed differentiation into HuC/D+ neuronal cells when compared to untreated differentiating cells. In conclusion, BCL-2 possess a protective function in fully differentiated ReNcell VM cells. We propose that the pro-survival signaling of BCL-2 is closely connected with its stimulatory effects on neurogenesis of human neural progenitor cells. |
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| 700 | 1 | _ | |a Kriehuber, Ralf |0 P:(DE-Juel1)133469 |b 3 |e Corresponding author |
| 773 | _ | _ | |a 10.1016/j.ijdevneu.2015.10.004 |g Vol. 48, p. 9 - 17 |0 PERI:(DE-600)2012538-0 |p 9 - 17 |t International journal of developmental neuroscience |v 48 |y 2016 |x 0736-5748 |
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