Please use this identifier to cite or link to this item:
https://doi.org/10.1074/jbc.274.43.30341
Title: | NF-κB/Rel proteins are required for neuronal differentiation of SH-SY5Y neuroblastoma cells | Authors: | Feng, Z. Porter, A.G. |
Issue Date: | 22-Oct-1999 | Citation: | Feng, Z., Porter, A.G. (1999-10-22). NF-κB/Rel proteins are required for neuronal differentiation of SH-SY5Y neuroblastoma cells. Journal of Biological Chemistry 274 (43) : 30341-30344. ScholarBank@NUS Repository. https://doi.org/10.1074/jbc.274.43.30341 | Abstract: | The expression, cellular localization, and activation of the NF-κB/Rel transcription factors are altered during neuronal differentiation, but the significance is unclear. Here we investigate the requirement for NF-κB/Rel proteins in neuronal differentiation. SH-SY5Y neuroblastoma cells were induced to differentiate with retinoic acid (RA) or 12-O-tetradecanoylphorbol 13-acetate (TPA), and differentiation was demonstrated by morphological criteria and the enhanced expression of Bcl-2. NF-κB was transiently activated after the addition of the differentiation inducers before the morphological signs of differentiation and the enhanced Bcl-2 synthesis. The onset of NF-κB activation coincided with a significant reduction in the amount of only one of four NF-κB-inhibitory proteins examined (I-κBβ). In contrast, NF-κB activation and the reduction in I-κBβ failed to occur in SH-SY5Y cells transformed with I-κBαM, a dominant-negative inhibitor of NF- κB/Rel proteins. These I-κBαM-expressing cells failed to differentiate into neuronal cell types when treated with RA or TPA, and the increased Bcl-2 synthesis was blocked. Therefore, NF-κB/Rel proteins are required for neuronal differentiation of SH-SY5Y neuroblastoma cells. | Source Title: | Journal of Biological Chemistry | URI: | http://scholarbank.nus.edu.sg/handle/10635/111988 | ISSN: | 00219258 | DOI: | 10.1074/jbc.274.43.30341 |
Appears in Collections: | Staff Publications |
Show full item record
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.