Overexpression of BETA2/neuroD induces neurite outgrowth in F11 neuroblastoma cells

Cited 37 time in scopus
Metadata Downloads
Title
Overexpression of BETA2/neuroD induces neurite outgrowth in F11 neuroblastoma cells
Author(s)
Jang Hyeon Cho; Il Sun Kwon; So Yeon Kim; Sung Ho Ghil; Ming Jer Tsai; Yeon Soo Kim; Young Don Lee; Hae Young Suh-Kim
Bibliographic Citation
Journal of Neurochemistry, vol. 77, no. 1, pp. 103-109
Publication Year
2001
Abstract
BETA2/NeuroD, a basic helix-loop-helix (bHLH) transcription factor, has been shown to play important roles in the development of the nervous system and the maintenance and formation of pancreatic and enteroendocrine cells. The gain of function of BETA2/NeuroD in neurogenesis has been shown in Xenopus embryos. In this study, we investigated the neurogenic potential of BETA2/NeuroD using neuroblastoma cell line, F11, which could be induced to differentiate into neurons in the presence of cAMP. To induce or block the expression of BETA2/NeuroD, expression vectors for the full-length and a C-terminal deletion mutant of BETA2 were constructed and their transactivation potential was verified using reporter genes containing the insulin promoter sequences. Overexpression of BETA2 with full-length construct induced neurite outgrowth in F11 cells in the absence of cAMP. In contrast, the C-terminal deletion mutant, BETA2(1-233), which has dominant negative activity, inhibited neurite outgrowth induced by cAMP in F11 cells. These results indicate that BETA2/NeuroD plays an important role in terminal differentiation of neuroblastoma cells. They also imply that BETA2/NeuroD or related bHLH factors plays an essential role for differentiation of F11 neuroblastoma cells.
Keyword
BETA2F11 cellsneurite outgrowthNeuroD
ISSN
0022-3042
Publisher
Wiley
DOI
http://dx.doi.org/10.1046/j.1471-4159.2001.00230.x
Type
Article
Appears in Collections:
1. Journal Articles > Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.