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Drosophila extracellular signal-regulated kinase involves the insulin-mediated proliferation of schneider cells

Title
Drosophila extracellular signal-regulated kinase involves the insulin-mediated proliferation of schneider cells
Authors
Kwon H.-B.Kim S.-H.Kim S.-E.Jang I.-H.Ahn Y.Lee W.-J.Choi K.-Y.
Ewha Authors
이원재
Issue Date
2002
Journal Title
Journal of Biological Chemistry
ISSN
0021-9258JCR Link
Citation
vol. 277, no. 17, pp. 14853 - 14858
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
The Drosophila insulin pathway is involved in the control of the proliferation and size of the cell. The stimulation of Schneider cells with human insulin has been observed to activate Drosophila extracellular signal regulated kinase (DERK). However, the role of DERK in the regulation of proliferation is unknown. In this study, we have identified a role of DERK in the proliferation of Drosophila Schneider cells. The inhibition of DERK activity by the overexpression of DMKP-3, an ERK-specific mitogen-activated protein kinase (MAPK) phosphatase, inhibited G 1 to S phase cell cycle progression as well as bromodeoxyuridine (BrdU) incorporation, which were previously increased by human insulin. However, DMKP-3 overexpression did not significantly reduce cell size that was also enlarged by insulin treatment, which suggests the specificity of the ERK pathway in proliferation but not for cell size. G 1 to S phase cell cycle progression and BrdU incorporation were also reduced by catalytically inactive DMKP-3 mutant, and they may be acquired by the trapping of DERK into cytosol. The depletion of DERK or DMKP-3 by inhibitory double-stranded RNA decreased and increased BrdU incorporation, respectively. Thus, we propose that DERK is involved in the proliferation of Schneider cells via the insulin pathway.
DOI
10.1074/jbc.M110366200
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일반대학원 > 바이오융합과학과 > Journal papers
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