Glucose induced MAPK signalling influences NeuroD1-mediated activation and nuclear localization.
Glucose induced MAPK signalling influences NeuroD1-mediated activation and nuclear localization.
复制标题
葡萄糖诱导的 MAPK 信号传导影响 NeuroD1 介导的激活和核定位。
DOI：
10.1016/s0014-5793(02)03318-5
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发表时间：
2002
期刊：
影响因子：
3.5
通讯作者：
Serup,Palle
中科院分区：
文献类型：
--
作者：
Petersen,HelleV;Jensen,JanN;Stein,Roland;Serup,Palle
The helix–loop–helix transcription factor NeuroD1 (also known as Beta2) is involved in β-cell survival during development and insulin gene transcription in adults. Here we show NeuroD1 is primarily cytoplasmic at non-stimulating glucose concentrations (i.e. 3 mM) in MIN6 β-cells and nuclear under stimulating conditions (i.e. 20 mM). Quantification revealed that NeuroD1 was in 40–45% of the nuclei at 3 mM and 80–90% at 20 mM. Treatment with the MEK inhibitor PD98059 or substitution of a serine for an alanine at a potential mitogen-activated protein kinase phosphorylation site (S274) in NeuroD1 significantly increased the cytoplasmic level at 20 mM glucose. The rise in NeuroD1-mediated transcription in response to glucose also correlated with the change in sub-cellular localization, a response attenuated by PD98059. The data strongly suggest that glucose-stimulation of the MEK–ERK signalling pathway influences NeuroD1 activity at least partially through effects on sub-cellular localization.
