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- W1964501276 abstract "Emerging evidence has shown that GSK3β plays a pivotal role in regulating the specification of axons and dendrites. Our previous study has shown a novel GSK3β interaction protein (GSKIP) able to negatively regulate GSK3β in Wnt signaling pathway. To further characterize how GSKIP functions in neurons, human neuroblastoma SH-SY5Y cells treated with retinoic acid (RA) to differentiate to neuron-like cells was used as a model. Overexpression of GSKIP prevents neurite outgrowth in SH-SY5Y cells. GSKIP may affect GSK3β activity on neurite outgrowth by inhibiting the specific phosphorylation of tau (ser396). GSKIP also increases β-catenin in the nucleus and raises the level of cyclin D1 to promote cell-cycle progression in SH-SY5Y cells. Additionally, overexpression of GSKIP downregulates N-cadherin expression, resulting in decreased recruitment of β-catenin. Moreover, depletion of β-catenin by small interfering RNA, neurite outgrowth is blocked in SH-SY5Y cells. Altogether, we propose a model to show that GSKIP regulates the functional interplay of the GSK3β/β-catenin, β-catenin/cyclin D1, and β-catenin/N-cadherin pool during RA signaling in SH-SY5Y cells. J. Cell. Biochem. 108: 1325–1336, 2009. © 2009 Wiley-Liss, Inc." @default.
- W1964501276 created "2016-06-24" @default.
- W1964501276 creator A5001965208 @default.
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- W1964501276 date "2009-12-15" @default.
- W1964501276 modified "2023-10-02" @default.
- W1964501276 title "GSKIP, an inhibitor of GSK3β, mediates the N-cadherin/β-catenin pool in the differentiation of SH-SY5Y cells" @default.
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- W1964501276 doi "https://doi.org/10.1002/jcb.22362" @default.
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