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Target Concepts:
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Query: UMLS:C0027819 (
neuroblastoma
)
27,800
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Emerging evidence has shown that GSK3beta plays a pivotal role in regulating the specification of axons and dendrites. Our previous study has shown a novel
GSK3beta interaction protein
(
GSKIP
) able to negatively regulate GSK3beta 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 GSK3beta activity on neurite outgrowth by inhibiting the specific phosphorylation of tau (ser396).
GSKIP
also increases beta-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 beta-catenin. Moreover, depletion of beta-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 GSK3beta/beta-catenin, beta-catenin/cyclin D1, and beta-catenin/N-cadherin pool during RA signaling in SH-SY5Y cells.
...
PMID:GSKIP, an inhibitor of GSK3beta, mediates the N-cadherin/beta-catenin pool in the differentiation of SH-SY5Y cells. 1983 Jul 2
