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DUSP6: Potential interactions with FXR1P in the nervous system

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Title DUSP6: Potential interactions with FXR1P in the nervous system
 
Creator Ma, Yun
Liu, Yixuan
He, Shuya
Jiang, Zhisheng
 
Subject Apoptosis
Co-localization
ERK1/2
Nervous system
SK-N-SH
 
Description 229-237
Fragile X syndrome (FXS) is a leading genetic cause of autism intellectual disorder and autism spectrum disorder
(ASD), with either limited treatment options or incurable. Fragile X-related gene 1 (FXR1) is a homolog of the Fragile
X mental retardation gene 1 (FMR1), the causative gene of FXS, and both are highly homologous and functionally identical.
In FXS, both PI3K (AKT/mTOR signaling pathway) and ERK1/2 (MAPK signaling pathway) expression levels were
abnormal. Dual specificity phosphatase 6 (DUSP6) is a member of the mitogen-activated protein kinases (MAPKs) that
participates in the crosstalk between the two signaling systems of MEK/ERK and mTOR. By interacting with multiple nodes
of MAPK and PI3K/AKT signaling pathways (including the mTOR complex), DUSP6 regulates cellular growth,
proliferation, metabolism and participates in pathological processes of cancer and cognitive impairment. However, whether
there is an interaction between FXR1P and DUSP6 and the effects of DUSP6 on the growth of SK-N-SH cells remains
elusive. As demonstrated by our results, FXR1P was identified in the cytoplasm and nucleus of SK-N-SH cells co-localized
with DUSP6, which might have regulated ERK1/2 signaling pathways in SK-N-SH cells. To a certain extent, FXR1P may
reverse the negative regulation of ERK1/2 by DUSP6. Moreover, we discovered that not only does DUSP6 inhibit
proliferation, but it also promotes the apoptosis of SK-N-SH cells.
 
Date 2022-03-25T05:17:04Z
2022-03-25T05:17:04Z
2022-02
 
Type Article
 
Identifier 0975-0959 (Online); 0301-1208 (Print)
http://nopr.niscair.res.in/handle/123456789/59366
 
Language en
 
Publisher NIScPR-CSIR, India
 
Source IJBB Vol.59(2) [February 2022]