DUSP6: Potential interactions with FXR1P in the nervous system

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dc.contributor.authorMa, Yunen_US
dc.contributor.authorLiu, Yixuanen_US
dc.contributor.authorHe, Shuyaen_US
dc.contributor.authorJiang, Zhishengen_US
dc.date.accessioned2023-08-09T06:01:39Z
dc.date.available2023-08-09T06:01:39Z
dc.date.issued2022-02
dc.description.abstractFragile 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 speci?city 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.en_US
dc.identifier.affiliationsInstitute of Biochemistry & Molecular Biologyen_US
dc.identifier.affiliationsInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Diseaseen_US
dc.identifier.affiliationsKey Laboratory of Ecological Environment and Critical Human Diseases Prevention of Hunan Province Department of Educationen_US
dc.identifier.affiliationsHunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang Medical School, University of South China, Hengyang, 421 001, Chinaen_US
dc.identifier.citationMa Yun, Liu Yixuan, He Shuya, Jiang Zhisheng. DUSP6: Potential interactions with FXR1P in the nervous system. Indian Journal of Biochemistry & Biophysics. 2022 Feb; 59(2): 229-237en_US
dc.identifier.issn0019-5189
dc.identifier.issn0975-1009
dc.identifier.placeIndiaen_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/221493
dc.languageenen_US
dc.publisherCSIR-NIScPRen_US
dc.relation.issuenumber2en_US
dc.relation.volume59en_US
dc.source.urihttps://doi.org/10.56042/ijbb.v59i2.54099en_US
dc.subjectApoptosisen_US
dc.subjectCo-localizationen_US
dc.subjectERK1/2en_US
dc.subjectNervous systemen_US
dc.subjectSK-N-SHen_US
dc.titleDUSP6: Potential interactions with FXR1P in the nervous systemen_US
dc.typeJournal Articleen_US
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