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  • mProX™ Human GRIK2 Stable Cell Line

    [CAT#: S01YF-1023-PY251]
    Product Category:
    Membrane Protein Stable Cell Lines
    Subcategory:

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    Product Information

    Target Family
    Other Targets
    Target Protein Species
    Human
    Host Cell Type
    HEK293;CHO-K1;UM-UC-3
    Target Classification
    Other Targets Drug Discovery Assays and Products
    Target Research Area
    CNS Research
    Related Diseases
    Neurodevelopmental Disorder With Impaired Language And Ataxia And With Or Without Seizures; Intellectual Developmental Disorder, Autosomal Recessive 6
    Gene ID
    Human:2898
    UniProt ID
    Human:Q13002

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    GRIK2, a gene encoding the kainate receptor subunit GluK2, has been implicated in various neurological disorders. A missense mutation in GRIK2 has been shown to increase dendritic excitability and synaptic integration, leading to altered neuronal function. Additionally, GRIK2 has been associated with the pathogenesis of Parkinson's disease, with the neuroprotective effects of a traditional Chinese formulation mediated through GRIK2-related signaling pathways. In the context of epilepsy, GRIK2 has been identified as a potential target for gene therapy in drug-resistant temporal lobe epilepsy, as downregulating GRIK2 expression reduces seizure activity. Furthermore, interstitial 6q deletions involving GRIK2 have been associated with epilepsy and Prader-Willi-like phenotypes. These findings highlight the diverse applications of GRIK2 in understanding and treating neurological disorders.

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    FAQ

    chat Cameron Garcia (Verified Customer)

    What is the significance of GRIK2 in neurodevelopmental disorders? Aug 15 2021

    chat Patrick Liam (Creative Biolabs Scientific Support)

    Variants in the GRIK2 gene, which encodes a kainate receptor subunit, are causative for early childhood developmental disorders, emphasizing the importance of clarifying the role of kainate receptors in early nervous system development. Aug 15 2021

    chat Jordan Garcia (Verified Customer)

    How does GRIK2 expression relate to cancer? Jan 20 2023

    chat Patrick Liam (Creative Biolabs Scientific Support)

    GRIK2-derived antigenic peptides are specifically expressed in bladder cancer stem cells, suggesting GRIK2's potential as a target for bladder cancer stem cell-targeting immunotherapy. Jan 20 2023

    Published Data

    Fig.1 Functional analysis of GRIK2 by siRNA-mediated mRNA knockdown.

    Cells derived from UM-UC3 with GRIK2 knockdown were utilized to generate Matrigel-invading cells. The scale of the black bar is 100 μm, and the mean number of invading cells along with their standard deviation (SD) was calculated for each data point. Significance levels (*P values) were determined to assess the differences observed.

    Ref: Inoue, Ryuta, et al. "GRIK2 has a role in the maintenance of urothelial carcinoma stem-like cells, and its expression is associated with poorer prognosis." Oncotarget 8.17 (2017): 28826.

    Pubmed: 28418868

    DOI: 10.18632/oncotarget.16259

    Research Highlights

    Nomura, Toshihiro. et al. "A pathogenic missense mutation in kainate receptors elevates dendritic excitability and synaptic integration through dysregulation of SK channels." The Journal of neuroscience : the official journal of the Society for Neuroscience, 2023.
    A considerable number of rare variants that contribute to neurodevelopmental disorders (NDDs) are found in genes that are responsible for encoding synaptic proteins, particularly ionotropic glutamate receptors (iGluRs). Despite this, the ways in which these damaging missense variants impact brain function are often not well understood. The authors of this study sought to investigate the physiological effects of a specific missense mutation in an iGluR gene that has been linked to NDDs.
    Nomura, Toshihiro. et al. "A pathogenic missense mutation in kainate receptors elevates dendritic excitability and synaptic integration through dysregulation of SK channels." The Journal of neuroscience : the official journal of the Society for Neuroscience, 2023.
    Pubmed: 37802657   DOI: 10.1523/JNEUROSCI.1259-23.2023

    Pan, Botao. et al. "Integrative multilevel exploration of the mechanism by which Er-Zhi-Wan alleviates the Parkinson's disease (PD)-like phenotype in the MPTP-induced PD mouse model." Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2023.
    The neuroprotective effects of Er-Zhi-Wan (EZW), a traditional Chinese formulation, in MPTP-induced Parkinson's disease (PD) models are not well understood. Thus, the aim of this study was to evaluate the neuroprotective effects of EZW in a mouse model of PD induced by MPTP. Using a combination of multilevel databases, network pharmacology, biological experiments, and LCMS/MS, the underlying pharmacological mechanisms of EZW in the prevention and treatment of PD were investigated. In vivo data demonstrated that pretreatment with EZW was able to protect against MPTP-induced motor dysfunction and rescue dopaminergic neurons from degeneration in mice. Network pharmacology analysis also revealed a complex, multi-component network that is responsible for the neuroprotective activity of EZW in PD treatment. Genes such as Grm2, Grm5, Drd2, and Grik2 were identified as important therapeutic targets, and subsequent experiments showed that EZW can regulate the mRNA levels of these genes and increase the phosphorylation of CREB to stimulate CREB signaling, thus reversing neuronal death after MPTP exposure. LC-MS/MS analysis further identified 53 compounds in EZW, highlighting the complexity of its neuroprotective network. This study provides important insight into the mechanism of EZW in MPTP-induced PD and supports its potential therapeutic role in neurodegenerative diseases.
    Pan, Botao. et al. "Integrative multilevel exploration of the mechanism by which Er-Zhi-Wan alleviates the Parkinson's disease (PD)-like phenotype in the MPTP-induced PD mouse model." Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2023.
    Pubmed: 37348406   DOI: 10.1016/j.biopha.2023.115021

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