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  • mProX™ Human ATP2B2 Stable Cell Line

    [CAT#: S01YF-1023-PY258]
    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;MDA-MB-231
    Target Classification
    Other Targets Drug Discovery Assays and Products
    Target Research Area
    CNS Research
    Related Diseases
    Deafness, Autosomal Dominant 82; Deafness, Autosomal Recessive 12
    Gene ID
    Human:493
    UniProt ID
    Human:P23634

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    ATP2B2, a gene involved in calcium signaling, has been studied in various contexts. In epilepsy, the expression of ATP2B2 and other related genes was found to be dysregulated in patients, suggesting their potential as biomarkers for the condition. In neurodevelopmental disorders, de novo variants in ATP2B2 were identified as a cause of variable symptoms such as dystonia, ataxia, intellectual disability, behavioral symptoms, and seizures. Additionally, ATP2B2 was investigated in the context of genetic hearing loss, and CRISPR-Cas9 ribonucleoprotein delivery was used to edit the gene and restore hearing function in mouse models. Finally, ATP2B2 was analyzed in head and neck squamous cell carcinomas, where low expression of the gene was associated with worse overall survival. These studies highlight the diverse applications of ATP2B2 in different fields of research.

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    FAQ

    chat Cameron Smith (Verified Customer)

    How does ATP2B2 affect auditory sensitivity? Oct 03 2020

    chat Patrick Liam (Creative Biolabs Scientific Support)

    Changes in cochlear ATP2B2 expression correlate with the maturation of auditory sensitivity, suggesting its involvement in the normal development of hearing. Oct 03 2020

    chat Casey Miller (Verified Customer)

    What is the impact of ATP2B2 mutations on hearing impairment? Dec 25 2021

    chat Patrick Liam (Creative Biolabs Scientific Support)

    Mutations in ATP2B2, a major calcium pump gene, cause deafness in mice, defining a new class of deafness genes that directly affect hair-cell physiology. Dec 25 2021

    Published Data

    Fig.1 In MDA-MB-231 breast cancer cells, the silencing of PMCA2 was undertaken, and its effects on cell viability as well as ionomycin-induced cell death were examined.

    SiRNA-mediated silencing of PMCA2 expression was carried out, followed by the assessment of cell viability in the presence of the calcium ionophore ionomycin, with a comparison between siPMCA2 and the siNT control. PMCA2 mRNA levels were evaluated at 48 h and 120 h post-siRNA treatment, showing significant differences (*P < 0.05) through two-way ANOVA analysis with Bonferroni post hoc analysis. Cell viability was depicted in representative dot plots featuring Hoechst 33342 and propidium iodide fluorescence in randomly selected cells (10,000 cells/dot plot) from three separate experiments (n = 3). Subsequent analysis of cell viability, under conditions of siNT and siPMCA2 transfection, either in the absence (0 μM) or presence (3 μM or 10 μM) of ionomycin, also revealed significant distinctions (*P < 0.05) via repeated-measures, two-way ANOVA with Bonferroni post hoc analysis. The bar graphs display the mean ± S.D. obtained from three independent experiments (n = 3), conducted in duplicate or triplicate wells.

    Ref: Curry, Merril, Sarah J. Roberts-Thomson, and Gregory R. Monteith. "PMCA2 silencing potentiates MDA-MB-231 breast cancer cell death initiated with the Bcl-2 inhibitor ABT-263." Biochemical and biophysical research communications 478.4 (2016): 1792-1797.

    Pubmed: 27613092

    DOI: 10.1016/j.bbrc.2016.09.030

    Research Highlights

    Taheri, Mohammad. et al. "Assessment of expression of calcium signaling related lncRNAs in epilepsy." Scientific reports, 2023.
    The study assessed the expression of three mRNA coding genes (SLC1A1, SLC25A12, and ATP2B2) and three long non-coding RNAs (LINC01231:1, lnc-SLC25A12-8:1, and lnc-MTR-1:1) involved in the calcium signaling pathway in 39 patients with refractory epilepsy and 71 healthy controls. Results showed higher expression of all genes (except lnc-SLC25A12) in epileptic patients compared to controls. Gender-based analysis revealed up-regulation of SLC1A1, SLC25A12, LINC01231, and lnc-MTR-1 in males, and higher expression of SLC1A1 and SLC25A12 in females with epilepsy. SLC25A12 was found to have the highest sensitivity (1.0) for differentiating epileptic cases from controls. The study concludes that dysregulation of calcium-signaling related genes may serve as potential biomarkers for epilepsy.
    Taheri, Mohammad. et al. "Assessment of expression of calcium signaling related lncRNAs in epilepsy." Scientific reports, 2023.
    Pubmed: 37865723   DOI: 10.1038/s41598-023-45341-7

    Poggio, Elena. et al. "ATP2B2 de novo variants as a cause of variable neurodevelopmental disorders that feature dystonia, ataxia, intellectual disability, behavioral symptoms, and seizures." Genetics in medicine : official journal of the American College of Medical Genetics, 2023.
    ATP2B2 is a gene that encodes a specific type of plasma-membrane calcium-transporting ATPase-2, found in sensory ear cells and specialized neurons. Prior research has connected ATP2B2/Atp2b2 variants to isolated hearing loss in patients and neurodevelopmental deficits accompanied by ataxia in mice. The objective of this study was to investigate the potential relationship between ATP2B2 and various neurological disorders in humans.
    Poggio, Elena. et al. "ATP2B2 de novo variants as a cause of variable neurodevelopmental disorders that feature dystonia, ataxia, intellectual disability, behavioral symptoms, and seizures." Genetics in medicine : official journal of the American College of Medical Genetics, 2023.
    Pubmed: 37675773   DOI: 10.1016/j.gim.2023.100971

    Please note: All products are "FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC OR CLINICAL PROCEDURES" For licensing inquiries, please contact
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