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  • mProX™ Human GABRA5 Stable Cell Line

    [CAT#: S01YF-1123-KX68]
    Product Category:
    Membrane Protein Stable Cell Lines
    Subcategory:
    Ion Channel Cell Lines

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    Product Information

    Target Protein
    GABRA5
    Target Family
    GABAA
    Target Protein Species
    Human
    Host Cell Type
    CHO-K1; HEK293
    Target Classification
    Ion Channel Cell Lines
    Target Research Area
    CNS Research
    Related Diseases
    Developmental And Epileptic Encephalopathy; Non-Specific Early-Onset Epileptic Encephalopathy
    Gene ID
    UniProt ID

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    Alpha-aminobutyric acid The GABRA5 gene in humans codes for a protein known as a receptor, alpha 5, or GABRA5. In the mammalian brain, GABA is the primary inhibitory neurotransmitter that operates through ligand-gated chloride channels called GABAA receptors. Benzodiazepines are among the drugs that can alter the chloride conductance of these channels by binding to the GABAA receptor. It has been determined that GABAA receptors have at least 16 different subunits. Three distinct alternative non-coding first exons have been used to describe transcript variations. The customized GABRA5 stable cell line can be used in antibody discovery and development, potential drug candidate screening and signaling pathway researches.

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    FAQ

    chat Melissa (Verified Customer)

    How GABRA5 works? Apr 07 2020

    chat Sherry Smith (Creative Biolabs Scientific Support)

    The ligand GABA is the endogenous compound that causes this receptor to open; once bound to GABA, the protein receptor changes conformation within the membrane, opening the pore in order to allow chloride anions (Cl−) and, to a lesser extent, bicarbonate ions (HCO3−) to pass down their electrochemical gradient. Apr 07 2020

    chat David (Verified Customer)

    How is GABRA5 associated with Alzheimer's Disease and other neurological disorders? Apr 10 2020

    chat Sherry Smith (Creative Biolabs Scientific Support)

    A severe reduction of GABRA5 has been observed in a subset of patients with Alzheimer's Disease (AD) and Parkinson's Disease (PD). Apr 10 2020

    Published Data

    Fig.1 Diversity of GABAAR subunit expression within various organs of the mouse.

    Representative gel electrophoresis images of homogenates from the entire brain (Br), stomach (St), lung (Lu), bladder (Bl), kidney (Ki), heart (Hr), and liver (Li) collected from adult male C57BL/6 mice, together with mRNA transcripts for different GABAAR subunits using RT-PCR. For several GABAAR subunits, corresponding amplicons with bands the same size as those seen in the brain were regularly found in a number of peripheral organs.

    Ref: Everington, Ethan A., et al. "Molecular characterization of GABA-A receptor subunit diversity within major peripheral organs and their plasticity in response to early life psychosocial stress." Frontiers in Molecular Neuroscience 11 (2018): 18.

    Pubmed: 29467616

    DOI: 10.3389/fnmol.2018.00018

    Research Highlights

    Expanding the phenotypic spectrum of the mutant GABRA1 gene, GABRA5 is a causal gene for early onset epileptic encephalopathy. This supports the increasing evidence that phenotypes of early onset epileptic encephalopathy are influenced by impairments in GABAergic neurotransmission.
    Hernandez, Ciria C., et al. "Altered inhibitory synapses in de novo GABRA5 and GABRA1 mutations associated with early onset epileptic encephalopathies." Brain 142.7 (2019): 1938-1954.
    Pubmed: 31056671   DOI: 10.1093/brain/awz123

    The molecular aim for treating obesity is the specific suppression of astrocytic GABA, which is suppressed by firing GABRA5LHA.
    Sa, Moonsun, et al. "Hypothalamic GABRA5-positive neurons control obesity via astrocytic GABA." Nature metabolism (2023): 1-20.
    Pubmed: 37653043   DOI: 10.1038/s42255-023-00877-w

    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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