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  • mProX™ Human PRKG1 Stable Cell Line

    [CAT#: S01YF-1023-PY50]
    Product Category:
    Membrane Protein Stable Cell Lines
    Subcategory:
    Kinase Cell Lines

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    Host Cell Type:
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    Based on this stable cell line, we also provide cell-based in vitro assays to evaluate the effects of your compounds or antibodies.

    Sub Cat Product Name Target Protein Species Host Cell Type Assay Types Inquiry Datasheet
    S01YF-1222-KX428 Magic™ Human PGK(PRKG1) in Vitro Assay Human Kinase Assay

    Product Information

    Target Family
    Kinases/Enzyme
    Target Protein Species
    Human
    Host Cell Type
    HEK293;CHO-K1;Neonatal rat ventricle cardiomyocytes (CMs)
    Target Classification
    Kinase Cell Lines
    Target Research Area
    Cardiovascular Research
    Related Diseases
    Aortic Aneurysm, Familial Thoracic 8; Familial Thoracic Aortic Aneurysm And Aortic Dissection
    Gene ID
    Human:5592
    UniProt ID
    Human:Q13976

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    PRKG1 (protein kinase, cGMP-dependent, type I) is associated with various traits and conditions. In Zhaotong cattle, PRKG1 is identified as a candidate gene related to meat quality traits. In aging rats, impaired nitric oxide mechanisms, including PRKG1, are implicated in lower urinary tract dysfunction. In male NongHua ma ducks, PRKG1 is considered an important candidate marker gene related to neck ring formation. In individuals with rape pollen allergy, PRKG1 is identified as one of five characteristic genes associated with the condition. Additionally, in individuals with functional somatic syndromes, such as chronic fatigue syndrome and fibromyalgia syndrome, altered DNA methylation of PRKG1 is observed, potentially contributing to the pathophysiology of these conditions. Overall, PRKG1 has implications in bone development and metabolism, meat quality traits, immune response, heat resistance, lower urinary tract function, neck ring formation, pollen allergy, and functional somatic syndromes.

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    FAQ

    chat Peyton Johnson (Verified Customer)

    How does PRKG1 influence achalasia disease? Jan 26 2021

    chat Patrick Liam (Creative Biolabs Scientific Support)

    Downexpression of miR-200c-3p contributes to achalasia disease by targeting the PRKG1 gene, suggesting its involvement in the disease's pathogenesis. Jan 26 2021

    chat Morgan Johnson (Verified Customer)

    What is the role of PRKG1 in skeletal muscle aging? Apr 03 2020

    chat Patrick Liam (Creative Biolabs Scientific Support)

    PRKG1-AS1, a long non-coding RNA, is identified as playing important roles in skeletal muscle aging, influencing cell viability and apoptosis. Apr 03 2020

    Published Data

    Fig.1 After 8 hours of glucose deprivation, autophagy activation was blunted by Prkg1 knockdown.

    Prkg1 was targeted for silencing in CMs, followed by an 8-hour treatment with NG to assess autophagy. Western blots were performed to analyze LC3-II, and corresponding densitometric analyses were conducted (N=4-5).

    Ref: Forte, Maurizio, et al. "NPPA/atrial natriuretic peptide is an extracellular modulator of autophagy in the heart." Autophagy 19.4 (2023): 1087-1099.

    Pubmed: 35998113

    DOI: 10.1080/15548627.2022.2115675

    Research Highlights

    Micale, Lucia et al. "Downexpression of miR-200c-3p Contributes to Achalasia Disease by Targeting the PRKG1 Gene." International journal of molecular sciences vol. 24,1 668. 30 Dec. 2022.
    Achalasia, a disorder affecting the smooth muscle motility of the esophagus, has an unknown origin. Building on prior findings that revealed decreased miR-200c-3p levels in achalasia patient tissues, linked to elevated PRKG1, SULF1, and SYDE1 gene expressions, the objective was to investigate the unexplored interplay between these genes and human miR-200c-3p, shedding light on their potential role in achalasia's development. Employing bioinformatics tools, researchers sought miR-200c-3p binding sites in PRKG1, SULF1, and SYDE1's 3'-UTR. Dual-luciferase assays, quantitative PCR, and immunoblot analysis were conducted, revealing miR-200c-3p's influence on gene expression and hinting at the NO/cGMP/PKG signaling pathway's involvement in achalasia's pathogenesis.
    Micale, Lucia et al. "Downexpression of miR-200c-3p Contributes to Achalasia Disease by Targeting the PRKG1 Gene." International journal of molecular sciences vol. 24,1 668. 30 Dec. 2022.
    Pubmed: 37767570   DOI: 10.1152/ajprenal.00092.2023

    Gotoh, Daisuke. et al. "Impaired nitric oxide mechanisms underlying lower urinary tract dysfunction in aging rats." American journal of physiology. Renal physiology, 2023.
    The research aimed to explore changes in bladder and urethral function as well as nitric oxide (NO)-related molecular alterations in aging rats. The rats were categorized into two groups: Group Y, consisting of young rats (12 weeks old), and Group A, comprised of aging rats (15 months old). A 24-hour voiding assessment was conducted, evaluating urodynamic parameters through awake cystometry (CMG) and urethral perfusion pressure (UPP) recordings under urethane anesthesia. They also examined mRNA expression levels of NO-, ischemia-, and inflammation-related markers in bladder and urethral tissues, along with cGMP levels in the urethra. Notably, Group A exhibited significantly higher body weight compared to Group Y. The 24-hour voiding assay yielded inconclusive results. In CMG, Group A showed a significant increase in the number of non-voiding contractions per voiding cycle and post-void residual volume, while voiding efficiency was significantly lower compared to Group Y. UPP recordings revealed significantly reduced urethral pressure and high-frequency oscillation (HFO) amplitude in Group A. Furthermore, the bladder of Group A exhibited significantly higher mRNA expression levels of Hif-1α, Vegf-a, and Tgf-β1, whereas the urethra showed significantly lower mRNA expression levels of Nos1 and Prkg1, along with reduced cGMP concentrations, when compared to Group Y. This research underscores the utility of aging rats as valuable models for studying the natural progression of age-related lower urinary tract dysfunctions, with a likely emphasis on impaired NO-mediated transmitter function as a crucial mechanism.
    Gotoh, Daisuke. et al. "Impaired nitric oxide mechanisms underlying lower urinary tract dysfunction in aging rats." American journal of physiology. Renal physiology, 2023.
    Pubmed: 37767570   DOI: 10.1152/ajprenal.00092.2023

    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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