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  • mProX™ Human FFAR4 Stable Cell Line

    [CAT#: S01YF-0923-PY70]
    Product Category:
    Membrane Protein Stable Cell Lines
    Subcategory:
    GPCR Cell Lines

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    Product Information

    Target Protein
    FFAR4
    Target Family
    Free Fatty Acid Family
    Target Protein Species
    Human
    Host Cell Type
    Huh-7;CHO-K1;HEK293
    Target Classification
    GPCR Cell Lines
    Target Research Area
    Metabolic Research
    Related Diseases
    Body Mass Index Quantitative Trait Locus 10;Body Mass Index Quantitative Trait Locus 11
    Gene ID
    Human: 338557
    UniProt ID
    Human: Q5NUL3

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    FFAR4, also known as GPR120, has been identified as a potential therapeutic target for various metabolic diseases. Recent studies have emphasized its role in Type 2 diabetes mellitus (T2DM), where it has been associated with beneficial glycemic control. Furthermore, FFAR4 has been linked to the regulation of cardiac oxylipin balance, promoting inflammation resolution in heart failure models. The receptor's involvement in macrophage foam cell formation has also been highlighted, suggesting its potential role in atherosclerosis prevention.

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    FAQ

    chat Kimberly (Verified Customer)

    What is the significance of FFAR4 in metabolic homeostasis and its potential therapeutic implications? Jun 06 2020

    chat Patrick Liam (Creative Biolabs Scientific Support)

    FFAR4 plays a crucial role in maintaining metabolic homeostasis. The cryo-electron microscopy structures of FFAR4 bound with its native ligand DHA have been elucidated, highlighting its therapeutic potential in treating diabetes. Jun 06 2020

    chat William (Verified Customer)

    How does FFAR4 influence inflammation and heart remodeling? Jul 26 2022

    chat Patrick Liam (Creative Biolabs Scientific Support)

    FFAR4 controls the balance between proinflammatory and proresolving oxylipins, both systemically and in the heart. This regulation helps to resolve inflammation and attenuate heart remodeling, especially in conditions like HFpEF secondary to metabolic syndrome. Jul 26 2022

    Published Data

    Fig.1 The receptor FFAR4, specializing in the recognition of extended-chain fatty acids, orchestrates oleate-triggered signaling pathways.

    Assessing FFAR4 knockdown effects in Huh7 cells: Open bars denote cells with stable FFAR4 shRNA expression, closed bars represent cells transfected with an empty pLKO vector, vertical-striped bars indicate additional FFAR4-GFP transfection, and horizontal-striped bars denote supplementary transfection with a non-functional FFAR4RH mutant. Oleate (OA) was employed. Data is presented as mean±s.e.m. Associated P-values are as follows: 15 min FFAR4 shRNA knockdown, P = 0.014; 15 min FFAR4 shRNA knockdown+FFAR4-GFP, P = 0.093; 180 min FFAR4 shRNA knockdown, P = 0.375; 180 min FFAR4 shRNA knockdown+FFAR4-GFP, P = 0.531; 15 min FFAR4 shRNA knockdown+FFAR4RH, P = 0.078; 180 min FFAR4 shRNA knockdown+FFAR4RH, P = 0.391 (Mann-Whitney U test).

    Ref: Rohwedder, Arndt, et al. "Lipid droplet formation in response to oleic acid in Huh-7 cells is mediated by the fatty acid receptor FFAR4." Journal of cell science 127.14 (2014): 3104-3115.

    Pubmed: 24876224

    DOI: 10.1242/jcs.145854

    Research Highlights

    Wang Z, et al. "Akkermansia muciniphila supplementation improves glucose tolerance in intestinal ." mSystems, 2023.
    The disruption of blood glucose utilization can lead to diabetes mellitus, a complex disease with both genetic and environmental factors. Free fatty acid receptors (FFARs) are believed to link these aspects together. Recently, FFAR4 has been identified as a potential target for diabetes treatment. Therefore, it is essential to understand how FFAR4 affects glucose homeostasis. Previous studies have shown that mice lacking FFAR4 have impaired glucose tolerance when fed a high-fat diet. However, the results for mice under a regular diet have been conflicting. This study aims to investigate the role of FFAR4 in glucose utilization rhythm and its possible mechanism. Results from both total Ffar4 knockout mice and mice with gut-specific Ffar4 deletion indicated a clear diurnal rhythm in glucose tolerance. Moreover, intestinal FFAR4 deficiency was found to cause significant changes in fecal microbiota at different time points. Further analysis revealed that Akkermansia muciniphila, an important bacteria in regulating intestinal hormone secretion, was the main target of FFAR4 at a specific time point. Additionally, supplementation of Akkermansia muciniphila significantly improved glucose tolerance in mice with gut-specific Ffar4 deletion at that time point. These findings suggest that intestinal FFAR4 plays a critical role in the regulation of glucose tolerance, particularly at specific time points. Moreover, alterations in the intestinal environment may contribute to the development of certain diseases.
    Pubmed: 37787527   DOI: 10.1128/msystems.00573-23

    Wei L, et al. "Double knockout of FFAR4 and FGF21 aggravates metabolic disorders in mice.." International journal of biological macromolecules, 2023.
    Multiple investigations have been conducted regarding the involvement of free fatty acid receptor 4 (FFAR4) in metabolic disorders, with conflicting results. To further understand the role of FFAR4 in regulating metabolic status, a team of researchers generated FFAR4/FGF21 double knockout (DKO) mice and examined the effects of FGF21, a fibroblast growth factor, on glucose and lipid metabolism in FFAR4 knockout mice on a high-fat diet. Results showed that levels of FGF21 were significantly elevated in FFAR4-deficient mice and the double deletion of FGF21 and FFAR4 resulted in severe metabolic disruptions. The study also found that FFAR4/FGF21 DKO mice had metabolic irregularities, possibly attributed to decreased energy expenditure. Overall, this study provided insight into the role of endogenous FGF21 as a key regulator in the absence of FFAR4.
    Pubmed: 37657572   DOI: 10.1016/j.ijbiomac.2023.126553

    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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