mProX™ Human FFAR3 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
To download a Certificate of Analysis, please enter a lot number in the search box below. Note: Certificate of Analysis not available for kit components.
Lot Number
Made to Order Inquiry
InquiryProduct Information
Product Properties
Protocols
Please visit our protocols page.
Customer Reviews
There are currently no Customer reviews or questions for mProX™ Human FFAR3 Stable Cell Line (S01YF-0923-PY68). Click the button above to contact us or submit your feedback about this product.
Anthony (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Paul (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Published Data
Fig.1 The mitigation of reactive oxygen species (ROS) damage in colonic epithelial cells by propionate occurred irrespective of any involvement of G protein-coupled receptors.
Assessment of ROS formation in NCM460 cells was conducted via DCFH-DA staining, involving both wild-type and NCM460 cells with knockdown of FFAR3. These cells were subjected to treatment with TNF-α and propionate.
Ref: Chen, Liuying, et al. "The role of NADPH oxidase 1 in alcohol-induced oxidative stress injury of intestinal epithelial cells." Cell Biology and Toxicology (2022): 1-20.
Pubmed: 35639301
DOI: 10.1007/s10565-022-09725-1
Research Highlights
Gudneppanavar R, et al. "Epigenetic histone modification by butyrate downregulates KIT and attenuates mast ." Journal of cellular and molecular medicine, 2023.
Butyrate, a short-chain fatty acid produced from bacterial fermentation, has been shown to reduce lung inflammation in asthma models by suppressing the activation of mast cells (MCs). MCs are known to play a crucial role in the inflammatory response to allergens in asthma. Their survival and proliferation are regulated by the growth factor, stem cell factor (SCF), through the KIT receptor. Although previous studies have demonstrated the ability of butyrate to suppress MC activation, its mechanism of action on SCF signalling and MC function is not yet fully understood. In this study, the researchers found that butyrate treatment caused modifications in MC histones through butyrylation and acetylation, as well as inhibited histone deacetylase (HDAC) activity. Additionally, butyrate treatment resulted in the downregulation of KIT receptor and its associated phosphorylation, thus attenuating SCF-mediated MC proliferation and cytokine secretion. Further investigation revealed that butyrate's suppression of MC function is mediated by its inhibition of the KIT/p38/Erk signalling pathway and its epigenetic effects on histones, acting as an HDAC inhibitor rather than through its traditional butyrate receptors, GPR41 and GPR43. The researchers suggest that these findings support butyrate as a potential treatment for allergy and asthma through its epigenetic modulation of MC function.
Pubmed:
37603611
DOI:
10.1111/jcmm.17924
Gao K, et al. "Oral administration of Bifidobacterium longum WHH2270 ameliorates type 2 diabetes ." Journal of food science, 2023.
A strain of Bifidobacterium longum known as WHH2270 has been identified as having strong potential as a hypoglycemic agent for treating type 2 diabetes mellitus. Its high level of inhibitory activity against alpha-glucosidase makes it a promising candidate for managing blood glucose levels. This abstract presents a promising avenue of research for the use of Bifidobacterium longum WHH2270 as a potential treatment for T2DM.
Pubmed:
37548634
DOI:
10.1111/1750-3841.16727
