mProX™ Human HCAR3 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 HCAR3 expression affects keratinocytes migration.
Representative images depict scratch assays conducted in N/TERT2G cells after 72 hours of transfection with specific siRNAs, with the open area highlighted in vibrant red. The scale bar spans 100µm. Quantitative analysis was carried out for scratch assays in both HEK (B) and N/TERT2G (C) cells, assessing the scratch area at various time points and normalizing it against the initial time point. These measurements were based on data obtained from five independent experiments, each conducted in triplicates. Additionally, we calculated the area under the curve (AUC) for the graphs presented in B and C, with data normalized to siCtrl, represented as a reference by a black dotted line. This analysis was performed across five independent experiments conducted in triplicates.
Ref: Pedro, M. Pilar, et al. "A GPCR screening in human keratinocytes identifies that the metabolite receptor HCAR3 controls epithelial proliferation, migration, and cellular respiration." bioRxiv (2023): 2023-05.
Pubmed: 37398171
DOI: 10.1101/2023.05.30.542853
Research Highlights
Pilar Pedro M, et al. "A GPCR screening in human keratinocytes identifies that the metabolite receptor ." bioRxiv : the preprint server for biology, 2023.
In this study, the authors investigated the role of G protein-coupled receptors (GPCRs) in regulating epithelial cell function. They focused on human primary keratinocytes, using them as a model to determine the specific GPCRs involved in controlling cell proliferation and differentiation. Through their research, the authors identified three key receptors - HCAR3, LTB4R, and GPR137 - that play a critical role in maintaining cell identity and promoting proliferation while inhibiting differentiation. They also found that HCAR3 regulates keratinocyte migration and cellular metabolism. Further analysis revealed that knockdown of HCAR3 resulted in reduced migration and respiration due to altered metabolite use and abnormal mitochondrial morphology. This study provides valuable insights into the complicated relationship between GPCR signaling and epithelial cell fate decisions.
Pubmed:
37398171
DOI:
10.1101/2023.05.30.542853
Kaddoura R, et al. "Identification of Specific Biomarkers and Pathways in the Treatment Response of ." Life (Basel, Switzerland), 2023.
Inflammatory bowel disease (IBD) is a chronic condition characterized by inflammation of the gastrointestinal tract. The use of infliximab, the first anti-tumor necrosis factor (TNF) agent approved for IBD, has shown limited success, high cost, and potential adverse effects. To enhance treatment outcomes, it is crucial to identify patients at risk for infliximab resistance. The current study utilized publicly available transcriptomics datasets from Gene Expression Omnibus (GEO) to identify differentially expressed genes (DEGs) that may serve as potential biomarkers for infliximab response in IBD. Enriched gene ontology clustering identified five commonly downregulated genes (SELE, TREM1, AQP9, FPR2, HCAR3) between IBD patients and healthy controls, as well as in infliximab non-responders compared to responders. The altered expression of these genes may contribute to impaired response to infliximab in IBD patients and could serve as potential biomarkers for early detection of compromised response.
Pubmed:
36983834
DOI:
10.3390/life13030680