Human FPR1 (fMet-Leu-Phe receptor) ELISA Kit
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name
Human FPR1 (fMet-Leu-Phe receptor) ELISA Kit
category
ELISA Kits
provider
FineTest
reference
EH14530
tested applications
ELISA
Documents del producto
Instrucciones
Data sheet
Product specifications
| Category | ELISA Kits |
| Reactivity | Human |
| Detection Method | Colorimetric |
| Assay Data | 4 hours |
| Assay Type | Sandwich ELISA, Double Antibody |
| Test Range | 0.313-20ng/ml |
| Sensitivity | 0.188ng/ml |
| Size 1 | 96T |
| Tested Applications | ELISA |
| Sample Type | Serum, Plasma, Cell Culture Supernatant, cell or tissue lysate, Other liquid samples |
| Availability | Shipped within 10-14 working days. |
| Storage | 2-8 °C for 12 months |
| UniProt ID | P21462 |
| Alias | FPR1,NFPR,FPR,formyl peptide receptor 1,fMLF-R,FPR,FMLP |
| Background | Elisa kits for FPR1 |
| Status | RUO |
FPR1 is a G protein-coupled receptor (GPCR) expressed predominantly on immune cells, such as neutrophils and macrophages, where it mediates chemotaxis and host defense responses. It recognizes formylated peptides derived from bacterial and mitochondrial proteins, triggering immune cell recruitment to infection or damaged tissues. FPR1 activation stimulates downstream signaling pathways, including PI3K/Akt, MAPK, and calcium mobilization, leading to cellular migration, degranulation, and reactive oxygen species (ROS) production. It plays a critical role in the innate immune system by detecting bacterial infections and sterile inflammation. Dysregulation of FPR1 signaling contributes to chronic inflammatory diseases, autoimmune disorders, and impaired immune responses. In cancer, FPR1 expression has been associated with tumor progression and metastasis, where it can enhance cell migration and immune evasion. FPR1 also influences tissue repair and wound healing by directing immune cells to sites of injury. Its role in immune surveillance, inflammation, and cancer progression makes it an important target for therapies aimed at modulating immune responses and improving host defense mechanisms.
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