|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for FPR2(NM_001462.3) Search again
Product ID:
HQP054728
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ALX, ALXR, FMLP-R-II, FMLPX, FPR2A, FPRH1, FPRH2, FPRL1, HM63, LXA4R
Gene Description:
formyl peptide receptor 2
Target Gene Accession:
NM_001462.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Gene References into function
- chemoattractant Trp-Lys-Tyr-Met-Val-D-Met activates eosinophils through the formyl peptide receptor and one of its homologues, formyl peptide receptor-like 1
- results indicate that the cytokine-like property of serum amyloid A is manifested through activation of the Gi-coupled formyl peptide receptor-like 1(FPRL1/LXA4R)
- investigated the direct effect of LXA4 as well as the effect on agonist-induced biological responses using transfected HL-60 cells expressing FPR, FPRL1 or FPRL2
- LXA(4) generated in or near the paracellular space via neutrophil-epithelial interactions can rapidly act on epithelial LXA(4)receptor to downregulate epithelial promotion of intestinal inflammation.
- Modulation of neutrophil FPRL1 by distinct peptide ligands activates a spectrum of cellular signaling events, including intracellular calcium concentration increase, phosphoinositide 3-kinase, extracellular signal-regulated kinase, and Akt activation.
- an annexin 1 peptide can activate FPR, FPRL1, and FPRL2; results indicate that annexin 1 participates in regulating leukocyte emigration into inflamed tissue by activating and desensitizing different receptors of the FPR family.
- The up-regulation of the A-SAA and FPRL1 genes in inflamed synovial tissue suggests an important role in the pathophysiology of inflammatory arthritis
- ligand-bound FPRL1 undergoes primarily clathrin-mediated and dynamin-dependent endocytosis
- Results show that humanin (HN) acts as a ligand for formyl peptide receptor-like 1 (FPRL1) and 2 (FPRL2).
- FPR and FPRL1, use distinct signaling pathways in activation of human neutrophils
- results showed that multiple domains in FPRL1 are involved in the receptor response to chemotactic agonists with the sixth transmembrane domain and the third extracellular loop playing a prominent role
- serum amyloid A plays a role in the modulation of inflammatory and immune responses via FPRL1, by inducing matrix-metalloproteinase-9 upregulation
- cells transfected with FPRL1 gene exhibited markedly reduced tumorigenicity in syngeneic mice
- FPRL1 is a pituitary adenylate cyclase activating polypeptide (PACAP) 27-specific receptor.
- In view of the wide range of endogenous ligands known to interact with FPRL-1, including the anti-inflammatory protein annexin-A1, we speculate that the novel effect here described may impact on the clinical immunosuppressive
- binding of SAA to FPRL1 may contribute to the destruction of bone and cartilage via the promotion of synoviocyte hyperplasia and angiogenesis
- Analysis of in vitro expression of lipoxin A(4) receptor (ALX) on human neutrophils and the in vivo anti-inflammatory effect of glucocorticoids.
- The N-formyl peptide receptors present in MSCs may play an important role in signaling stem cell adhesion, migration, and homing to injured and inflamed tissue for repair.
- association of the PDGFRbeta with lipid raft microdomains renders it susceptible to LXA(4)-mediated dephosphorylation by possible reactivation of oxidatively inactivated SHP-2.
- Exocytosis of FPRL1 results in down-regulation of cytoplasmic FRPL1 in patients with pyoderma.
- Both intra- and extracellular Ca2+ play a role in controlling pro-inflammatory functions stimulated by PACAP which acts through a VPAC-1, FPRL1/Galphai/PI3K/ERK pathway and a VPAC-1/Galphas/PKA/p38 pathway to fully activate monocytes
- To specifically inhibit the FPRL1 response the antagonist WRW(4) should be used.
- Piroxicam inhibits the neutrophil responses triggered through formyl peptide receptor, but not through formyl peptide receptor like 1 and this inhibition is due to a reduced binding of the activating ligand to its cell surface receptor.
- FPRL-1 is capable of activating nuclear factor-kappa B (NF-kappaB) signaling through inhibitor-kappa B kinase (IKK) phosphorylation in human astrocytoma or Chinese hamster ovary cells.
- level of LXA4 in synovial fluid and lipoxin A4 receptor expression in synovial tissues obtained from patients with rheumatoid arthritis and osteoarthritis
- Proinflammatory effect of VIP is mediated via the specific G protein-coupled receptor VIP/pituitary adenylate cyclase-activating protein (VPAC1) receptor as well as via FPRL1.
- Our results indicate that severe asthma is characterized by decreased airway LXA4 levels and luekocyte AKX receptor availability.
- FPRL1 is a potent mediator in the activation of CRAC channels
- The chemokine FPRL1 plays a role in the production of chemokine CCL2 by serum amyloid A.