FPR2 Antibodies

N-formyl peptide receptor 2 (FPR2)

Low affinity receptor for N-formyl-methionyl peptides, which can be strong neutrophil chemotactic factors (PubMed:1374236). Binding of FMLP to the receptor causes activation of neutrophils (PubMed:1374236).

This response is mediated via a G-protein that activates a phosphatidylinositol- calcium second messenger system (PubMed:1374236). The activation of LXA4R could result in an anti-inflammatory outcome counteracting the actions of proinflammatory signals such as LTB4 (leukotriene B4) (PubMed:9547339).

Gene Information

Human
Gene Name:	FPR2
Uniprot:	P25090
Entrez:	2358

Family

Belongs to:
G-protein coupled receptor 1 family

Alternative Names

ALXR; FMLP-R-I; FMLP-R-II; FMLPX; formyl peptide receptor 2; Formyl peptide receptor-like 1RFP; FPR2; FPR2A; FPRH1FMLP-related receptor I; FPRL1; FPRL1LXA4 receptor; HM63; HM63FPRH2; lipoxin A4 receptor (formyl peptide receptor related); Lipoxin A4 receptor; LXA4 Receptor; LXA4RFMLP-R-I; N-formyl peptide receptor 2; RFP

Molecular Weight

Mass (kDA):
38.964 kDA

Genomic Context

Human
Location:	19q13.41
Sequence:	19; NC_000019.10 (51752026..51770531)

Tissue Specificity

Expressed abundantly in the lung and neutrophils. Also found in the spleen and testis.

Subcellular Localizations

Cell membrane; Multi-pass membrane protein. Associates with Amyloid-beta protein 42, product of APP, at the cell surface and the complex is then rapidly internalized.

Diseases

• Inflammation
• Pertussis
• Alzheimer's Disease
• Inflammatory Response
• Arthritis
• Tissue Adhesions
• Rheumatoid Arthritis
• Neurodegenerative Disorders
• Hiv Infections
• Asthma
• Immunologic Deficiency Syndromes
• Neoplasms

• Infective Disorder
• Atherosclerosis
• Malignant Neoplasms
• Innate Immune Response
• Bacterial Infections
• Chronic Inflammation
• Inflammatory Disorder

Pathways

• Chemotaxis
• Secretion
• Inflammatory Response
• Pathogenesis
• Cell Migration
• Cell Proliferation
• Immune Response
• Phagocytosis
• Neutrophil Chemotaxis
• Virulence
• Cell Adhesion
• Cell Activation
• Neutrophil Activation

• Leukocyte Migration
• Wound Healing
• Localization
• Cell Death
• Exocytosis
• Innate Immune Response
• Endocytosis

PTMs

• Phosphorylation
• Formylation
• Cleavage
• Acetylation

• Dephosphorylation
• Biotinylation
• Reduction
• Glycosylation

• Methylation

Research Areas

• Immunology

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/FPR2

What Are The Best Uses Of The FPR2 Marker?

What are the best uses of the FPR2 Markers? Here are some examples. Boster scientists may submit results for applications, species, and even special samples. In some instances they will be awarded product credits. These are valid for scientists across the world. Visit the Boster website for more information. Learn more about the FPR2 Marker. It's a versatileand powerful molecule.

FPR2 Marker was used to treat supernatants of cells

Human peripheral blood monocytes and PMNs were isolated and resuspended in culture medium containing 30% fetal calf serum, 100 units/ml penicillin-streptomycin, and 2 mM L-glutamine. Incubation was performed for 3 days at 37°C, and medium was replaced every 3 days with fresh medium. For future experiments, cells were lysed by centrifugation before being fixed in ice cold the RPMI.

The cells were incubated at 5 x 10105 cells per milliliter, differentiated using 50 ng/ml myristate acetate, washed, and replated for 48 h. After 48 hours, the medium was replaced with fresh media (M0) or with 20 ng/ml IFN-g 100 ng/ml LPS (Sigma-Aldrich), or 20 ng/ml IL-4 (BD Biosciences). After 24 h, the cells were collected and analyzed to determine the expression of proteins and RNA expression.

This study demonstrates that treatment with FPR2 can trigger gene expression changes. FPR2 is found in the brainstem hippocampus, and spinal cords as well as the cerebellum and the striatum as well as cerebral cortex. It has also been shown that FPR2 expression is rapid in microglia, neurons including the cerebellum and thalamus and hippocampus.

FPR2 Marker was used to treat supernatants that were derived from cell cultures. Supernatants were filtered out by centrifugation. We found that cells containing FPR2 had an increase in the expression of the protein the mRNA. Cell culture supernatants can be used for further research. If you're trying to figure out how to utilize supernatants from cell culture we recommend FPR2 Marker.

FPR2 Marker was demonstrated to inhibit TNF-a production in apoptotic cells. It is associated with signalling pathways that stimulate anti-inflammatory responses. FPR2 inhibits the tyrosine-phosphorylation of STAT3 as well as suppressing TNFa release. FPRs could be involved in the transmission of signals from neutrophils that have died, it is believed.

We also looked into the effects of Ac2-26 treatment on cell proliferative capacity. U937 cells had significantly lower levels of CD38 induction. However, CD38 expression was significantly upregulated in cells that were treated with M(LPS+ IFN-g) however not in M0 and M(IL-4). As the results showed, FPR2 activation did not correlate with an increase in CD38 levels in human macrophages.

Cathelicidin was used to treat supernatants derived from cell culture

Boster Bio researchers used cell culture supernatants containing Cathelicidin LL 37 in a study published in Science Translational Medicine. This substance was found in a variety human cancer cell types. LL-37 blocks the replication of SARS-CoV-2 through an immediate mechanism. The drug binds with the SARS/CoV-2-ACE-2 receptor directly and cloaks it non-specific manner. In cell culture as well as in mouse models, LL-337 inhibits pseudovirions' growth through disruption of the membranes.

A549 cells were harvested from the exponential growth phase before being resuspended into RPMI-1640 medium. Cells were then kept at 37°C for 24 h with 0 25, 35 and umol/l Cathelicidin L37. The cells that were not treated served as controls. Supernatants were analyzed after nine hours, and IL-10, TNF-a and IL-1b levels were measured using ELISA. The Wuhan Boster Bio kit was used to determine the presence of the supernatants.

Mixing PBMCs and 10 percent FBS was used to create supernatants. The supernatant was then treated with 400 ul RNaseA and five U of propidium Iodide. The supernatant then was incubated for another five minutes at 4degC and the CFSE fluorescence was examined using flow cytometry.

The MDM generated LL37 transcript and levels of peptides fluctuated over the four-day time frame, with significant differences between Group I and Group II. On day 4, Group-I showed significantly higher levels than Group-II, while Group III only had marginal growth. Researchers conclude that Cathelicidin-LL-37 treatment reduces the transcription of the gene LL-37 and cell proliferation in human tumor cells.

Cathelicidin LL-37 inhibits tumor cells from growing by regulating the cytotoxicity of natural killer cells. It prevents the growth of different cancer cell lines, including human lung adenocarcinoma A549 cells. It also inhibits cell proliferation in vitro as well as in live. These properties have significant implications for cancer research.

TB is an important public health problem that causes more than 3 million deaths every year. In addition to the wide spread of antibiotic-resistant strains of Mtb, co-infection with HIV has negative effects on TB. Therefore alternative TB treatments are required to lessen the burden on TB patients. Both HIV patients and TB patients can be treated with cathelicidin LL-37 to reduce toxicities.

In a study using engineered hUC-MSCs, the antimicrobial activity of the compounds inhibited nine different bacteria species. BL-hUC–MSCs had greater antimicrobial activity and anti-inflammatory capabilities than LB-hUC–MSCs. These results suggest that hUC-MSCs may be a new treatment option for patients suffering from sepsis. Combining BPI21 and Cathelicidin LL-37 could be beneficial for sepsis patients.

The Boster Bio cell culture supernatants were treated with Cathelicidin LL37 and used for TUNEL immunoassay. After three washes with PBS, TUNEL was added. Images were captured after five fields for each group. Boster scientists are allowed to submit their findings after obtaining positive results. This is open to researchers from all over the globe.

The cell culture supernatants were treated with Formyl peptide-like 1 ligand

In a previous study we discovered that HTR8/SVneo Humantrophoblast Cells showed significantly lower apoptotic responses against the FPR1 ligand. FPR1. The experiment was performed with HTR8/SVneo cells obtained from The American Type Culture Collection and cultured on a Corning 3736-cell plate with 1% sodium pyruvate and penicillin and streptomycin.

In a different study, we discovered that HTR8/SVneo LPS-treated cells showed significantly higher levels FPR1 which is a determinant of preeclampsia. This suggests that functional FPR2 might reduce preeclampsia risk. FPR1 knockdown also stopped the development a morphological type in rats.

In a separate study, we identified a area of rOVAFLIPr's activity in human thymus cells. Particularly, rOVA FLIPr stimulates long-lived memory T cells. They are also able to produce recall responses when given rOVA-FLIPr. These results show the therapeutic potential for the rOVAFLIPr.

Lung cell suspensions were prepared as previously described (19). Fluorochrome-labeled antibodies were used to detect CD11b and CD11c. To sort cells using the data, they were analyzed using FACSJazz and FlowJo-V10 software from Three Star, Ashland, OR, USA.

The effects of FPR2/ALX upon neutrophil migration and adhesion were also studied. The effects of Formyl peptide receptor-like 1 ligand weren't observed in cells that were not infected, however, they were evident in vivo neutrophils. These results suggest that FPR2/ALX ligand may exert an effect of protection in the immune response to sepsis.

After transfection, Boster Bio cell culture supernatants treated with Formyl peptide receptors were examined for antigen-specific killing activity. The protein was purified by breaking up the cell-culture supernatants with a French press at 25 Kpsi pressure in homogenization buffer.

Researchers discovered that neutrophils express more S100A8/A9 with this ligand than normal. This suggests that it stimulates TLRs within the immune system. Similar interactions were observed between S100A8/A9 and Formyl peptide-like 1 ligand. Both S100A8 ligands as well as S100A9 ligands were found to are associated with TB disease progress.

After treatment, mice were killed when the volume of tumor exceeded 3,300mm3. The immunostaining and flow cytometry tests were carried out using the identical FACS buffer, containing 1 % FBS, 1 percent EDTA, and 0.1 percent sodium azide. To prevent non-specific binding, the anti-mouse antibody CD16/32 was employed. The samples were then stained and flow analyzed with fluorescence-conjugated antibodies.

Immunofluorescence staining was carried out on neutrophils from bone marrow or S100A9KO mice. Mtb infection was carried out in B6 and S100A9KO mice. To study the immune response, we utilized the mCherry Mtb virus. Flow cytometry was used to analyze both Gr-1 and CD11b.