C3a Receptor Rabbit pAb
C3a Receptor Rabbit pAb
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- 背景知识
Application
| WB, IHC-P, IHC-F, IF |
|---|---|
| Primary Accession | Q16581 |
| Reactivity | Human, Horse |
| Predicted | Rat, Rabbit, Horse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 53864 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human C3a Receptor/C3aR |
| Epitope Specificity | 401-482/482 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SUBCELLULAR LOCATION | Cell membrane; Multi-pass membrane protein. |
| SIMILARITY | Belongs to the G-protein coupled receptor 1 family. |
| Post-translational modifications | Among the sulfation sites Tyr-174 is essential for binding of C3a anaphylatoxin. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | Complement C3 precursor contains complement C3 beta chain, complement C3 alpha chain, C3a anaphylatoxin, complement C3b alpha chain, complement C3c fragment, complement C3dg fragment, complement C3g fragment, complement C3d fragment and complement C3f fragment. C3a, C4a, and C5a are potent anaphylatoxins that are released during complement activation, a system of ligand-surface protein interactions specific to cells of hematopoietic lineage that aids in the elimination of pathogens. C3a and C5a secretion correlates with pathophysiological phenotypes such as asthma and bacterial meningitis. Binding of these proteins to their respective G protein-coupled receptors (C3aR, C5aR), which are present on the surface of myeloid leukocytes, induces proinflammatory events such as cellular degranulation, smooth muscle contraction, arachidonic acid metabolism, cytokine release, leukocyte activation and cellular chemotaxis. C3aR is expressed in brain and activated B-lymphocytes whereas C5aR is prevalent on the surface of hepatocyte, lung, smooth muscle, and endothelial cells. Upon activation, C3aR and C5aR are susceptible to rapid GRK-mediated phosphorylation and clathrin-coated vesicle targeting. C5aR utilizes the Ras-Raf-ERK1/2 cascade and couples to Gi/G16 proteins. |
| Gene ID | 719 |
|---|---|
| Other Names | C3a anaphylatoxin chemotactic receptor, C3AR, C3a-R, C3AR1, AZ3B, C3R1, HNFAG09 |
| Target/Specificity | Widely expressed in several differentiated hematopoietic cell lines, in the lung, spleen, ovary, placenta, small intestine, throughout the brain, heart, and endothelial cells. Mostly expressed in lymphoid tissues. |
| Dilution | WB=1:500-2000,IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500 |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| Name | C3AR1 |
|---|---|
| Synonyms | AZ3B, C3R1, HNFAG09 |
| Function | Receptor for the chemotactic and inflammatory peptide anaphylatoxin C3a. This receptor stimulates chemotaxis, granule enzyme release and superoxide anion production. |
| Cellular Location | Cell membrane; Multi-pass membrane protein. |
| Tissue Location | Widely expressed in several differentiated hematopoietic cell lines, in the lung, spleen, ovary, placenta, small intestine, throughout the brain, heart, and endothelial cells. Mostly expressed in lymphoid tissues |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Complement C3 precursor contains complement C3 beta chain, complement C3 alpha chain, C3a anaphylatoxin, complement C3b alpha chain, complement C3c fragment, complement C3dg fragment, complement C3g fragment, complement C3d fragment and complement C3f fragment. C3a, C4a, and C5a are potent anaphylatoxins that are released during complement activation, a system of ligand-surface protein interactions specific to cells of hematopoietic lineage that aids in the elimination of pathogens. C3a and C5a secretion correlates with pathophysiological phenotypes such as asthma and bacterial meningitis. Binding of these proteins to their respective G protein-coupled receptors (C3aR, C5aR), which are present on the surface of myeloid leukocytes, induces proinflammatory events such as cellular degranulation, smooth muscle contraction, arachidonic acid metabolism, cytokine release, leukocyte activation and cellular chemotaxis. C3aR is expressed in brain and activated B-lymphocytes whereas C5aR is prevalent on the surface of hepatocyte, lung, smooth muscle, and endothelial cells. Upon activation, C3aR and C5aR are susceptible to rapid GRK-mediated phosphorylation and clathrin-coated vesicle targeting. C5aR utilizes the Ras-Raf-ERK1/2 cascade and couples to Gi/G16 proteins.
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