Complement Component C5a R1 Antibody (P12/1) Summary
| Immunogen |
C5aR – peptide: Met1 – Asn31
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| Localization |
Multi pass membrane protein.
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| Specificity |
Recognizes the C5a receptor (C5aR) CD88, which is predominantly expressed on cells of the myeloid lineage. Clone P12/1 was raised against a synthetic peptide comprising the N-terminal extracellular domain of the C5aR (met1-Asn31). Clone P12/1 does not inhibit the binding of C5a to its receptor.
|
| Isotype |
IgG2a
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| Clonality |
Monoclonal
|
| Host |
Mouse
|
| Gene |
C5AR1
|
| Purity |
Protein G purified
|
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Applications/Dilutions
| Dilutions |
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| Positive Control |
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Packaging, Storage & Formulations
| Storage |
Store at 4C short term. Aliquot and store at -20C long term. Avoid freeze-thaw cycles.
|
| Buffer |
PBS
|
| Preservative |
0.09% Sodium Azide
|
| Concentration |
1 mg/ml
|
| Purity |
Protein G purified
|
Alternate Names for Complement Component C5a R1 Antibody (P12/1)
- C5a anaphylatoxin chemotactic receptor
- C5A
- C5aR
- C5a-R
- C5AR1
- C5ARC5a anaphylatoxin receptor
- C5R1C5a ligand
- CD88 antigen
- CD88
- complement component 5 receptor 1 (C5a ligand)
- complement component 5 receptor 1
- complement component 5a receptor 1
- Complement Component C5a R1
- Complement Component C5aR1
Background
The human anaphylatoxin C5a (CD88) is a 74 residue glycopeptide which is generated by proteolytic cleavage of the complement factor C5 in the course of complement activation. A variety of biological effects evoked by C5a can be demonstrated, rendering this molecule an important mediartor of inflammation, with granulocytes and macrophages as the main target cells. All cellular responses to C5a are specifically mediated by interactions with the membrane bound C5a receptor, a seven transmembrane GTP binding coupled receptor that belongs to the rhodopsin supergene family. C5a receptor 1 expression has been reported in myeloid blood cells, brain, liver, lung, spleen, heart, kidney, and intestinal tract. ESTs have been isolated from B cell/lung/testis, nerve, and placenta libraries.