Receptor, Anaphylatoxin C5a
"Receptor, Anaphylatoxin C5a" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
A G-protein-coupled receptor that signals an increase in intracellular calcium in response to the potent ANAPHYLATOXIN peptide COMPLEMENT C5A.
| Descriptor ID |
D044087
|
| MeSH Number(s) |
D12.776.543.750.695.024 D12.776.543.750.705.833.550
|
| Concept/Terms |
Receptor, Anaphylatoxin C5a- Receptor, Anaphylatoxin C5a
- CD88 Antigen
- Antigen, CD88
- Receptor, Complement 5a
- CD88 Antigens
- Anaphylatoxin C5a Receptor
- Antigens, CD88
- C5a Receptors
- Receptors, C5a
- Complement 5a Receptor
|
Below are MeSH descriptors whose meaning is more general than "Receptor, Anaphylatoxin C5a".
Below are MeSH descriptors whose meaning is more specific than "Receptor, Anaphylatoxin C5a".
This graph shows the total number of publications written about "Receptor, Anaphylatoxin C5a" by people in this website by year, and whether "Receptor, Anaphylatoxin C5a" was a major or minor topic of these publications.
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| Year | Major Topic | Minor Topic | Total |
|---|
| 2001 | 0 | 2 | 2 |
| 2004 | 0 | 1 | 1 |
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Below are the most recent publications written about "Receptor, Anaphylatoxin C5a" by people in Profiles.
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Age-related changes in polymorphonuclear neutrophil characteristics in infants born to human immunodeficiency virus type 1 seropositive mothers. Pediatr Allergy Immunol. 2004 Apr; 15(2):172-82.
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Altered expression of CD88 and associated impairment of complement 5a-induced neutrophil responses in human immunodeficiency virus type 1-infected patients with and without pulmonary tuberculosis. J Infect Dis. 2001 Feb 15; 183(4):662-5.
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Defective neutrophil degranulation induced by interleukin-8 and complement 5a and down-regulation of associated receptors in children vertically infected with human immunodeficiency virus type 1. Clin Diagn Lab Immunol. 2001 Jan; 8(1):21-30.