Type |
Details |
Score |
Publication |
First Author: |
Mouse Genome Informatics (MGI) and The National Center for Biotechnology Information (NCBI) |
Year: |
2010 |
Journal: |
Database Download |
Title: |
Consensus CDS project |
|
|
|
|
•
•
•
•
•
|
Publication |
First Author: |
Mouse Genome Informatics Group |
Year: |
2003 |
Journal: |
Database Procedure |
Title: |
Automatic Encodes (AutoE) Reference |
|
|
|
|
•
•
•
•
•
|
Publication |
First Author: |
Bairoch A |
Year: |
1999 |
Journal: |
Database Release |
Title: |
SWISS-PROT Annotated protein sequence database |
|
|
|
|
•
•
•
•
•
|
Publication |
First Author: |
Mouse Genome Informatics Scientific Curators |
Year: |
2005 |
|
Title: |
Obtaining and Loading Genome Assembly Coordinates from Ensembl Annotations |
|
|
|
|
•
•
•
•
•
|
Publication |
First Author: |
Mouse Genome Informatics |
Year: |
2010 |
Journal: |
Database Release |
Title: |
Protein Ontology Association Load. |
|
|
|
|
•
•
•
•
•
|
Publication |
First Author: |
Mouse Genome Informatics Scientific Curators |
Year: |
2005 |
|
Title: |
Obtaining and loading genome assembly coordinates from NCBI annotations |
|
|
|
|
•
•
•
•
•
|
Publication |
First Author: |
Yu S |
Year: |
2019 |
Journal: |
J Biol Chem |
Title: |
The complement receptor C5aR2 promotes protein kinase R expression and contributes to NLRP3 inflammasome activation and HMGB1 release from macrophages. |
Volume: |
294 |
Issue: |
21 |
Pages: |
8384-8394 |
|
•
•
•
•
•
|
Allele |
Name: |
complement component 5a receptor 2; endonuclease-mediated mutation 1, Shanghai Model Organisms Center |
Allele Type: |
Endonuclease-mediated |
Attribute String: |
Null/knockout |
|
•
•
•
•
•
|
Allele |
Name: |
transgene insertion 9, Peter Heeger |
Allele Type: |
Transgenic |
Attribute String: |
Inserted expressed sequence |
|
•
•
•
•
•
|
Allele |
Name: |
complement component 5a receptor 1; targeted mutation 1, Shanghai Model Organisms Center |
Allele Type: |
Targeted |
Attribute String: |
Humanized sequence, Inserted expressed sequence |
|
•
•
•
•
•
|
Strain |
Attribute String: |
coisogenic, endonuclease-mediated mutation, mutant strain |
|
•
•
•
•
•
|
Allele |
Name: |
complement component 5a receptor 2; targeted mutation 1, Shanghai Model Organisms Center |
Allele Type: |
Targeted |
Attribute String: |
Humanized sequence, Inserted expressed sequence |
|
•
•
•
•
•
|
Strain |
Attribute String: |
transgenic, mutant stock |
|
•
•
•
•
•
|
Allele |
Name: |
complement component 5a receptor 2; targeted mutation 1.1, Jorg Kohl |
Allele Type: |
Targeted |
Attribute String: |
Conditional ready, Reporter |
|
•
•
•
•
•
|
Strain |
Attribute String: |
coisogenic, mutant strain, targeted mutation |
|
•
•
•
•
•
|
Protein Domain |
Type: |
Family |
Description: |
The activation of the complement cascade produces a number of small fragments that are bioactive: potent chemoattractants and secretagogues that act on immune and non-immune cells []. Similar peptides can also be released by the actions of non-complement proteases, for instance during clotting []. Initially these were termed anaphylatoxins because of their effect on mast cell histamine release, but were reclassified as complement component peptides. They include C3a and C5a, which are involved immune response [], neural development and organ regeneration [, ]. A third peptide, C4a, has a similar structure, but it is inactive in humans []. Since the primary function of complement component peptides is in inflammation, they are important targets for the development of anti-inflammatory therapies [].The anaphylatoxin chemotactic receptors (also known as complement peptide receptors) are a group of rhodopsin-like G-protein coupled receptors (GPCRs) [, , , ]. There are three subtypes: C3a anaphylatoxin chemotactic receptor (C3AR1) [], C5a anaphylatoxin chemotactic receptor (C5AR1) []and C5a anaphylatoxin chemotactic receptor C5L2 (C5AR2) []. Both C3AR1 and C5AR1 receptors are classical GPCRs. However, C5AR2 appears to be permanently uncoupled from G proteins but can associate with beta-arrestin []. Nevertheless, it has been shown that activation of both C5AR1 and C5AR2 is required for a full pro-inflammatory response, particularly in mice []. Several receptor antagonists have been reported [, , , ], although none, so far, have been show to be effective in humans. This entry represents C3a anaphylatoxin chemotactic receptors and C5a anaphylatoxin chemotactic receptor 1/2. |
|
•
•
•
•
•
|
Protein Domain |
Type: |
Family |
Description: |
The activation of the complement cascade produces a number of small fragments that are bioactive: potent chemoattractants and secretagogues that act on immune and non-immune cells []. Similar peptides can also be released by the actions of non-complement proteases, for instance during clotting []. Initially these were termed anaphylatoxins because of their effect on mast cell histamine release, but were reclassified as complement component peptides. They include C3a and C5a, which are involved immune response [], neural development and organ regeneration [, ]. A third peptide, C4a, has a similar structure, but it is inactive in humans []. Since the primary function of complement component peptides is in inflammation, they are important targets for the development of anti-inflammatory therapies [].The anaphylatoxin chemotactic receptors (also known as complement peptide receptors) are a group of rhodopsin-like G-protein coupled receptors (GPCRs) [, , , ]. There are three subtypes: C3a anaphylatoxin chemotactic receptor (C3AR1) [], C5a anaphylatoxin chemotactic receptor (C5AR1) []and C5a anaphylatoxin chemotactic receptor C5L2 (C5AR2) []. Both C3AR1 and C5AR1 receptors are classical GPCRs. However, C5AR2 appears to be permanently uncoupled from G proteins but can associate with beta-arrestin []. Nevertheless, it has been shown that activation of both C5AR1 and C5AR2 is required for a full pro-inflammatory response, particularly in mice []. Several receptor antagonists have been reported [, , , ], although none, so far, have been show to be effective in humans. This entry represents C5AR2, also known as complement component 5a receptor 2. |
|
•
•
•
•
•
|
Publication |
First Author: |
Pandey S |
Year: |
2021 |
Journal: |
Mol Cell |
Title: |
Intrinsic bias at non-canonical, β-arrestin-coupled seven transmembrane receptors. |
Volume: |
81 |
Issue: |
22 |
Pages: |
4605-4621.e11 |
|
•
•
•
•
•
|
Publication |
First Author: |
Hartmann K |
Year: |
1997 |
Journal: |
Blood |
Title: |
C3a and C5a stimulate chemotaxis of human mast cells. |
Volume: |
89 |
Issue: |
8 |
Pages: |
2863-70 |
|
•
•
•
•
•
|
Publication |
First Author: |
Bellows-Peterson ML |
Year: |
2012 |
Journal: |
J Med Chem |
Title: |
De novo peptide design with C3a receptor agonist and antagonist activities: theoretical predictions and experimental validation. |
Volume: |
55 |
Issue: |
9 |
Pages: |
4159-68 |
|
•
•
•
•
•
|
Publication |
First Author: |
Takafuji S |
Year: |
1994 |
Journal: |
Int Arch Allergy Immunol |
Title: |
Degranulation from human eosinophils stimulated with C3a and C5a. |
Volume: |
104 Suppl 1 |
Issue: |
1 |
Pages: |
27-9 |
|
•
•
•
•
•
|
Publication |
First Author: |
Schraufstatter IU |
Year: |
2009 |
Journal: |
J Immunol |
Title: |
C3a and C5a are chemotactic factors for human mesenchymal stem cells, which cause prolonged ERK1/2 phosphorylation. |
Volume: |
182 |
Issue: |
6 |
Pages: |
3827-36 |
|
•
•
•
•
•
|
Publication |
First Author: |
Bera MM |
Year: |
2011 |
Journal: |
J Immunol |
Title: |
Th17 cytokines are critical for respiratory syncytial virus-associated airway hyperreponsiveness through regulation by complement C3a and tachykinins. |
Volume: |
187 |
Issue: |
8 |
Pages: |
4245-55 |
|
•
•
•
•
•
|
Publication |
First Author: |
Yu M |
Year: |
2012 |
Journal: |
Invest Ophthalmol Vis Sci |
Title: |
A novel role of complement in retinal degeneration. |
Volume: |
53 |
Issue: |
12 |
Pages: |
7684-92 |
|
•
•
•
•
•
|
Publication |
First Author: |
Banda NK |
Year: |
2012 |
Journal: |
J Immunol |
Title: |
Role of C3a receptors, C5a receptors, and complement protein C6 deficiency in collagen antibody-induced arthritis in mice. |
Volume: |
188 |
Issue: |
3 |
Pages: |
1469-78 |
|
•
•
•
•
•
|
Protein Domain |
Type: |
Family |
Description: |
The activation of the complement cascade produces a number of small fragments that are bioactive: potent chemoattractants and secretagogues that act on immune and non-immune cells []. Similar peptides can also be released by the actions of non-complement proteases, for instance during clotting []. Initially these were termed anaphylatoxins because of their effect on mast cell histamine release, but were reclassified as complement component peptides. They include C3a and C5a, which are involved immune response [], neural development and organ regeneration [, ]. A third peptide, C4a, has a similar structure, but it is inactive in humans []. Since the primary function of complement component peptides is in inflammation, they are important targets for the development of anti-inflammatory therapies [].The anaphylatoxin chemotactic receptors (also known as complement peptide receptors) are a group of rhodopsin-like G-protein coupled receptors (GPCRs) [, , , ]. There are three subtypes: C3a anaphylatoxin chemotactic receptor (C3AR1) [], C5a anaphylatoxin chemotactic receptor (C5AR1) []and C5a anaphylatoxin chemotactic receptor C5L2 (C5AR2) []. Both C3AR1 and C5AR1 receptors are classical GPCRs. However, C5AR2 appears to be permanently uncoupled from G proteins but can associate with beta-arrestin []. Nevertheless, it has been shown that activation of both C5AR1 and C5AR2 is required for a full pro-inflammatory response, particularly in mice []. Several receptor antagonists have been reported [, , , ], although none, so far, have been show to be effective in humans. This entry represents C3AR1, also known as complement component 3a receptor 1 and C3aR []. It appears to be widely expressed in different lymphoid tissues, providing evidence for a central role in inflammatory processes []. This receptor stimulates chemotaxis [], granule enzyme release [, ]and increases phosphorylated-ERK1/2 production []. C3AR1 may provide a theraputic avenue for the treatment of asthma [], retinal degeneration [], and rheumatoid arthritis []. |
|
•
•
•
•
•
|
Publication |
First Author: |
Kalant D |
Year: |
2005 |
Journal: |
J Biol Chem |
Title: |
C5L2 is a functional receptor for acylation-stimulating protein. |
Volume: |
280 |
Issue: |
25 |
Pages: |
23936-44 |
|
•
•
•
•
•
|
Publication |
First Author: |
Ames RS |
Year: |
1996 |
Journal: |
J Biol Chem |
Title: |
Molecular cloning and characterization of the human anaphylatoxin C3a receptor. |
Volume: |
271 |
Issue: |
34 |
Pages: |
20231-4 |
|
•
•
•
•
•
|
Publication |
First Author: |
Monk PN |
Year: |
2007 |
Journal: |
Br J Pharmacol |
Title: |
Function, structure and therapeutic potential of complement C5a receptors. |
Volume: |
152 |
Issue: |
4 |
Pages: |
429-48 |
|
•
•
•
•
•
|
Publication |
First Author: |
Amara U |
Year: |
2008 |
Journal: |
Adv Exp Med Biol |
Title: |
Interaction between the coagulation and complement system. |
Volume: |
632 |
|
Pages: |
71-9 |
|
•
•
•
•
•
|
Publication |
First Author: |
Peng Q |
Year: |
2009 |
Journal: |
Inflamm Allergy Drug Targets |
Title: |
The role of anaphylatoxins C3a and C5a in regulating innate and adaptive immune responses. |
Volume: |
8 |
Issue: |
3 |
Pages: |
236-46 |
|
•
•
•
•
•
|
Publication |
First Author: |
Carmona-Fontaine C |
Year: |
2011 |
Journal: |
Dev Cell |
Title: |
Complement fragment C3a controls mutual cell attraction during collective cell migration. |
Volume: |
21 |
Issue: |
6 |
Pages: |
1026-37 |
|
•
•
•
•
•
|
Publication |
First Author: |
Klos A |
Year: |
2009 |
Journal: |
Mol Immunol |
Title: |
The role of the anaphylatoxins in health and disease. |
Volume: |
46 |
Issue: |
14 |
Pages: |
2753-66 |
|
•
•
•
•
•
|
Publication |
First Author: |
Lienenklaus S |
Year: |
1998 |
Journal: |
J Immunol |
Title: |
Human anaphylatoxin C4a is a potent agonist of the guinea pig but not the human C3a receptor. |
Volume: |
161 |
Issue: |
5 |
Pages: |
2089-93 |
|
•
•
•
•
•
|
Publication |
First Author: |
Fukuoka Y |
Year: |
1989 |
Journal: |
Dermatologica |
Title: |
Characterization of receptors to the anaphylatoxins on isolated cells. |
Volume: |
179 Suppl 1 |
|
Pages: |
35-40 |
|
•
•
•
•
•
|
Publication |
First Author: |
Lee DK |
Year: |
2001 |
Journal: |
Brain Res Mol Brain Res |
Title: |
Identification of four novel human G protein-coupled receptors expressed in the brain. |
Volume: |
86 |
Issue: |
1-2 |
Pages: |
13-22 |
|
•
•
•
•
•
|
Publication |
First Author: |
Gerard C |
Year: |
1994 |
Journal: |
Annu Rev Immunol |
Title: |
C5A anaphylatoxin and its seven transmembrane-segment receptor. |
Volume: |
12 |
|
Pages: |
775-808 |
|
•
•
•
•
•
|
Publication |
First Author: |
Roglic A |
Year: |
1996 |
Journal: |
Biochim Biophys Acta |
Title: |
cDNA cloning of a novel G protein-coupled receptor with a large extracellular loop structure. |
Volume: |
1305 |
Issue: |
1-2 |
Pages: |
39-43 |
|
•
•
•
•
•
|
Publication |
First Author: |
Gerard NP |
Year: |
1991 |
Journal: |
Nature |
Title: |
The chemotactic receptor for human C5a anaphylatoxin. |
Volume: |
349 |
Issue: |
6310 |
Pages: |
614-7 |
|
•
•
•
•
•
|
Publication |
First Author: |
Joost P |
Year: |
2002 |
Journal: |
Genome Biol |
Title: |
Phylogenetic analysis of 277 human G-protein-coupled receptors as a tool for the prediction of orphan receptor ligands. |
Volume: |
3 |
Issue: |
11 |
Pages: |
RESEARCH0063 |
|
•
•
•
•
•
|
Publication |
First Author: |
Ames RS |
Year: |
2001 |
Journal: |
J Immunol |
Title: |
Identification of a selective nonpeptide antagonist of the anaphylatoxin C3a receptor that demonstrates antiinflammatory activity in animal models. |
Volume: |
166 |
Issue: |
10 |
Pages: |
6341-8 |
|
•
•
•
•
•
|
Publication |
First Author: |
Mathieu MC |
Year: |
2005 |
Journal: |
Immunol Lett |
Title: |
The C3a receptor antagonist SB 290157 has agonist activity. |
Volume: |
100 |
Issue: |
2 |
Pages: |
139-45 |
|
•
•
•
•
•
|
Publication |
First Author: |
Otto M |
Year: |
2004 |
Journal: |
J Biol Chem |
Title: |
C5a mutants are potent antagonists of the C5a receptor (CD88) and of C5L2: position 69 is the locus that determines agonism or antagonism. |
Volume: |
279 |
Issue: |
1 |
Pages: |
142-51 |
|
•
•
•
•
•
|
Publication |
First Author: |
Crass T |
Year: |
1996 |
Journal: |
Eur J Immunol |
Title: |
Expression cloning of the human C3a anaphylatoxin receptor (C3aR) from differentiated U-937 cells. |
Volume: |
26 |
Issue: |
8 |
Pages: |
1944-50 |
|
•
•
•
•
•
|
Protein |
Organism: |
Mus musculus/domesticus |
Length: |
344
 |
Fragment?: |
false |
|
•
•
•
•
•
|
Protein |
Organism: |
Mus musculus/domesticus |
Length: |
477
 |
Fragment?: |
false |
|
•
•
•
•
•
|
Protein |
Organism: |
Mus musculus/domesticus |
Length: |
477
 |
Fragment?: |
false |
|
•
•
•
•
•
|
Protein |
Organism: |
Mus musculus/domesticus |
Length: |
358
 |
Fragment?: |
false |
|
•
•
•
•
•
|
Protein |
Organism: |
Mus musculus/domesticus |
Length: |
477
 |
Fragment?: |
false |
|
•
•
•
•
•
|
Protein |
Organism: |
Mus musculus/domesticus |
Length: |
226
 |
Fragment?: |
true |
|
•
•
•
•
•
|
Protein |
Organism: |
Mus musculus/domesticus |
Length: |
358
 |
Fragment?: |
false |
|
•
•
•
•
•
|
Protein |
Organism: |
Mus musculus/domesticus |
Length: |
351
 |
Fragment?: |
false |
|
•
•
•
•
•
|
Protein |
Organism: |
Mus musculus/domesticus |
Length: |
301
 |
Fragment?: |
true |
|
•
•
•
•
•
|
Protein |
Organism: |
Mus musculus/domesticus |
Length: |
181
 |
Fragment?: |
true |
|
•
•
•
•
•
|