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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Complement component 3a receptor 1

C3aR, C3AR1
receptor for anaphylatoxin complement component C3a, [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: C5a, V1a, HAD, CAN, MAST
Papers using C3aR antibodies
Regulation of stably transfected platelet activating factor receptor in RBL-2H3 cells. Role of multiple G proteins and receptor phosphorylation.
Koch Karl-Wilhelm, In PLoS ONE, 1993
... Anti-human C3aR was obtained from Santa Cruz Biotechnology (Santa Cruz, CA), PE-labeled ...
Papers on C3aR
Deficiency of the complement component 3 but not factor B aggravates Staphylococcus aureus septic arthritis in mice.
Jin et al., Göteborg, Sweden. In Infect Immun, Feb 2016
Mice lacking the complement component 3 (C3(-/-)), complement factor B (fB(-/-)), receptor for C3 derived anaphylatoxin C3a (C3aR(-/-)) and wild-type (WT) control mice were intravenously or intraarticularly inoculated with Staphylococcus aureus Newman strain.
Astrocyte-Microglia Cross Talk through Complement Activation Modulates Amyloid Pathology in Mouse Models of Alzheimer's Disease.
Zheng et al., Houston, United States. In J Neurosci, Feb 2016
Previously, we identified a neuron-glia signaling pathway whereby Aβ acts as an upstream activator of astroglial nuclear factor kappa B (NF-κB), leading to the release of complement C3, which acts on the neuronal C3a receptor (C3aR) to influence dendritic morphology and cognitive function.
Potent complement C3a receptor agonists derived from oxazole amino acids: Structure-activity relationships.
Fairlie et al., Brisbane, Australia. In Bioorg Med Chem Lett, Jan 2016
Potent ligands for the human complement C3a receptor (C3aR) were developed from the almost inactive tripeptide Leu-Ala-Arg corresponding to the three C-terminal residues of the endogenous peptide agonist C3a.
Complement Split Products C3a/C5a and Receptors: Are They Regulated by Circulating Angiotensin II Type 1 Receptor Autoantibody in Severe Preeclampsia?
Zhang et al., Qingdao, China. In Gynecol Obstet Invest, Nov 2015
Levels of C3a, C5a and AT1-AA in serum were measured by enzyme-linked immunosorbent assay and C3aR and C5aR in placenta by Western blotting.
Complement anaphylatoxin receptors C3aR and C5aR are required in the pathogenesis of experimental autoimmune uveitis.
Lin et al., Tianjin, China. In J Leukoc Biol, Oct 2015
UNASSIGNED: Recent studies have suggested that reagents inhibiting complement activation could be effective in treating T cell mediated autoimmune diseases such as autoimmune uveitis.
Molecules Great and Small: The Complement System.
Heeger et al., New York City, United States. In Clin J Am Soc Nephrol, Oct 2015
The subsequent local complement activation yields production of the anaphylatoxins C3a and C5a, which bind to their respective receptors (C3aR and C5aR) on both partners to augment effector T-cell proliferation and survival, while simultaneously inhibiting regulatory T-cell induction and function.
Role of Complement on Broken Surfaces After Trauma.
Brenner et al., Ulm, Germany. In Adv Exp Med Biol, 2014
In addition, key complement components and the corresponding receptors (such as C3aR, C5aR) have been detected on "exposed surfaces" of the damaged regions.
Complement modulation of T cell immune responses during homeostasis and disease.
Tenner et al., Irvine, United States. In J Leukoc Biol, 2014
Here, we will review recent data demonstrating the influence of complement proteins C1q, C3b/iC3b, C3a (and C3aR), and C5a (and C5aR) and complement regulators DAF (CD55) and CD46 (MCP) on T cell function during homeostasis and disease.
Complement anaphylatoxins as immune regulators in cancer.
Parsa et al., Chicago, United States. In Cancer Med, 2014
Several types of immune cells express the cognate receptors for the complement anaphylatoxins, C3aR and C5aR, and demonstrate functional modulation in response to complement stimulation.
Absence of signaling into CD4⁺ cells via C3aR and C5aR enables autoinductive TGF-β1 signaling and induction of Foxp3⁺ regulatory T cells.
Medof et al., Cleveland, United States. In Nat Immunol, 2013
Signaling through the G protein-coupled receptors for the complement fragments C3a and C5a (C3aR and C5aR, respectively) by dendritic cells and CD4(+) cells provides costimulatory and survival signals to effector T cells.
G protein-coupled receptor crosstalk and signaling in hematopoietic stem and progenitor cells.
Drost et al., Tübingen, Germany. In Ann N Y Acad Sci, 2012
A variety of G protein-coupled receptors (GPCRs) is expressed in hematopoietic stem and progenitor cells (HPCs), including the chemokine receptor CXCR4, the leukotriene receptor CysLT1, the sphingosine 1-phosphate receptor S1P1, the cannabinoid receptor CB2, and the complement receptor C3aR.
Role of C3a receptors, C5a receptors, and complement protein C6 deficiency in collagen antibody-induced arthritis in mice.
Holers et al., Aurora, United States. In J Immunol, 2012
Clinical disease activity in C3aR(-/-), C5aR(-/-), and C6-deficient (C6-def) mice was decreased by 52, 94, and 65%, respectively, as compared with wild-type mice.
Participation of complement 3a receptor (C3aR) in the sensitization phase of Th2 mediated allergic contact dermatitis.
Werfel et al., Hannover, Germany. In Exp Dermatol, 2012
might participate in conjunction with other complement effector functions down-stream of C3/C3b in the protection of Th2 induced allergic contact dermatitis
Distinct roles for C3a and C5a in complement-induced tubulointerstitial injury.
Quigg et al., Chicago, United States. In Kidney Int, 2011
distinct roles of C3a and C5a receptor signaling in complement-induced tubulointerstitial injury
Distinct and shared roles of β-arrestin-1 and β-arrestin-2 on the regulation of C3a receptor signaling in human mast cells.
Ali et al., Philadelphia, United States. In Plos One, 2010
shows that both beta-arrestin-1 and beta-arrestin-2 play a novel and shared role in inhibiting G protein-dependent ERK1/2 phosphorylation. These findings reveal a new level of complexity for C3aR regulation by beta-arrestins in human mast cells
Regulation of C3a receptor signaling in human mast cells by G protein coupled receptor kinases.
Ali et al., Philadelphia, United States. In Plos One, 2010
a new level of complexity for C3aR regulation
Complement-mediated regulation of the IL-17A axis is a central genetic determinant of the severity of experimental allergic asthma.
Wills-Karp et al., Cincinnati, United States. In Nat Immunol, 2010
Mechanistically, we demonstrate that IL-17A and AHR were regulated by allergen-driven production of anaphylatoxins, as mouse strains deficient in complement factor 5 (C5) or the complement receptor C5aR mounted robust IL-17A responses, whereas mice deficient in C3aR had fewer IL-17-producing helper T cells (T(H)17 cells) and less AHR after allergen challenge.
Locally produced complement fragments C5a and C3a provide both costimulatory and survival signals to naive CD4+ T cells.
Medof et al., Cleveland, United States. In Immunity, 2008
Here, we demonstrate that locally produced C5a and C3a anaphylatoxins interacting with their G protein-coupled receptors (GPCRs), C5aR and C3aR, on APCs and T cells both upstream and downstream of CD28 and CD40L signaling are integrally involved in T cell proliferation and differentiation.
C5L2 is critical for the biological activities of the anaphylatoxins C5a and C3a.
Yeh et al., Toronto, Canada. In Nature, 2007
Furthermore, like mice incapable of C3a/complement 3a receptor (C3aR) signalling, C5L2-deficient mice are hypersensitive to lipopolysaccharide (LPS)-induced septic shock, show reduced ovalbumin (OVA)-induced airway hyper-responsiveness and inflammation, and are mildly delayed in haematopoietic cell regeneration after gamma-irradiation.
6-Sulfo LacNAc, a novel carbohydrate modification of PSGL-1, defines an inflammatory type of human dendritic cells.
Rieber et al., Dresden, Germany. In Immunity, 2002
Yet they express anaphylatoxin receptors (C5aR and C3aR) and the Fcgamma receptor III (CD16), which recruit cells to inflammatory sites.
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