Complement Component 3a Receptor 1 (C3AR1) ELISA Kits

Zebrafish Complement Component 3a Receptor 1 (C3AR1) interaction partners

1. Neural crest cells are coattracted via the complement fragment C3a and its receptor C3aR, revealing an unexpected role of complement proteins in early vertebrate development.

Human Complement Component 3a Receptor 1 (C3AR1) interaction partners

1. C3aR has roles in platelet function, thrombus formation and in vivo hemostasis

2. C3aR-positive cells are found more often in patients with inflammatory cardiomyopathy. The relevance of C3aR-positive cells in patients with non-ischaemic cardiomyopathy should be further evaluated as potential predictors or modulators of adverse cardiac remodelling, the substrate of progressive heart failure.

3. Studies indicate that the complement response lie the active fragments, C3a and C5a, acting through their specific receptors, C3aR, C5aR1 and C5aR2 to direct the cellular response to inflammation.

4. High C3aR1 expression is associated with acute myeloid leukemia-M2.

5. these findings suggest a critical role for C3a through autocrine/paracrine induction of C3aR in the pathogenesis of cigarette smoke-induced sterile inflammation and provide new therapeutic targets for the treatment of emphysema.

6. Medulloblastoma cells express C3aR, and siRNA-mediated knockdown of C3aR inhibits proliferation of these cells in vitro.

7. Observed a positive correlation between the expression of anaphylatoxin-receptors C3aR and C5aR with platelet activation in patients with coronary artery disease.

8. The obesity-induced down-regulation of complement C3 and C3aR which is specific to subcutaneous adipose tissue.

9. In patients with IgAN, urinary and renal C3a and C5a and renal expression of C3aR and C5aR are significantly correlated with the activity and severity of renal injury.

10. C3aR and CD46 activation via intrinsic generation of their respective ligands is an integral part of human Th1 (but not Th2) immunity.

11. functional regulation of C3aR by NHERFs in human mast cells

12. significantly decreased expression of C3aR mRNA and protein expression in placentas with preeclampsia compared to controls

13. study demonstrates that although C3a causes phosphorylation of its receptor at multiple sites, Ser459, Thr463, Ser465, Thr466 and Ser470 participate in C3aR desensitization

14. Complement C3a receptor activation contributes to the pathogenesis of preeclampsia.

15. a new level of complexity for C3aR regulation

16. 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

17. Mutant gonococci lacking the pilin glycan did not bind to the I-domain when it is in a closed, low-affinity conformation and cannot induce an active conformation to complement receptor 3 during pex cell challenge.

18. results indicate that normal human hematopoietic stem and progenitor cells express functional C3aR and that the C3aR-C3a axis sensitizes the responses of these cells to SDF-1

19. Sulfation of tyrosine 174 in the human C3a receptor is essential for binding of C3a anaphylatoxin.

20. determination of whether the levels of complement factors C3a, C4a, and C5a are elevated at the site of inflammation in chronic obstructive pulmonary disease and in asthma

Mouse (Murine) Complement Component 3a Receptor 1 (C3AR1) interaction partners

1. C3aR has roles in platelet function, thrombus formation and in vivo hemostasis

2. C3aR(-/-) animals also have altered neural progenitor cell proliferation, but demonstrate an opposing phenotype to animals subjected to pharmacological blockade of C3aR.

3. Development of burn-induced mechanical allodynia, thermal allodynia, weight bearing changes and edema was assessed in C3aR(-/-), C5aR1(-/-) and C5aR2(-/-) mice and compared to their wild type controls over three days. Burn-induced mechanical allodynia, thermal allodynia and weight bearing changes developed normally C3aR(-/-), C5aR1(-/-) and C5aR2(-/-) mice.

4. Complement component 3a receptor 1 role in the lung cancer progression.

5. The complement 3a receptor (C3aR1) participates in microglial signaling under pathological conditions and was recently shown to be activated by the neuropeptide TLQP-21.

6. whilst the C3aR modulates some elements of disease pathogenesis, overall it is not critical in effector responses and glomerular injury caused by autoimmunity to MPO

7. study provided detailed insights into the C3aR expression pattern in immune and stromal cells under steady-state conditions

8. proposal that C3aR activation alters the tumor inflammatory milieu, thereby promoting tumor growth

9. The roles of C3, CfB, and C3a receptor in the severity of S. aureus induced septic arthritis are reported.

10. increased circulating lipopolysaccharide induces upregulation of complement C3a receptor on neutrophils and activation of the complement cascade.

11. showed that C3a receptor/C5a receptor-deficient mice developed much less severe uveitis than did control mice using all retinal examination methods

12. these findings suggest a critical role for C3a through autocrine/paracrine induction of C3aR in the pathogenesis of cigarette smoke-induced sterile inflammation and provide new therapeutic targets for the treatment of emphysema.

13. C3a/C3aR signaling during host immune response suppresses Fas expression and caspase-3 activity while increasing Bcl-2 proto-oncogene protein expression, providing protection to myeloid and lymphoid cells against L. monocytogenes-induced apoptosis.

14. This study indicated that C3a and C5a-mediated functions are not critical to the development of experimental autoimmune uveitis.

15. The binding of TLQP-21 to C3AR1 not only has effects on signaling but also modulates cellular functions

16. C3a receptor promotes viral containment in mice inoculated with vaccinia virus at sites of allergic skin inflammation.

17. The role of the anaphylatoxin C3a receptor in acute dextran sulfate sodium-induced colitis in mice, was investigated.

18. ALI in H5N1-infected mice was caused by excessive complement activation, as demonstrated by deposition of C3, C5b-9, and MBL-C in lung tissue, and by up-regulation of MBL-associated serine protease-2 and the complement receptors C3aR and C5aR.

19. Chitin induces the generation of C3a in the lung, and chitin-dependent allergic sensitization to Aspergillus requires C3aR signaling, which suppresses regulatory dendritic cells and T cells and induces allergy-promoting T cells.

20. The receptor for complement component C3a mediates protection from intestinal ischemia-reperfusion injuries by inhibiting neutrophil mobilization.