anti-Complement Component 5 (C5) 抗体产品概述

Human Complement Component 5 (C5) interaction partners

1. S. aureus-induced coagulation in human whole blood was mainly attributable to C5a-induced mRNA upregulation, monocyte tissue factors expression, and plasma TF activity.

2. In addition, an in vitro experiment revealed C5aR deficiency promoted the development of regulatory T cells whereas C5a activation abolished the differentiation of regulatory T cells.

3. Urinary C5a correlates with the degree of kidney donor acute kidney injury. In the absence of clinical donor AKI, donor urinary C5a concentrations associate with recipient delayed graft function.

4. REVIEW: Emerging roles in cancer progression and treatment

5. the placental C5a/C5aR pathway contributed to the development of pre eclampsia by regulating placental trophoblasts dysfunctions.

6. Aspergillus fumigatus conidial metalloprotease Mep1p cleaves host major complement components C3, C4, and C5.

7. Furthermore, Apigenin reduced the proliferation of human NPC cells triggered by C5a through negative regulation of C5aR/PCAF/STAT3 axis. These might provide a new insight into the function of Apigenin in cancer treatment, and also provide a potential strategy for treating human NPC through inhibition of C5aR expression on cancer cells

8. Study identified that peripheral mRNA expression levels of two complement genes (C5, SERPING1) made unique contributions to the variance in superior frontal cortical thickness. Vertex-wise maps of the association between gene expression levels and thickness across the cortex suggested that this relationship was especially strong with SERPING1 in the superior frontal region.

9. these data demonstrate that Mesenchymal Stem Cells inhibit the activation of pathogenic C5 via up-regulation of FH, which improves our understanding of the immunomodulatory mechanisms of MSCs in the treatment of lupus nephritis.

10. recombinant C5a potentiated TNFalpha-induced NF-kappaB activation in renal tubular epithelial cells

11. tumoral C5a is an independent adverse prognostic biomarker for clinical outcome of Clear Cell Renal Cell Carcinoma patients after nephectomy.

12. C5a synergises with P. aeruginosa LPS in both PD-L1 expression and the production of IL-10 and TGF-beta.

13. these results not only confirm the critical role of C5b-9 in complement-mediated hemolysis and but also highlight the critical role of C5b-9 in inflammasome activation.

14. Mean cerebrospinal fluid C5 levels increased in patients with depression and schizophrenia.

15. elevated in the cerebrospinal fluid of preterm newborns

16. Up-regulation of granulocyte and monocyte CD11b during plasma separation was C5-dependent.

17. This study provides the preclinical rationale for the combined blockade of PD-1/PD-L1 and C5a to restore antitumor immune responses, inhibit tumor cell growth, and improve outcomes of patients with lung cancer

18. Diagnosis and therapeutic management of neonatal hemochromatosis cannot only be based on C5b9 expression in liver samples as it is not specific of this disease.

19. C5a-C5aR enriched clear cell renal cell carcinoma patients significantly had a poorer overall survival and recurrence free survival after nephrectomy.

20. The complement activation factors Bb, C3a, C5a, and MAC were increased significantly in early-onset severe pre-eclampsia (EOSPE) (all P<.01) and late-onset severe pre-eclampsia (LOSPE). (P value: .027, <.001, .001, and <.001, respectively) compared with E/L-control. C1q and C4d were increased significantly in LOSPE (P value: .003 and .014, respectively) compared with L-control.

Mouse (Murine) Complement Component 5 (C5) interaction partners

1. Carboxypeptidase N is key for inactivation of systemic C5a, whereas Carboxypeptidase B2 functions as an on-demand supplementary anaphylatoxin inhibitor in inactivating excessive C5a formed locally.

2. C5a plays a role in the progression of experimental arthritis(rheumatoid arthritis mouse model) with Porphyromonas gingivalis infection in SKG mice

3. Together, the data indicates that respiratory syncytial virus infection could apparently increase C5a and C5aR expression in the pathogenesis of respiratory syncytial virus-infected asthma mice, meanwhile C5a receptor antagonist prevents some of the CD4(+)T cells immune changes that are induced by respiratory syncytial virus.

4. However, serum C5 levels did not differ between nPM and filtered air cohorts. These findings demonstrate white matter C5 deposition and microglial activation secondary to nPM exposure. The C5 upregulation appears to be localized to the brain.

5. this study shows a novel role for C5a in B-1 cell homeostasis

6. Complement C5 but not C3 is expendable for tissue factor activation by cofactor-independent antiphospholipid antibodies.

7. We present evidence that mice deficient in C5aR or treated with AON-D21 are poor hematopoietic stem/progenitor cells mobilizers, thereby establishing a critical role for the C5a/C5adesArg-C5aR axis in the mobilization process.

8. C5 and C5aR have critical roles in the development of C3 glomerulopathy.

9. In mice that lost the ability to express complement C5, there was a lower frequency of metastasis, and males no longer had a higher frequency of metastasis than females.

10. C5 contributes effectively to liver steatosis and inflammation in non-alcoholic fatty liver disease pathogenesis

11. C5a in vitro caused activation (phosphorylation) of MAPKs and Akt in cardiomyocytes, which required availability of both C5a receptors. These data suggest that polymicrobial sepsis causes cardiac dysfunction that appears to be linked to activation of MAPKs and Akt in heart.

12. data suggest a novel role for the anaphylatoxin C5a as a master switch of the delicate pHi balance in neutrophils resulting in profound inflammatory and metabolic changes that contribute to hyperlactatemia during sepsis.

13. n the complex but clinically relevant DH model the local and systemic inflammatory immune response features both, C5-dependent and C5-independent characteristics. Activation of caspase-3 in lung tissue after DH was C5-dependent whereas local inflammation in lung tissue was C5-independent.

14. The C5a/C5aR pathway is essential for up-regulating SphK1 expression through p38 MAPK activation in acute liver failure.in mice.

15. We induced anti-myeloperoxidase vasculitis in bone marrow chimaeric mice and found that circulating and not bone marrow-derived C5 was required for disease

16. Choroidal neovascularization lesions trigger a systemic immune response, augmenting local ocular inflammation via the infiltration of IL-17-producing gamma-delta T-cells, which are presumably recruited to the eye in a C5a-dependent manner.

17. Identify complement 5a as the major C3 activation product that was involved in macrophage polarization and DOCA-salt-induced vascular injury.

18. Data (including data from studies in knockout mice) suggest that C5aR/C5aR (complement C5a/anaphylatoxin C5a Receptor) signaling pathway is involved in neurocognitive injury in uninfected pups induced by malaria in pregnancy.

19. Carboxypeptidase B2 deficiency reveals that complement C5a exacerbates infection in a murine polymicrobial sepsis model.

20. our results suggest that the detrimental effects of C5a in this model are partly mediated through CCR5 activation downstream of C5aR1, which may be evaluated for potential therapeutic exploitation in ALI/ARDS.