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anti-Human C5A Antibodies:
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Mouse (Murine) Monoclonal C5A Primary Antibody for ELISA - ABIN2688863
Hugli: Structure and function of the anaphylatoxins. in Springer seminars in immunopathology 1984
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.
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.
recombinant C5a potentiated TNFalpha-induced NF-kappaB activation in renal tubular epithelial cells
tumoral C5a is an independent adverse prognostic biomarker for clinical outcome of Clear Cell Renal Cell Carcinoma patients after nephectomy.
C5a synergises with P. aeruginosa LPS in both PD-L1 expression and the production of IL-10 and TGF-beta.
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.
Mean cerebrospinal fluid C5 levels increased in patients with depression and schizophrenia.
elevated in the cerebrospinal fluid of preterm newborns
Up-regulation of granulocyte and monocyte CD11b during plasma separation was C5-dependent.
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
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.
C5a-C5aR enriched clear cell renal cell carcinoma patients significantly had a poorer overall survival and recurrence free survival after nephrectomy.
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.
C5a/C5aR pathway promotes gastric cancer pathogenesis by suppressing p21/p-p21 expression via activation of PI3K/AKT signaling.
this study shows that C5 acts in the control of serum triglycerides and cholesterol, liver cholesterol deposition, liver homeostasis and C5 promotes a pro-inflammatory liver environment in our mouse model of alcoholic liver disease
a library of 61 peptides based on the C-terminus of C5a was assayed for the ability to selectively modulate C5aR2 function.
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.
Data show the expression of a neoepitope which was exposed on complement C5 (C5) after binding to eculizumab in vivo.
Plasma levels of sC5b-9 were significantly increased in patients with thrombotic microangiopathy after allogeneic stem cell transplantation.
C5 gene analysis revealed two novel mutations as causative of C5 deficiency in 3 north African families
The protein encoded by this gene is the fifth component of complement, which plays an important role in inflammatory and cell killing processes. This protein is comprised of alpha and beta polypeptide chains that are linked by a disulfide bridge. An activation peptide, C5a, which is an anaphylatoxin that possesses potent spasmogenic and chemotactic activity, is derived from the alpha polypeptide via cleavage with a convertase. The C5b macromolecular cleavage product can form a complex with the C6 complement component, and this complex is the basis for formation of the membrane attack complex, which includes additional complement components. Mutations in this gene cause complement component 5 deficiency, a disease where patients show a propensity for severe recurrent infections. Defects in this gene have also been linked to a susceptibility to liver fibrosis and to rheumatoid arthritis.
C3 and PZP-like alpha-2-macroglobulin domain-containing protein 4
, C5a anaphylatoxin
, anaphylatoxin C5a analog
, complement C5