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Human Polyclonal CP Primary Antibody for IHC, IHC (p) - ABIN4297774
Hametner, Wimmer, Haider, Pfeifenbring, Brück, Lassmann: Iron and neurodegeneration in the multiple sclerosis brain. in Annals of neurology 2014
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Human Polyclonal CP Primary Antibody for IHC (fro), ELISA - ABIN2472948
Perusicová, Fric, Cacáková, Mardesicová, Stolba, Kocna: [The effect of Sinecal fiber on compensation in type 2 diabetics]. in Vnitr?ní lékar?ství 1990
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Human Polyclonal CP Primary Antibody for IHC (fro), ELISA - ABIN2472949
Mazumder, Sampath, Fox: Regulation of macrophage ceruloplasmin gene expression: one paradigm of 3'-UTR-mediated translational control. in Molecules and cells 2005
Show all 2 Pubmed References
Human Polyclonal CP Primary Antibody for FACS, IHC (p) - ABIN391512
Jiang, Liu, Zheng, Chen, Maimaitiming, Chen, Liu, Jiang, Fuqua, Dunaief, Vulpe, Anderson, Wang, Chen: Hephaestin and ceruloplasmin facilitate iron metabolism in the mouse kidney. in Scientific reports 2018
Maternal blood ceruloplasmin level was found to be lower in neural tube defect-affected pregnancies as compared to healthy controls.
Increased serum transferrin and ceruloplasmin turnover in diet-controlled patients with type 2 diabetes has been reported.
Strong correlations between the meconium concentrations of CP, LF and MPO (show MPO Antibodies) indicate a possible role of these complementary proteins in maintaining homeostasis of the intrauterine environment of the fetus. CP, LF and MPO (show MPO Antibodies) measured in meconium may serve as biomarkers for assessment of impairment of oxidative balance during intrauterine life with its potential impact on disease development in adulthood.
A woman in her 50s who initially presented with movement disorder was diagnosed with aceruloplasminemia, a rare autosomal recessive disorder resulting in accumulation of iron deposits in major organs. Genetic testing confirmed mutations in the ceruloplasmin gene (c.1864 + 1G>C).
Higher circulating ceruloplasmin levels were associated with increased atrial fibrillation risk.
for ATP7B (show ATP7B Antibodies) mutations, the more severe impact on ATP7B (show ATP7B Antibodies) protein was, the younger onset age and lower Cp level presented. The feasibility of presymptomatic DNA diagnosis and predicting clinical manifestation or severity of Wilson disease (WD) would be facilitated with identified mutations and genotype-phenotype correlation precisely revealed in the study.
Ceruloplasmin is supposed to be related with advanced T stage and perineural invasion, having a possibility as a candidate prognostic marker for bile duct cancer.
Mechanistically, ceruloplasmin could specifically interact with the hepatitis B virus middle surface protein.
The present study determined that ARE, CLP (show CALML3 Antibodies), CAT, and MPO (show MPO Antibodies) levels are different between the pediatric patients with sepsis and healthy controls. ARE level can be a potent biomarker for sepsis in critical patients in intensive care units.
Ceruloplasmin was independently and negatively associated with liver fibrosis in chronic hepatitis b.
We thus used hephaestin (Heph (show HEPH Antibodies)) and ceruloplasmin (Cp) single-knockout mice and Heph (show HEPH Antibodies)/Cp double-knockout mice to investigate the roles of multicopper ferroxidases(MCF) in pancreatic iron homeostasis. We found that both HEPH (show HEPH Antibodies) and CP were expressed in the mouse pancreas, and that ablation of either MCF had limited effect on the pancreatic iron levels.
Hephaestin (show HEPH Antibodies) and ceruloplasmin have roles in facilitating iron metabolism in the mouse kidney
In D-galactosamine-sensitized mice CP+Cu(II) increased the LPS (show TLR4 Antibodies)-induced lethality from 54 to 100%, while administration of antibodies against MIF (show MIF Antibodies) prevented the lethal effect. The enhancement by CP+Cu(II) of the pro-inflammatory signal of MIF (show MIF Antibodies) is discussed
mice with mutation of Cp and Heph (show HEPH Antibodies), iron accumulates in glia, while neurons have low iron levels. Both neurons and glia degenerate and mice become ataxic unless given an iron chelator.
Data (including data from studies in knockout mice) suggest that ceruloplasmin and hephaestin (show HEPH Antibodies) play distinct roles in regulation of gene expression in various regions of the brain and are involved in iron homeostasis.
Evidence supports a regulatory role of both proteins (Ceruloplasmin (CP) and beta-amyloid protein precursor (APP (show APP Antibodies))) in defence against iron-induced oxidative damage after TBI, which presents as a tractable therapeutic target.
Genetic interactions between Cp, Mon1a (show MON1A Antibodies), and the Slc40a1 (show SLC40A1 Antibodies) locus are involved in iron metabolism.
ceruloplasmin should provide a protective shield against inadvertent oxidant production by myeloperoxidase (show MPO Antibodies) during inflammation
The mouse ceruloplasmin gene has been mapped to chromosome 3.
The protein encoded by this gene is a metalloprotein that binds most of the copper in plasma and is involved in the peroxidation of Fe(II)transferrin to Fe(III) transferrin. Mutations in this gene cause aceruloplasminemia, which results in iron accumulation and tissue damage, and is associated with diabetes and neurologic abnormalities. Two transcript variants, one protein-coding and the other not protein-coding, have been found for this gene.
, hypothetical protein
, ceruloplasmin (ferroxidase)