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anti-Human Hepcidin Anticorps:
anti-Mouse (Murine) Hepcidin Anticorps:
anti-Rat (Rattus) Hepcidin Anticorps:
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Human Polyclonal Hepcidin Primary Antibody pour ELISA - ABIN450057
Ward, Roberts, Brookes, Joy, Martin, Ismail, Spychal, Iqbal, Tselepis: Increased hepcidin expression in colorectal carcinogenesis. dans World journal of gastroenterology 2008
Human Polyclonal Hepcidin Primary Antibody pour WB - ABIN2776909
Theurl, Theurl, Seifert, Mair, Nairz, Rumpold, Zoller, Bellmann-Weiler, Niederegger, Talasz, Weiss: Autocrine formation of hepcidin induces iron retention in human monocytes. dans Blood 2008
Human Polyclonal Hepcidin Primary Antibody pour WB - ABIN4892228
Bose, Megyesi, Shah, Hiatt, Hall, Karaduta, Swaminathan: Evidence Suggesting a Role of Iron in a Mouse Model of Nephrogenic Systemic Fibrosis. dans PLoS ONE 2015
Serum hepcidin is a pathogenic factor of anemia in ANCA-associated vasculitis and can be used as an additional marker in active forms of the disease.
We also identified an association between hepcidin and HDL3-C at baseline, which indicates that the HDL3-C level may reflect the change in cholesterol efflux from peripheral arteries and partly explain the relationship between hepcidin and the change of arterial stiffness
These findings suggest that serum hepcidin may be a uremic toxin and play an important role in erythropoietin resistance. However, future prospective studies are needed to confirm our results
Hepcidin is lower in more severely anemic children with sickle cell disease independent of inflammation or markers of erythropoiesis.
serum hepcidin level has a role in iron status in children with cystic fibrosis
Athree-dimensional (3D) model of hepcidin-25 with bound copper(II) is presented.
our data demonstrate that hypoxia strongly potentiates the peroxide-mediated induction of hepcidin via STAT3 signaling pathway. Moreover, oxidases such as NOX4 or artificially overexpressed urate oxidase (UOX) can induce hepcidin
High hepcidin maternal serum levels could be an early marker of preeclampsia.
Suggest IL-6 can induce hepcidin in systemic lupus erythematosus flares.
Serum hepcidin was associated with more severe anemia in advanced CKD patients.
Data suggest that magnitude of up-regulation of serum hepcidin levels in response to acute exercise in adults is dependent on pre-exercise iron nutritional status (ferritin levels) and on circulating pro-inflammatory cytokines (prominently interleukin-6). [REVIEW]
The present study provides new evidence that ASP decreases hepcidin expression, which can reduce iron burden and inhibit tumor proliferation. These findings might aid ASP developed as a potential candidate for cancer treatment in patients with iron overload.
Postexercise supplementation with protein and carbohydrate and vitamins D3 and K2 did not blunt the postexercise hepcidin response in highly trained athletes.
A decrease in serum FGF23 and hepcidin levels was observed in chronic hemodialysis patients treated with lanthanum carbonate.
These observations suggest correlations between serum hepcidin and progression of chronic HBV infection, and may shed a new light on the development of biomarkers for HBV-related disease surveillance.
Increasing adiposity in the pediatric population is associated with increasing IL-6, which stimulates hepcidin synthesis, leading to functional iron deficiency due to inhibition of iron absorption and mobilization from iron stores.
Suggest that pentoxifylline may be a clinically and biologically meaningful modulator of hepcidin-25 in dialysis of patients with ESA-hyporesponsive anaemia.
Among low birth weight infants, gestational age, IL-6, erythropoietin, and soluble transferrin receptor were associated with Hep25 levels. Therefore, prematurity, inflammation, hypoxia, and erythropoietic activity may be important perinatal factors that affect hepcidin levels.
genetic association studies in cohort of infants in Spain: Data suggest that serum hepcidin levels increase in infants during first year of life and are positively associated with iron status only in infants with wild-type HFE gene (not in infants with genetic polymorphisms C282Y, H63D, and S65C). (HFE, homeostatic iron regulator)
Data suggest that circulating hepcidin levels (a biomarker for iron-deficiency anemia) may be regulated by dietary factors other than iron; here, one-time high-dose vitamin D3 reduces plasma hepcidin levels in adults one week post-dosing, without changes in plasma pro-inflammatory cytokine or ferritin concentrations.
The study describes a role for C and hepcidin in obesity and highlights the relevance of iron regulation in the control of adipose tissue function.
results indicate that a 0.25% carbonyl iron diet is sufficient to induce maximal hepatic hepcidin response. Importantly these results also demonstrate that in a chronic setting of iron administration, the amount of excess hepatic iron may not further influence hepcidin regulation and that expression of hepcidin plateaus at lower hepatic iron levels. These studies provide further insights into the regulation of this import
Increased serum hepcidin contributes to the anemia of chronic kidney disease in a murine model.
bone marrow transplantation between wild-type and TLR4 knockout mice revealed that hepatic TLR4-dependent hepcidin expression was comparable to macrophage TLR4-dependent hepcidin expression induced by LPS
Hepc decreases in Cyp1b1-/- and gestational vitamin A deficiency mice resulted in stellate activation and lipogenesis suppression.
data indicate that unlike with many other infections, hepcidin is decreased following M.tb infection, and show that hepcidin ablation does not influence M.tb growth in vivo
Hepcidin expression involves epigenetic regulation by histone deacetylase 3.
Serum hepcidin levels were measured by competitive ELISA in wild-type and Inhbb-/- mice at baseline and 4 hours after LPS challenge. Although Smad1/5/8 signaling is not activated by inflammatory stimuli in the absence of activin B, this has no impact on the induction of hepcidin expression.
Anti-hemojuvelin antibody corrects anemia caused by inappropriately high hepcidin levels
hepcidin mRNA upregulation depends on M1 macrophage polarization
Our data provide evidence that the interplay of these two hormones could help improve the understanding of the pathogenesis of atherosclerosis and NAFLD.
downregulation of hepcidin by siRNA increased iron uptake in bone and liver, which aggravated unloading-induced bone loss.
These data suggest that, in Hjv(-/-) females, Bmp6 can provide a signal adequate to maintain hepcidin to a level sufficient to avoid extrahepatic iron loading.
The authors generated mice with cardiomyocyte-specific deletion of hepcidin, or knock-in of hepcidin-resistant ferroportin. They find that while both models maintain normal systemic iron homeostasis, the mice nonetheless develop fatal contractile and metabolic dysfunction as a consequence of cardiomyocyte iron deficiency.
Erythroferrone and matriptase-2 independently regulate hepcidin expression.
Acute tacrolimus treatment transiently increases hepcidin in wild-type mice. FKBP12 preferentially targets the BMP receptor ALK2. ALK2 mutants defective in binding FKBP12 increase hepcidin expression in a ligand-independent manner, through BMP-SMAD signaling.
Hamp1 mRNA and plasma hepcidin levels are not good predictors of tissue iron levels, at least in males
The lack of effect of erythropoietin on hepcidin expression in mask mice can not be explained by changes in erythroferrone synthesis, as splenic erythroferrone content increased after erythropoietin administration in both C57BL/6 and mask mice.
these results characterise a new model of rapidly inducible hepcidin disruption, and demonstrate the critical contribution of hepcidin to the hypoferraemia of inflammation
Hepatic gene expression of hepcidin is regulated in beta-thalassemia by ATOH8.
This study shows that hepcidin knockdown in zebrafish using morpholinos leads to iron overload.
The data also show that the antibacterial activity of hepcidin-2 depends upon the disulfide bridges.
data support an alternative mechanism for hepcidin regulation during zebrafish embryonic development, which is independent of hemojuvelin.
Hepcidin expression is regulated by a transferrin-a-dependent pathway in the zebrafish embryo.
this study demonstrates that urine hepcidin-25 concentrations strongly correlate with hepatic hepcidin mRNA abundance, plasma hepcidin-25 levels, iron transferrin saturation and non-heme liver iron levels.
Data suugest that hepcidin might had antiinflammatory function and is a candidate regulator of the cross-talk between iron regulation and inflammation.
report the full-length cDNA sequences of porcine hepcidin and liver-expressed antimicrobial peptide-2 (LEAP-2)
HEP/FPN axis seems to have a central role in infections, with microorganisms within macrophages or that survive in the bloodstream or other cellular spaces. In addition, HEP may be responsible for iron flux regulation as a molecular bridge for iron trafficking and response to infection.
cloning, sequencing and expression analysis
Hepcidin peptide is up-regulated by iron and bacterial components in the trout liver.
The product encoded by this gene is involved in the maintenance of iron homeostasis, and it is necessary for the regulation of iron storage in macrophages, and for intestinal iron absorption. The preproprotein is post-translationally cleaved into mature peptides of 20, 22 and 25 amino acids, and these active peptides are rich in cysteines, which form intramolecular bonds that stabilize their beta-sheet structures. These peptides exhibit antimicrobial activity. Mutations in this gene cause hemochromatosis type 2B, also known as juvenile hemochromatosis, a disease caused by severe iron overload that results in cardiomyopathy, cirrhosis, and endocrine failure.
, liver-expressed antimicrobial peptide 1
, putative liver tumor regressor
, hepcidin antimicrobial peptide 1
, hepcidin antimicrobial peptide
, antimicrobial peptide
, iron regulatory peptide
, preprohepcidin 1
, antimicrobial peptide hepcidin
, putative hepcidin antibacterial peptide