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anti-Human Hepcidin Antibodies:
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Human Polyclonal Hepcidin Primary Antibody for WB - ABIN2776909
Theurl, Theurl, Seifert, Mair, Nairz, Rumpold, Zoller, Bellmann-Weiler, Niederegger, Talasz, Weiss: Autocrine formation of hepcidin induces iron retention in human monocytes. in Blood 2008
Human Polyclonal Hepcidin Primary Antibody for WB - ABIN4892228
Bose, Megyesi, Shah, Hiatt, Hall, Karaduta, Swaminathan: Evidence Suggesting a Role of Iron in a Mouse Model of Nephrogenic Systemic Fibrosis. in PLoS ONE 2015
Human Polyclonal Hepcidin Primary Antibody for ELISA - ABIN450057
Ward, Roberts, Brookes, Joy, Martin, Ismail, Spychal, Iqbal, Tselepis: Increased hepcidin expression in colorectal carcinogenesis. in World journal of gastroenterology 2008
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 (show FTL Antibodies) concentrations.
Hepcidin can very well be utilized as a potential prognostic marker to follow patients with breast cancer metastatic to bone.
Data suggest that hematologic parameters in children consuming lacto-ovo vegetarian diets are comparable with those of control children, but ferritin (show FTL Antibodies) levels are lower; inclusion of novel serum biomarkers, soluble transferrin receptor and hepcidin, in nutritional assessment can better detect subclinical iron deficiency in children following vegetarian diet. This study was conducted in Poland with children ages 4.5-9 years.
results suggest that lower Hepcidin-25, as well as higher sTfR and sTfR/Hepcidin-25 ratio were significant predictors of favorable hemoglobin response within a month after IV administration of ferric carboxymaltose in patients with CKD
unreported iron metabolism-related genes in non-classic hereditary hemochromatosis (show HFE Antibodies) patients that were predicted to be potentially pathogenic were three novel mutations in TFR2 (show TFR2 Antibodies) [two missense (p.Leu750Pro and p.Ala777Val) and one intronic splicing mutation (c.967-1G>C)], one missense mutation in HFE (show HFE Antibodies) (p.Tyr230Cys), and one mutation in the 5'-UTR (show UTS2R Antibodies) of HAMP gene (c.-25G>A)
increased intracellular iron content in recombinant-TfR1 (show TFRC Antibodies) HepG2 cells did not increase hepcidin responses compared to wild-type cells, resembling hemochromatosis (show HFE Antibodies)
Review of the role of hepcidin in iron metabolism disorders.
The bone morphogenetic protein (BMP) pathway regulates expression of hepcidin through transcriptional activation via BMP-responsive elements (REs) 1 and 2 on the promoter. A search for GC-rich sequences on the hepcidin promoter indicated 13 regions across the distal (A to F), middle (G to I), and proximal (J to M) areas.
Of the non-HFE (show HFE Antibodies) forms of iron overload, TFR2 (show TFR2 Antibodies)-, HFE2 (show HFE2 Antibodies)-, and HAMP-related forms are predicted to be rare, with pathogenic allele frequencies in the range of 0.00007 to 0.0005. Significantly, SLC40A1 (show SLC40A1 Antibodies) variants that have been previously associated with autosomal-dominant ferroportin (show SLC40A1 Antibodies) disease were identified in several populations (pathogenic allele frequency 0.0004), being most prevalent among Africans
Data (including data from studies using knockout mice) suggest that MT2 (show MT2 Antibodies)/TMPRSS6 (show TMPRSS6 Antibodies) suppresses hepcidin expression in hepatocytes independently of HJV (show HFE2 Antibodies); MT2 (show MT2 Antibodies)/TMPRSS6 (show TMPRSS6 Antibodies) cleaves ALK2 (show ACRV1 Antibodies), ALK3 (show BMPR1A Antibodies), ACTRIIA (show ACVR2A Antibodies), BMPR2 (show BMPR2 Antibodies), HFE (show HFE Antibodies), and, to a lesser extent, HJV (show HFE2 Antibodies) and TFR2 (show TFR2 Antibodies); thus, MT2 (show MT2 Antibodies)/TMPRSS6 (show TMPRSS6 Antibodies) suppresses hepcidin expression by cleaving multiple components of the hepcidin induction pathway. (MT2 (show MT2 Antibodies)/TMPRSS6 (show TMPRSS6 Antibodies) = matriptase-2 (show TMPRSS6 Antibodies); HJV (show HFE2 Antibodies) = hemojuvelin (show HFE2 Antibodies))
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 (show HDAC3 Antibodies).
Serum hepcidin levels were measured by competitive ELISA in wild-type and Inhbb (show INHBB Antibodies)-/- mice at baseline and 4 hours after LPS (show TLR4 Antibodies) challenge. Although Smad1 (show SMAD1 Antibodies)/5/8 signaling is not activated by inflammatory stimuli in the absence of activin B (show Actbeta Antibodies), this has no impact on the induction of hepcidin expression.
Anti-hemojuvelin (show HFE2 Antibodies) 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 (show TSC2 Antibodies).
downregulation of hepcidin by siRNA increased iron uptake in bone and liver, which aggravated unloading-induced bone loss.
These data suggest that, in Hjv (show HFE2 Antibodies)(-/-) females, Bmp6 (show BMP6 Antibodies) 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 (show SLC40A1 Antibodies). 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 (show TMPRSS6 Antibodies) independently regulate hepcidin expression.
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 (show HFE2 Antibodies).
Hepcidin expression is regulated by a transferrin-a (show Tf Antibodies)-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 (show Tf Antibodies) 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 (show LEAP2 Antibodies))
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