Contacto

Human Hepcidin (HAMP) CLIA Kit

618,75 (96 tests)

Human Hepcidin (Hepc) CLIA Kit is a CLIA kit against Hepcidin (Hepc).

Proveedor

Abbexa

Reference

abx195730

Tested Applications

CLIA

Reactivity

Human

Status

RUO

Si quieres saber los precios con descuentos por volumen o bien más características del producto, contáctanos!

Características de producto

tested_applications
CLIA
reactivity
Human
category
CLIA Kits
Immunogen / Target
Hepcidin (HAMP)
size_1
96 tests
storage
Shipped at 4 °C. Upon receipt, store the kit according to the storage instruction in the kit's manual.
test_range
31.2 pg/ml - 2000 pg/ml
sensitivity
18.8 pg/ml
detection_method
Chemiluminescent
assay_type
Sandwich
assay_data
Quantitative
availability
Shipped within 5-12 working days.
dry_ice
No
note
This product is for research use only.

The range and sensitivity is subject to change. Please contact us for the latest product information. For accurate results, sample concentrations must be diluted to mid-range of the kit. If you require a specific range, please contact us in advance or write your request in your order comments.

Please note that our ELISA and CLIA kits are optimised for detection of native samples, rather than recombinant proteins. We are unable to guarantee detection of recombinant proteins, as they may have different sequences or tertiary structures to the native protein.
background
Hepcidin is a protein that in humans is encoded by the HAMP gene. Hepcidin is a key regulator of the entry of iron into the circulation in mammals. Hepcidin is a regulator of iron metabolism. Hepcidin inhibits iron transport by binding to the iron export channel ferroportin which is located on the basolateral surface of gut enterocytes and the plasma membrane of reticuloendothelial cells (macrophages). Hepcidin ultimately breaks down the transporter protein in the lysosome. Inhibiting ferroportin prevents iron from being exported and the iron is sequestered in the cells. By inhibiting ferroportin, hepcidin prevents enterocytes from allowing iron into the hepatic portal system, thereby reducing dietary iron absorption. The iron release from macrophages is also reduced by ferroportin inhibition. Increased hepcidin activity is partially responsible for reduced iron availability seen in anemia of chronic inflammation, such as renal failure. Target