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Hepcidin/HAMP Protein, Mouse, Recombinant (GST)

Catalog No. TMPK-01170 Copy Product Info
Hepcidin, the main regulator of iron metabolism, is synthesized and released by hepatocytes in response to increased body iron concentration and inflammation. Deregulation of hepcidin expression is a common feature of genetic and acquired iron disorders: in Hereditary Hemochromatosis (HH) and iron-loading anemias low hepcidin causes iron overload, while in Iron Refractory Iron Deficiency Anemia (IRIDA) and anemia of inflammation (AI), high hepcidin levels induce iron-restricted erythropoiesis.

Hepcidin/HAMP Protein, Mouse, Recombinant (GST)

Catalog No. TMPK-01170
Copy Product Info

Hepcidin, the main regulator of iron metabolism, is synthesized and released by hepatocytes in response to increased body iron concentration and inflammation. Deregulation of hepcidin expression is a common feature of genetic and acquired iron disorders: in Hereditary Hemochromatosis (HH) and iron-loading anemias low hepcidin causes iron overload, while in Iron Refractory Iron Deficiency Anemia (IRIDA) and anemia of inflammation (AI), high hepcidin levels induce iron-restricted erythropoiesis.

Hepcidin/HAMP Protein, Mouse, Recombinant (GST)
Pack SizePriceUSA StockGlobal StockQuantity
5 μg$567-10 days7-10 days
10 μg$887-10 days7-10 days
20 μg$1437-10 days7-10 days
50 μg$2787-10 days7-10 days
100 μg$4657-10 days7-10 days
200 μg$8397-10 days7-10 days
500 μg$1,8507-10 days7-10 days
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In stock · Estimated delivery: USA Stock (1-2 days) Global Stock (5-7 days)
For research use only—not for human use. No sales to individuals. Use as intended only.
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Biological Activity
Activity has not been tested. It is theoretically active, but we cannot guarantee it. If you require protein activity, we recommend choosing the eukaryotic expression version first.
Description
Hepcidin, the main regulator of iron metabolism, is synthesized and released by hepatocytes in response to increased body iron concentration and inflammation. Deregulation of hepcidin expression is a common feature of genetic and acquired iron disorders: in Hereditary Hemochromatosis (HH) and iron-loading anemias low hepcidin causes iron overload, while in Iron Refractory Iron Deficiency Anemia (IRIDA) and anemia of inflammation (AI), high hepcidin levels induce iron-restricted erythropoiesis.
Species
Mouse
Expression System
E. coli
TagN-GST
Accession NumberQ9EQ21
Synonyms
PLTR,LEAP-1,LEAP1,HFE2B,Hepc1,Hepc,Hamp1
Construction
Asp59-Thr83
Protein Purity
> 95% as determined by Tris-Bis PAGE
Molecular Weight29.05 kDa (predicted) same as Tris-Bis PAGE result.
Endotoxin< 1.0 EU/μg of the protein as determined by the LAL method.
FormulationLyophilized from a solution filtered through a 0.22 μm filter, containing 50 mM Tris-HCl, 150 mM NaCl, 2 mM DTT (pH 7.5). Typically, 8% trehalose is incorporated as a protective agent before lyophilization.
Reconstitution
Reconstitute the lyophilized protein in distilled water. The product concentration should not be less than 100 μg/ml. Before opening, centrifuge the tube to collect powder at the bottom. After adding the reconstitution buffer, avoid vortexing or pipetting for mixing.
Stability & Storage
It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.
ShippingIn general, lyophilized powders are shipped with blue ice, while solutions are shipped with dry ice.
Research Background
Hepcidin, the main regulator of iron metabolism, is synthesized and released by hepatocytes in response to increased body iron concentration and inflammation. Deregulation of hepcidin expression is a common feature of genetic and acquired iron disorders: in Hereditary Hemochromatosis (HH) and iron-loading anemias low hepcidin causes iron overload, while in Iron Refractory Iron Deficiency Anemia (IRIDA) and anemia of inflammation (AI), high hepcidin levels induce iron-restricted erythropoiesis.

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