Human Hepcidin 25 (Hepc-25) Peptide (OVA)

Este producto es parte de HAMP - Hepcidin
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442€ (100 µg)

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935106861
info@markelab.com
name
Human Hepcidin 25 (Hepc-25) Peptide (OVA)
category
Proteins and Peptides
provider
Abbexa
reference
abx651222
tested applications
SDS-PAGE

Description

Human Hepcidin 25 (Hepc 25) Peptide (OVA) is a OVA conjugated peptide synthesized from the Hepcidin-25 region of Human Hepcidin.

Documents del producto

Instrucciones
Data sheet
Descargar

Product specifications

Category
Proteins and Peptides
Immunogen Target
Hepcidin 25 (Hepc 25)
Origin
Human
Conjugation
OVA
Observed MW
Concentration: Prior to lyophilization: 1.5 mg/ml
Sequence Fragment: Thr61-Met80
Expression
Synthetic
Purity
> 90%
Size 1
100 µg
Size 2
200 µg
Size 3
500 µg
Size 4
1 mg
Size 5
5 mg
Form
Lyophilized To keep the original salt concentration, we recommend reconstituting to the original concentration prior to lyophilization (see Concentration) in ddH2O. If a lower concentration is required, dilute in 10 mM PBS, pH 7.4. If a higher concentration is required, the product can be reconstituted directly in 10 mM PBS, pH 7.4, though please note that this will change the overall salt concentration. The stock concentration should be between 0.1-1.0 mg/ml. Do not vortex.
Tested Applications
SDS-PAGE
Buffer
Prior to lyophilization: 10 mM PBS, pH 7.4.
Availability
Shipped within 5-7 working days.
Storage
Store at 2-8 °C for up to one month. Store at -80 °C for up to one year. Avoid repeated freeze/thaw cycles.
Dry Ice
No
UniProt ID
P81172
Gene ID
57817
Alias
HEPC,PLTR,HFE2B,LEAP1,Putative liver tumor regressor,PLTR
Background
Protein HAMP
Status
RUO
Note
This product is for research use only.   Not for human consumption, cosmetic, therapeutic or diagnostic use.

Descripción

Hepcidin Antimicrobial Peptide (HAMP) is a small, liver-derived peptide hormone that serves as the master regulator of systemic iron homeostasis and possesses antimicrobial properties. Hepcidin controls iron levels by binding to the iron export protein ferroportin, leading to its internalization and degradation, thereby reducing iron release from enterocytes, macrophages, and hepatocytes into the bloodstream. This regulation is critical for preventing iron overload and ensuring adequate iron availability for erythropoiesis. HAMP expression is modulated by factors such as systemic iron levels, inflammation, erythropoietic demand, and hypoxia. Inflammatory cytokines, particularly IL-6, stimulate HAMP production via the JAK-STAT pathway, contributing to the anemia of chronic disease by sequestering iron in storage sites. Conversely, inadequate HAMP expression leads to conditions such as hereditary hemochromatosis and iron-loading anemias. In addition to its role in iron metabolism, HAMP exhibits antimicrobial activity by directly targeting bacterial pathogens, making it a key component of the innate immune response. Therapeutic manipulation of HAMP is being explored for treating iron disorders and related conditions.

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