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SLC40A1/Ferroportin-1 (F9U5S) Rabbit mAb #48322

Filter:
  • WB
  • IHC
Western blot analysis of extracts from various cell lines using SLC40A1/Ferroportin-1 (F9U5S) Rabbit mAb (upper) or GAPDH (D16H11) XP® Rabbit mAb #5174 (lower). Negative expression of SLC40A1/Ferroportin-1 protein in REC-1 and BT-20 cells is consistent with the predicted expression pattern.

To Purchase # 48322

Supporting Data

REACTIVITY H
SENSITIVITY Endogenous
MW (kDa) 62
Source/Isotype Rabbit IgG
Application Key:
  • WB-Western Blotting 
  • IHC-Immunohistochemistry 
Species Cross-Reactivity Key:
  • H-Human 
  • Related Products

Product Information

Product Usage Information

Application Dilution
Western Blotting 1:1000
Immunohistochemistry (Paraffin) 1:125 - 1:500

Storage

Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

For a carrier free (BSA and azide free) version of this product see product #59679.

Protocol

Specificity / Sensitivity

SLC40A1/Ferroportin-1 (F9U5S) Rabbit mAb recognizes endogenous levels of total SLC40A1/Ferroportin-1 protein. Non-specific staining was observed in pancreatic acinar cells by immunohistochemistry. This antibody is not recommended for immunohistochemical analysis of mouse tissues.

Species Reactivity:

Human

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu265 of human SLC40A1/Ferroportin-1 protein.

Background

Ferroportin-1 (FPN1), also known as solute carrier family 40 member 1 (SLC40A1) or iron-regulated transporter 1 (IREG1), is a multi-pass membrane protein that transports iron from the inside of the cell into the blood. As the only known iron exporter, FPN1 is critical for maintaining systemic iron homeostasis (1). FPN1 activity is regulated by hepcidin, a peptide hormone secreted by the liver in response to iron loading and inflammation. Circulating hepcidin binds to FPN1 and induces its internalization and degradation, thereby reducing iron efflux to the plasma (2,3). Expression of FPN1 may also be regulated post-transcriptionally by several microRNAs that directly target its 3' untranslated region (4-6). Mutations in the SLC40A1 gene encoding FPN1 are associated with type IV hemochromatosis (7) as well as several neural tube and patterning defects, including spina bifida, exencephaly, and forebrain truncations (8). Loss of FPN1 in the brains of Alzheimer's disease (AD) mouse models and patients has been shown to promote ferroptosis, leading to neuronal death and memory impairment. Therefore, targeting of FPN1 may be a promising therapeutic approach for AD (9).
For Research Use Only. Not For Use In Diagnostic Procedures.
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