Human Ferroportin/SLC40A1 Antibody Summary
Accession # Q9NP59
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Detection of Ferroportin/SLC40A1 in HEK293 Human Cell Line Transfected with Human Ferroportin/SLC40A1 and eGFP by Flow Cytometry. HEK293 human embryonic kidney cell line transfected with human Ferroportin/SLC40A1 and eGFP was stained with either (A) Rabbit Anti-Human Ferroportin/SLC40A1 Monoclonal Antibody (Catalog # MAB9924) or (B) Rabbit IgG Isotype Control (Catalog # MAB1050) followed by APC-conjugated Anti-Rabbit IgG Secondary Antibody (Catalog # F0111). View our protocol for Staining Membrane-associated Proteins.
Ferroportin/SLC40A1 in Human Liver. Ferroportin/SLC40A1 was detected in immersion fixed paraffin-embedded sections of human liver using Rabbit Anti-Human Ferroportin/SLC40A1 Monoclonal Antibody (Catalog # MAB9924) at 1 µg/mL for 1 hour at room temperature followed by incubation with the Anti-Mouse IgG VisUCyte™ HRP Polymer Antibody (Catalog # VC001). Tissue was stained using DAB (brown) and counterstained with hematoxylin (blue). Specific staining was localized to cytoplasm in Kupffer cells. View our protocol for IHC Staining with VisUCyte HRP Polymer Detection Reagents.
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
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 in humans is encoded by the SLC40A1 gene and is part of the Ferroportin (Fpn) Family. Ferroportin 1 is an iron-regulated transporter that is essential for iron homeostasis, playing a key role in intestinal iron absorption, as well as cellular iron release and efflux. Ferroportin can be regulated at many different levels including transcriptionally, post-transcriptionally, through mRNA stability and post-translationally, through protein turnover. Mutations affecting the SLC40A1 gene result in a disorder of iron metabolism characterized by iron overload. Excess iron is deposited in a variety of organs leading to their failure, and resulting in serious illnesses including cirrhosis, hepatomas, diabetes, cardiomyopathy and arthritis.
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