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SAB4200575

Sigma-Aldrich

Anti-SLC40A1 antibody produced in rabbit

IgG fraction of antiserum

Sinonimo/i:

Ferroportin-1(FPN1), HFE4, IREG1, MST079, MSTP079, MTP1, SLC11A3, solute carrier family 40 (iron-regulated transporter) member 1,

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About This Item

Codice UNSPSC:
12352203
NACRES:
NA.41

Origine biologica

rabbit

Forma dell’anticorpo

IgG fraction of antiserum

Tipo di anticorpo

primary antibodies

Forma fisica

buffered aqueous solution

PM

~60 kDa

Reattività contro le specie

rat, human

tecniche

immunoblotting: 1:1,000-1:2,000 using rat kidney extracts (S1 fraction)
immunohistochemistry: 1:50-1:100 using formalin-fixed paraffin-embedded human duodenum

N° accesso UniProt

Condizioni di spedizione

dry ice

Temperatura di conservazione

−20°C

modifica post-traduzionali bersaglio

unmodified

Informazioni sul gene

Descrizione generale

SLC40A1 (also known as ferroportin, FPN1), also called iron-regulated transporter 1 (IREG1), is an iron transporter expressed in liver, duodenum and kidney. SLC40A1 is also expressed in the brain, duodenal mucosa, in neuronal cells and endothelial cells of the blood-brain barrier.

Immunogeno

synthetic peptide corresponding to an internal sequence of human SLC40A1, conjugated to KLH.

Applicazioni

Anti-SLC40A1 antibody produced in rabbit has been used in western blotting and immunohistochemistry.

Azioni biochim/fisiol

Ferroportin 1(FPN1) plays a central role in systemic iron homeostasis and is critical for normal intestinal iron absorption. SLC40A1 is essential for development of the mouse embryo, forebrain patterning and neural tube closure. Hepcidin binds to and inhibits solute carrier family FPN1, thus preventing enterocytes of the intestines from secreting iron into the hepatic portal system, thereby functionally reducing iron absorption. Ferroportin in neuronal cells is required for cellular Fe2+ export, a process critical for normal neuronal function. It has been shown to interact with amyloid precursor protein (APP), to facilitate the iron export process from neuronal cells. Mutations in the FPN1 gene have been linked to hereditary hemochromatosis, a common disorder characterized by iron overload and multi-organ damage.

Stato fisico

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Esclusione di responsabilità

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Codice della classe di stoccaggio

10 - Combustible liquids

Classe di pericolosità dell'acqua (WGK)

WGK 2

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


Certificati d'analisi (COA)

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The iron exporter ferroportin/Slc40a1 is essential for iron homeostasis
Donovan A, et al.
Cell Metabolism, 1(3), 191-200 (2005)
Natascha A Wolff et al.
Journal of cellular and molecular medicine, 15(2), 209-219 (2009-12-18)
Ferroportin 1 (FPN1) is an iron export protein expressed in liver and duodenum, as well as in reticuloendothelial macrophages. Previously, we have shown that divalent metal transporter 1 (DMT1) is expressed in late endosomes and lysosomes of the kidney proximal
Differential regulation of estrogen in iron metabolism in astrocytes and neurons
Xu M, et al.
Journal of Cellular Physiology, 234(4), 4232-4242 (2019)
James A Duce et al.
Cell, 142(6), 857-867 (2010-09-08)
Alzheimer's Disease (AD) is complicated by pro-oxidant intraneuronal Fe(2+) elevation as well as extracellular Zn(2+) accumulation within amyloid plaque. We found that the AD β-amyloid protein precursor (APP) possesses ferroxidase activity mediated by a conserved H-ferritin-like active site, which is
Jinzhe Mao et al.
Development (Cambridge, England), 137(18), 3079-3088 (2010-08-13)
Neural tube defects (NTDs) are some of the most common birth defects observed in humans. The incidence of NTDs can be reduced by peri-conceptional folic acid supplementation alone and reduced even further by supplementation with folic acid plus a multivitamin.

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