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Key Documents

HPA046646

Sigma-Aldrich

Anti-FLVCR1 antibody produced in rabbit

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

Synonym(s):

Anti-AXPC1, Anti-FLVCR, Anti-MFSD7B, Anti-PCA, Anti-feline leukemia virus subgroup C cellular receptor 1

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About This Item

UNSPSC Code:
12352203
Human Protein Atlas Number:
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

product line

Prestige Antibodies® Powered by Atlas Antibodies

form

buffered aqueous glycerol solution

species reactivity

human

technique(s)

immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:50-1:200

immunogen sequence

KSDLRRHNINIGITNVDVKAIPADSPTDQEPKTVMLSKQSESAI

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... FLVCR1(28982)

General description

The gene FLVCR1 (feline leukemia virus subgroup C cellular receptor 1) is mapped to human chromosome 1q32. The gene encodes two proteins, FLVCR1a (a heme exporter in the plasma membrane) and FLVCR1b (a heme exporter in the mitochondria). FLVCR1a has 12 transmembrane domains and FLVCR1b has six transmembrane domains.

Immunogen

feline leukemia virus subgroup C cellular receptor 1 recombinant protein epitope signature tag (PrEST)

Application

All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project and as a result, are supported by the most extensive characterization in the industry.

The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. We also provide Prestige Antibodies® protocols and other useful information.

Biochem/physiol Actions

Both isoforms of FLVCR1 (feline leukemia virus subgroup C cellular receptor 1) help in maintaining heme concentration, thereby allowing proper expansion and differentiation of erythroid precursors. Downregulation or absence of FLVCR1′s activity results in diamond-Blackfan anemia. FLVCR1a was first recognized as a membrane receptor for feline leukemia virus subgroup C. Absence of FLVCR1a in mice causes hemorrhages, edema and skeletal abnormalities. On the other hand, absence of FLVCR1b results in mitochondrial heme accumulation and defects in erythroid differentiation. Mutation in the FLVCR1 gene is associated with posterior column ataxia and retinitis pigmentosa (PCARP).

Features and Benefits

Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.

Every Prestige Antibody is tested in the following ways:
  • IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
  • Protein array of 364 human recombinant protein fragments.

Linkage

Corresponding Antigen APREST78727

Physical form

Solution in phosphate buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide.

Legal Information

Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

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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Storage Class Code

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Mutations of FLVCR1 in posterior column ataxia and retinitis pigmentosa result in the loss of heme export activity.
Yanatori I, et al.
Blood Cells, Molecules and Diseases, 49, 60-66 (2012)
Alteration of heme metabolism in a cellular model of Diamond-Blackfan anemia.
Mercurio S, et al.
European Journal of Haematology, 96, 367-374 (2016)
The mitochondrial heme exporter FLVCR1b mediates erythroid differentiation.
Chiabrando D, et al.
The Journal of Clinical Investigation, 122, 4569-4579 (2012)
Anjali M Rajadhyaksha et al.
American journal of human genetics, 87(5), 643-654 (2010-11-13)
The study of inherited retinal diseases has advanced our knowledge of the cellular and molecular mechanisms involved in sensory neural signaling. Dysfunction of two specific sensory modalities, vision and proprioception, characterizes the phenotype of the rare, autosomal-recessive disorder posterior column
Sonia Mercurio et al.
Haematologica, 100(6), 720-729 (2015-03-22)
Feline leukemia virus subgroup C receptor 1 (Flvcr1) encodes two heme exporters: FLVCR1a, which localizes to the plasma membrane, and FLVCR1b, which localizes to mitochondria. Here, we investigated the role of the two Flvcr1 isoforms during erythropoiesis. We showed that

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