Anti -FLVCR (Feline Leukemia Virus Subgroup C Receptor-related Protein 1, Feline Leukemia Virus Subgroup C Receptor, hFLVCR, FLVCR1)

For Research Use Only. Not for use in diagnostic procedures.

Chromosome: 1; NC_000001.10 (213031597..213072705). Location: 1q32.3

Polyclonal

IgG

Rabbit

Recognizes human FLVCR1.

Affinity Purified
Purified by Protein A affinity chromatography.

Supplied as a liquid in PBS, pH 7.2.

May be stored at 4 degree C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20 degree C. Aliquots are stable for at least 12 months. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Small volumes of anti-FLVCR1 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

FLVCR is responsible for exporting cytoplasmic heme. It may be required to protect developing erythroid cells from heme toxicity. It causes suceptibility to FeLV-C in vitro.

Antibodies; Abs to Cancer Markers, Leukemia

Western Blot (WB)

Suitable for use in Western Blot.

59,863 Da[Similar Products]

feline leukemia virus subgroup C cellular receptor 1

feline leukemia virus subgroup C receptor-related protein 1

Feline leukemia virus subgroup C receptor-related protein 1

FLVCR; Feline leukemia virus subgroup C receptor; hFLVCR??[Similar Products]

FLVC1_HUMAN

This gene encodes a member of the major facilitator superfamily of transporter proteins. The encoded protein is a heme transporter that may play a critical role in erythropoiesis by protecting developing erythroid cells from heme toxicity. This gene may play a role in posterior column ataxia with retinitis pigmentosa and the hematological disorder Diamond-Blackfan syndrome. [provided by RefSeq, Jan 2011]

Function: Isoform 1: Heme transporter that exports cytoplasmic heme. It can also export coproporphyrin and protoporphyrin IX, which are both intermediate products in the heme biosynthetic pathway. Does not export bilirubin. Heme export depends on the presence of HPX and may be required to protect developing erythroid cells from heme toxicity. Heme export also provides protection from heme or ferrous iron toxicities in liver and brain. Causes susceptibility to FeLV-C in vitro. Required during er****opoiesis to maintain intracellular free heme balance since in proerythroblasts, heme synthesis intensifies and it's accumulation is toxic for cells. Ref.1 Ref.7 Ref.12 Ref.15Isoform 2: Heme transporter that promotes heme efflux from the mitochondrion to the cytoplasm. Essential for erythroid differentiation. Ref.1 Ref.7 Ref.12 Ref.15

Subunit structure: Interacts with HPX. Ref.12

Subcellular location: Isoform 1: Cell membrane; Multi-pass membrane protein

By similarity Ref.8 Ref.15. Isoform 2: Mitochondrion membrane; Multi-pass membrane protein

By similarity Ref.8 Ref.15.

Tissue specificity: Found all hematopoietic tissues including peripheral blood lymphocytes. Some expression is found in pancreas and kidney. Ref.1

Developmental stage: Down-regulated in haemopoietic progenitor cells undergoing differentiation and hemoglobinization. Abundant in fetal liver. Ref.7

Post-translational modification: N-Glycosylated. Ref.8

Involvement in disease: Posterior column ataxia with retinitis pigmentosa (PCARP) [MIM:609033]: A neurodegenerative syndrome beginning in infancy with areflexia and retinitis pigmentosa. Nyctalopia (night blindness) and peripheral visual field loss are usually evident during late childhood or teenage years, with subsequent progressive constriction of the visual fields and loss of central retinal function over time. A sensory ataxia caused by degeneration of the posterior columns of the spinal cord results in a loss of proprioceptive sensation that is clinically evident in the second decade of life and gradually progresses. Scoliosis, camptodactyly, achalasia, gastrointestinal dysmotility, and a sensory peripheral neuropathy are variable features of the disease. Affected individuals have no clinical or radiological evidence of cerebral or cerebellar involvement.Note: The disease is caused by mutations affecting the gene represented in this entry. Defective neuronal heme transmembrane export due to FLVCR1 mutations may abrogate the neuroprotective effects of neuroglobin and initiate an apoptotic cascade that results in the selective degeneration of photoreceptors in the neurosensory retina and sensory neurons in the posterior spinal cord. Ref.16 Ref.17

Sequence similarities: Belongs to the major facilitator superfamily. Feline leukemia virus subgroup C receptor (TC 2.A.1.28.1) family. [View classification]

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