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Mouse Anti-FLVCR1 Recombinant Antibody (CBXF-0768) (CBMAB-F0927-CQ)

This product is a mouse antibody that recognizes FLVCR1. The antibody CBXF-0768 can be used for immunoassay techniques such as: WB.
See all FLVCR1 antibodies
Published Data
Fig.1 Western blot analysis of HA-tagged E3−, E3−E6−, and hFLVCR1 proteins in cell lysate fractions from FLVCR1-transduced MDTF cells.
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Fig.2 Western blot with antibodies against hFLVCR1.
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Summary

Host Animal
Mouse
Specificity
Human
Clone
CBXF-0768
Antibody Isotype
IgG2b
Application
WB

Basic Information

Specificity
Human
Antibody Isotype
IgG2b
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Concentration
1 mg/mL
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
feline leukemia virus subgroup C cellular receptor 1
Introduction
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.
Entrez Gene ID
28982
UniProt ID
Q9Y5Y0
Alternative Names
Feline Leukemia Virus Subgroup C Cellular Receptor 1; FLVCR; Feline Leukemia Virus Subgroup C Receptor-Related Protein 1; Ataxia, Posterior Column 1, With Retinitis Pigmentosa; Feline Leukemia Virus Subgroup C Receptor; MFSD7B;
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 is required to maintain intracellular free heme balance, protecting cells from heme toxicity. Heme export provides protection from heme or ferrous iron toxicities in liver, brain, sensory neurons and during erythtopoiesis, a process in which heme synthesis intensifies. Causes susceptibility to FeLV-C in vitro.

Isoform 2:
Heme transporter that promotes heme efflux from the mitochondrion to the cytoplasm. Essential for erythroid differentiation.
Biological Process
Blood vessel development Source: Ensembl
Cellular iron ion homeostasis Source: Reactome
Embryonic digit morphogenesis Source: Ensembl
Embryonic skeletal system morphogenesis Source: Ensembl
Erythrocyte differentiation Source: MGI
Erythrocyte maturation Source: UniProtKB-KW
Head morphogenesis Source: Ensembl
Heme biosynthetic process Source: Reactome
Heme export Source: UniProtKB
Heme transport Source: MGI
In utero embryonic development Source: Ensembl
Mitochondrial transport Source: MGI
Multicellular organism growth Source: Ensembl
Regulation of organ growth Source: Ensembl
Spleen development Source: Ensembl
Cellular Location
Isoform 1: Cell membrane
Isoform 2: Mitochondrion membrane
Involvement in disease
Posterior column ataxia with retinitis pigmentosa (PCARP):
The disease is caused by variants 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. 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. Defects in FLVCR1 are a cause of a sensory neuropathy resulting in pain insensitivity. Patients have decreased sensing of pain, temperature and touch. Self-injury, ulcers and amputations are commonly observed in affected individuals.
Topology
Cytoplasmic: 1-107
Helical: 108-128
Extracellular: 129-147
Helical: 148-168
Cytoplasmic: 169-174
Helical: 175-195
Extracellular: 196-199
Helical: 200-220
Cytoplasmic: 221-240
Helical: 241-261
Extracellular: 262-275
Helical: 276-296
Cytoplasmic: 297-331
Helical: 332-352
Extracellular: 353-372
Helical: 373-393
Cytoplasmic: 394-401
Helical: 402-422
Extracellular: 423-424
Helical: 425-445
Cytoplasmic: 446-459
Helical: 460-480
Extracellular: 481-490
Helical: 491-511
Cytoplasmic: 512-555
PTM
N-Glycosylated.

Sheykhhasan, M., Tanzadehpanah, H., Ahmadieh Yazdi, A., Mahaki, H., Seyedebrahimi, R., Akbari, M., ... & Dama, P. (2022). FLVCR1-AS1 and FBXL19-AS1: Two Putative lncRNA Candidates in Multiple Human Cancers. Non-Coding RNA, 9(1), 1.

Han, Y., Wang, X., Mao, E., Shen, B., & Huang, L. (2021). lncRNA FLVCR1‑AS1 drives colorectal cancer progression via modulation of the miR‑381/RAP2A axis. Molecular Medicine Reports, 23(2), 1-1.

Pan, Z., Ding, J., Yang, Z., Li, H., Ding, H., & Chen, Q. (2020). LncRNA FLVCR1-AS1 promotes proliferation, migration and activates Wnt/β-catenin pathway through miR-381-3p/CTNNB1 axis in breast cancer. Cancer Cell International, 20, 1-12.

Yan, Z., Zhang, W., Xiong, Y., Wang, Y., & Li, Z. (2020). Long noncoding RNA FLVCR1-AS1 aggravates biological behaviors of glioma cells via targeting miR-4731-5p/E2F2 axis. Biochemical and biophysical research communications, 521(3), 716-720.

Yan, H., Li, H., Silva, M. A., Guan, Y., Yang, L., Zhu, L., ... & Ren, C. (2019). LncRNA FLVCR1-AS1 mediates miR-513/YAP1 signaling to promote cell progression, migration, invasion and EMT process in ovarian cancer. Journal of Experimental & Clinical Cancer Research, 38(1), 1-13.

Liu, Y., Guo, G., Zhong, Z., Sun, L., Liao, L., Wang, X., ... & Chen, H. (2019). Long non-coding RNA FLVCR1-AS1 sponges miR-155 to promote the tumorigenesis of gastric cancer by targeting c-Myc. American Journal of Translational Research, 11(2), 793.

Bao, W., Cao, F., Ni, S., Yang, J., Li, H., Su, Z., & Zhao, B. (2019). lncRNA FLVCR1‑AS1 regulates cell proliferation, migration and invasion by sponging miR‑485‑5p in human cholangiocarcinoma. Oncology letters, 18(3), 2240-2247.

Zhang, K., Zhao, Z., Yu, J., Chen, W., Xu, Q., & Chen, L. (2018). LncRNA FLVCR1‐AS1 acts as miR‐513c sponge to modulate cancer cell proliferation, migration, and invasion in hepatocellular carcinoma. Journal of cellular biochemistry, 119(7), 6045-6056.

Gao, X., Zhao, S., Yang, X., Zang, S., & Yuan, X. (2018). Long non-coding RNA FLVCR1-AS1 contributes to the proliferation and invasion of lung cancer by sponging miR-573 to upregulate the expression of E2F transcription factor 3. Biochemical and biophysical research communications, 505(3), 931-938.

Peng, C., Song, Y., Chen, W., Wang, X., Liu, X., Wang, F., ... & Gao, C. (2018). FLVCR1 promotes the proliferation and tumorigenicity of synovial sarcoma through inhibiting apoptosis and autophagy. International Journal of Oncology, 52(5), 1559-1568.

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For research use only. Not intended for any clinical use.

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