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Human Polyclonal FLVCR1 Primary Antibody for ELISA, WB - ABIN250325
Quigley, Yang, Worthington, Phillips, Sabo, Sabath, Berg, Sassa, Wood, Abkowitz: Identification of a human heme exporter that is essential for erythropoiesis. in Cell 2004
Show all 2 Pubmed References
Human Monoclonal FLVCR1 Primary Antibody for RNAi, ELISA - ABIN565398
Alves, Costa, Sorgine, Nascimento-Silva, Teodosio, Bárcena, Castro-Faria-Neto, Bozza, Orfao, Oliveira, Maya-Monteiro: Heme-oxygenases during erythropoiesis in K562 and human bone marrow cells. in PLoS ONE 2011
Cat (Feline) Polyclonal FLVCR1 Primary Antibody for ELISA, WB - ABIN547368
Rey, Duffy, Brown, Kennedy, Dick, Dror, Tailor: Enhanced alternative splicing of the FLVCR1 gene in Diamond Blackfan anemia disrupts FLVCR1 expression and function that are critical for erythropoiesis. in Haematologica 2008
This is the first time that FLVCR expression has been investigated in bovine tissues and the first to suggest that expression could be increased in cancers.
Altogether, these findings showed a direct association between FLVCR1 mRNA levels and hyperglycemia, suggesting that increased adipose tissue heme exportation might disrupt, or is the consequence of, impaired systemic glucose metabolism during the progression to type 2 diabetes.
Mutation in FLVCR1 gene is associated with Posterior column ataxia with retinitis pigmentosa coexisting with sensory-autonomic neuropathy and leukemia.
Using fibroblasts and lymphoblastoid cell lines from patients with sensory neurodegeneration, we here show that the FLVCR1-mutations reduce heme export activity, enhance oxidative stress and increase sensitivity to programmed cell death. Our data link heme metabolism to sensory neuron maintenance and suggest that intracellular heme overload causes early-onset degeneration of pain-sensing neurons in humans
RPS19-downregulated erythroleukemia cells show reduced FLVCR1a and FLVCR1b mRNA levels associated with heme overload.
Data shows that FLVCR1a participates in the control of intestinal mucosa homeostasis by exporting the excess of de novo synthesized heme from intestinal cells.
Flvcr1 regulates differentiation of erythroid progenitors by controlling intracellular heme accumulation.
both HIF2alpha and ETS1 are involved in the transcriptional regulation of Flvcr1a and that HIF2alpha is absolutely required for Flvcr1a induction upon hypoxia
FLVCR1b regulates erythropoiesis by controlling mitochondrial heme efflux, whereas FLVCR1a expression is required to prevent hemorrhages and edema.
FLVCR1 mutants failed to fold properly in the ER, were rapidly degraded in the lysosomes, and therefore, could not export heme out of cells. Thus, accumulation of heme in FLVCR1-mutant cells could cause cellular toxicity.
Study identified sequence variants in the known disease-causing genes SLC6A3 and FLVCR1, and present evidence to strongly support the pathogenicity of variants identified in TUBGCP6, BRAT1, SNIP1, CRADD, and HARS.
Posterior column ataxia with retinitis pigmentosa is caused by mutations in FLVCR1.
relative protein expression of 2 heme transporters, Feline Leukemia Virus, Subgroup C, Receptor 1 (FLVCR1) and Breast Cancer Resistance Protein, was assessed in placental tissue in relation to maternal/neonatal iron status and placental iron concentration
These results suggest that aberrant FLVCR1 causes a selective degeneration of a subpopulation of neurons in the retina and the posterior columns of the spinal cord via dysregulation of heme or iron homeostasis.
hemopexin directly interacts with FLVCR
the FLVCR gene on 1q31 is not involved in Diamond-Blackfan anemia in families studied
results suggest that multiple FLVCR1 regions are critical for mediating efficient feline leukemia virus subgroup C (FeLV-C) infection and that these regions are distinct from the FeLV-C envelope binding site
Alternative splicing of FLVCR1 transcripts and subsequent FLVCR1 insufficiency is an additional contributing factor to the erythropoietic defect observed in Diamond-Blackfan anemia.
study found that primary and immortalized murine macrophages downregulate Flvcr mRNA levels upon LPS stimulation; findings point to a new role for FLVCR and heme export in macrophages responses to infection and inflammation
These studies identify a novel and unexpected role for FLVCR, a major facilitator superfamily metabolite transporter, in T cell development
Flvcr1a maintains a free heme pool that regulates heme synthesis and degradation as well as cytochromes P450 expression and activity.
FLVCR is redundant in stem cells but has critical and contrasting stage-specific roles in discrete hematopoietic lineages
Hemochromatosis is associated not only with excessive accumulation of free iron in the retina and retinal pigment epithelium but also with excessive accumulation of heme.
data show that FLVCR exports heme & is required by erythroid progenitors to complete terminal differentiation; data show that FLVCR functions in macrophage heme-iron recycling and that systemic iron balance involves heme-iron trafficking via FLVCR
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.
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-like
, feline leukemia virus subgroup C cellular receptor
, eline leukemia virus subgroup C cellular receptor 1