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Biological redox reactions require electron donors and acceptor. Zusätzlich bieten wir Ihnen G Protein-Coupled Receptor 172B Antikörper (42) und G Protein-Coupled Receptor 172B Kits (4) und viele weitere Produktgruppen zu diesem Protein an.
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We here report a case of transient MADD, caused by a heterozygous intronic variation, c.1134+11G>A, in the SLC52A1 gene encoding RFVT1. This variation creates a binding site for the splice inhibitory hnRNP A1 protein and causes exon 4 skipping. Riboflavin deficiency and maternal malnutrition during pregnancy might have been the determining factor in the outcome of this case.
In HT-29 cells, the RFVT1 protein level was drastically lower. In tumor tissues of patients with CRC, RFVT1 content was reduced at both protein and mRNA levels compared to normal mucosa.
results are the first to reveal the identity of the minimal SLC52A1 promoter and to establish an important role for Sp-1 in its activity
data suggest that MMND is a distinct clinical subgroup of childhood onset MND patients where the known genetic defects are so far negative.
summary of recent findings on the cloning, nomenclature, functional characterization and genetic diseases of RFVT1/SLC52A1, RFVT2/SLC52A2 and RFVT3/SLC52A3 [review]
Intestinal riboflavin uptake process undergoes differentiation-dependent upregulation and suggest that this is mediated (at least in part) via transcriptional mechanisms of SLC52A1 and SLC52A3.
We demonstrated that TFAP-2gamma is one of the transcription factors involved in the PAR-2 expression in human villous trophoblast cells.
Identification/characterization riboflavin trasporter (RFT1) as a novel riboflavin transporter.
mRFVT2 was involved in hepatic riboflavin homeostasis
Biological redox reactions require electron donors and acceptor. Vitamin B2 is the source for the flavin in flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN) which are common redox reagents. This gene encodes a member of the riboflavin (vitamin B2) transporter family. Haploinsufficiency of this protein can cause maternal riboflavin deficiency. Multiple alternatively spliced variants, encoding the same protein, have been identified.
G protein-coupled receptor 172B
, G protein-coupled receptor 172A
, riboflavin transporter 1
, G-protein coupled receptor GPCR42
, PERV-A receptor 2
, porcine endogenous retrovirus A receptor 2
, solute carrier family 52, riboflavin transporter, member 1
, PERV-A receptor
, endogenous retrovirus A receptor
, PERV-A receptor 2 homolog
, porcine endogenous retrovirus A receptor 2 homolog
, solute carrier family 52, riboflavin transporter, member 2