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MRP6Multidrug Resistance Protein 6
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5C indicated that only DADS stimulated MRP3 gene expression and showed that DADS and DATS promoted MRP4 and MRP6 gene expression as seen in Fig.
In the in vitro studies, we showed that colo 205 cells after exposure to DAS, DADS and DATS for 24 and 48 h that DAS and DADS promoted Mdr3 gene expression at the 48 h treatment but did not affect MRP1, MRP4 and MRP6 gene expression levels (Fig.
Genotype group A consisted of patients who were homozygous or compound heterozygous for mutations likely to produce either no MRP6 protein or no functional MRP6, whereas genotype group B consisted of patients with an MRP6 enzyme with reduced activity due to missense mutations.
The effect was even more pronounced in patients who were likely to have either no MRP6 protein or no functional MRP6 because of nonsense, frameshift, or splice site mutations, thus indicating a compound effect of PXE genotype and variation in genes encoding antioxidant enzymes.
Nevertheless, the connection between MRP6 deficiency and oxidative stress remains unclear.
Furthermore, the data indicated that MRP3 may contribute to the drug-resistant phenotype in EPP85-181RDB, EPP85-181RNOV and HT-29RNOV cells as well as that MRP6 may be involved in the MDR of the cell line HT-29RDB.
The implication of a defect or deficiency of MRP6 in the development of PXE, especially in the mineralization process, is still unknown.
Thus, the identification of the physiological substrate of MRP6 will shed light on the role of SPP1 and other extracellular matrix proteins in PXE.
Expression of human MRP6, a homologue of the multidrug resistance protein gene MRP1, in tissues and cancer cells.
Because of the minor amount of MRP6 produced in tissues frequently affected, PXE was considered a metabolic disorder with undetermined circulating molecules leading to the mineralization of elastic fibers in the skin, Bruch's membrane, and vessel walls (4, 14, 18).
The question is whether an MRP6 deficiency has an effect on the production of proteins that are actively involved in inhibiting calcification.