Guido J.R. Zaman

TL;DR: The complementary DNA for rat cmoat, a homolog of the human multidrug resistance gene (hMRP1), was isolated and shown to be expressed in the canalicular membrane of hepatocytes and likely accounts for the TR− phenotype.

TL;DR: It is demonstrated that overexpression of the MRP gene in human cancer cells increases the ATP-dependent glutathione S-conjugate carrier activity in plasma membrane vesicles isolated from these cells, suggesting that MRP can cause multidrug resistance by promoting the export of drug modification products from cells.

TL;DR: It is demonstrated that depletion of intracellular glutathione by DL-buthionine (S,R)-sulfoximine results in a complete reversal of resistance to doxorubicin, daunorubICin, vincristine, and VP-16 in lung carcinoma cells transfected with a MRP cDNA expression vector, and this results support the hypothesis that MRP functions as a glutATHione S-conjugate carrier.

TL;DR: The presence of MRP in bronchiolar epithelium, heart muscle, and macrophages would agree with the glutathione S-conjugate carrier activity previously detected in these cells, and in 46 of 119 untreated tumors from various histogenetic origins MRP staining was seen.

TL;DR: The results suggest that this ubiquitous GS-X pump, which mediates the cellular excretion of many drugs, glutathione S-conjugates of lipophilic xenobiotics and endogenous cysteinyl leukotrienes, is dispensable in mice, making treatment of MDR with MRP-specific reversal agents potentially feasible.