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Carol O. Cardarelli

Researcher at Laboratory of Molecular Biology

Publications -  31
Citations -  4686

Carol O. Cardarelli is an academic researcher from Laboratory of Molecular Biology. The author has contributed to research in topics: Multiple drug resistance & Drug resistance. The author has an hindex of 23, co-authored 31 publications receiving 4593 citations. Previous affiliations of Carol O. Cardarelli include Johns Hopkins University School of Medicine & National Institutes of Health.

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Expression of a full-length cDNA for the human "MDR1" gene confers resistance to colchicine, doxorubicin, and vinblastine

TL;DR: The construction of a full-length cDNA is reported for the human MDR1 gene and it is shown that this reconstructed cDNA, when inserted into a retroviral expression vector containing the long terminal repeats of Moloney leukemia virus or Harvey sarcoma virus, functions to confer the complete multidrug-resistance phenotype.
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HIV-1 protease inhibitors are substrates for the MDR1 multidrug transporter.

TL;DR: It is indicated that cells in patients that express the MDR1 transporter will be relatively resistant to the anti-viral effects of the HIV-1 protease inhibitors, and that absorption, excretion, and distribution of these inhibitors in the body may be affected by the multidrug transporter.
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Multiple drug-resistant human KB carcinoma cells independently selected for high-level resistance to colchicine, adriamycin, or vinblastine show changes in expression of specific proteins.

TL;DR: It is suggested that only a limited number of protein changes occur in multidrug-resistant cell lines, which are associated with a loss of translatable mRNA for these proteins.
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Partial purification and reconstitution of the human multidrug-resistance pump: characterization of the drug-stimulatable ATP hydrolysis.

TL;DR: It is demonstrated that the partially purified P-glycoprotein, when reconstituted in an artificial membrane, catalyzes drug-stimulated ATP hydrolysis, similar to other ion-transporting ATPases.
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α-Galactosidase A deficient mice: A model of Fabry disease

TL;DR: The similarity of the pathophysiological process in the mutant mice and in patients with Fabry disease is indicated, indicating the importance of an animal model for exploring therapeutic strategies for patients withFabry disease.