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Norbert Kartner

Researcher at University of Toronto

Publications -  52
Citations -  8919

Norbert Kartner is an academic researcher from University of Toronto. The author has contributed to research in topics: Cystic fibrosis transmembrane conductance regulator & P-glycoprotein. The author has an hindex of 31, co-authored 52 publications receiving 8786 citations. Previous affiliations of Norbert Kartner include Ontario Institute for Cancer Research.

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Cell surface P-glycoprotein associated with multidrug resistance in mammalian cell lines.

TL;DR: The plasma membranes of hamster, mouse, and human tumor cell lines that display multiple resistance to drugs were examined and increased expression of a 170,000-dalton surface antigen was found to be correlated with multidrug resistance.
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Purification and functional reconstitution of the cystic fibrosis transmembrane conductance regulator (CFTR)

TL;DR: In this paper, a recombinant CFTR protein from a high-level baculovirus-infected insect cell line was purified to homogeneity, and the protein exhibited regulated chloride channel activity, providing evidence that the protein itself is the channel.
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Detection of P-glycoprotein in multidrug-resistant cell lines by monoclonal antibodies

TL;DR: Monoclonal antibodies whose binding to plasma membranes of different multidrug-resistant mammalian cells correlates with the degree of drug resistance are produced and might serve as diagnostic reagents for clinically unresponsive tumours16.
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Amplification of P-glycoprotein genes in multidrug-resistant mammalian cell lines.

TL;DR: Southern blot analysis of hamster, mouse and human DNA using this cDNA as a probe showed that P-glycoprotein is conserved and is probably encoded by a gene family, and that members of this putative family are amplified in multidrug-resistant cells.
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Expression of the cystic fibrosis gene in non-epithelial invertebrate cells produces a regulated anion conductance

TL;DR: It is demonstrated that CFTR can function in heterologous nonepithelial cells and lend support to the possibility thatCFTR may itself be a regulated anion channel.