Changing the Subcellular Location of the Oncoprotein Bcr-Abl Using Rationally Designed Capture Motifs |
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| Authors: | Andrew S. Dixon Jonathan E. Constance Tomoyuki Tanaka Terence H. Rabbitts Carol S. Lim |
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| Affiliation: | (1) Department of Pharmaceutics and Pharmaceutical Chemistry College of Pharmacy, University of Utah, 421 Wakara Way, Rm. 318, Salt Lake City, Utah 84108, USA;(2) Department of Pharmacology and Toxicology, College of Pharmacy, University of Utah, Salt Lake City, Utah 84108, USA;(3) Section of Experimental Therapeutics Leeds Institute of Molecular Medicine, St. James’s University Hospital, Leeds, LS9 7TF, UK; |
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| Abstract: | Purpose Bcr-Abl, the causative agent of chronic myelogenous leukemia (CML), localizes in the cytoplasm where its oncogenic signaling leads to proliferation of cells. If forced into the nucleus Bcr-Abl causes apoptosis. To achieve nuclear translocation, binding domains for capture of Bcr-Abl were generated and attached to proteins with signals destined for the nucleus. These resulting proteins would be capable of binding and translocating endogenous Bcr-Abl to the nucleus. |
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