Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3056268 | Experimental Neurology | 2009 | 5 Pages |
Abstract
This study reports that the cysteine 22 → glycine 22 substitution in the HIV-1 Tat 1–86 B significantly attenuates its neurotoxicity. Consistent with previous studies, direct interactions of rat hippocampal cells with Tat 1–86 B were shown to cause dose-dependent and time-dependent neurotoxicity associated with activation of caspases from the mitochondrial apoptotic pathway. Despite the similar binding/uptake properties, Cys22 Tat 1–86 B failed to induce significant neurotoxicity and activation of caspases 9 and 3/7 in hippocampal primary cultures. Results of the study underscore the important role of cysteine-rich domain in mechanism of Tat-mediated neurotoxicity.
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Authors
Michael Y. Aksenov, Marina V. Aksenova, Charles F. Mactutus, Rosemarie M. Booze,