Publication: Improper protein trafficking contributes to artemisinin sensitivity in cells lacking the KDAC Rpd3p
Issued Date
2014-11-03
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ISSN
18733468
00145793
00145793
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2-s2.0-84908248007
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Mahidol University
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SCOPUS
Bibliographic Citation
FEBS Letters. Vol.588, No.21 (2014), 4018-4025
Suggested Citation
Amornrat Naranuntarat Jensen, Worathad Chindaudomsate, Kanate Thitiananpakorn, Skorn Mongkolsuk, Laran T. Jensen Improper protein trafficking contributes to artemisinin sensitivity in cells lacking the KDAC Rpd3p. FEBS Letters. Vol.588, No.21 (2014), 4018-4025. doi:10.1016/j.febslet.2014.09.021 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/33209
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Title
Improper protein trafficking contributes to artemisinin sensitivity in cells lacking the KDAC Rpd3p
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Abstract
© 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. Lysine deacetylases (KDACs) inhibitors may have therapeutic value in anti-malarial combination therapies with artemisinin. To evaluate connections between KDACs and artemisinin, Saccharomyces cerevisiae deletion mutants in KDAC genes were assayed. Deletion of RPD3, but not other KDAC genes, resulted in strong sensitivity to artemisinin, which was also observed in sit4Δ mutants with impaired endoplasmic reticulum (ER) to Golgi protein trafficking. Decreased accumulation of the transporters Pdr5p, Fur4p, and Tat2p was observed in rpd3Δ and sit4Δ cells. The unfolded protein response is induced in rpd3Δ cells consistent with retention of proteins in the ER. Disruption of protein trafficking appears to sensitize cells to artemisinin and targeting these pathways may be useful as part of artemisinin based anti-malarial therapy.