K
Kai Zhang
Researcher at Texas Tech University
Publications - 50
Citations - 1378
Kai Zhang is an academic researcher from Texas Tech University. The author has contributed to research in topics: Leishmania & Leishmania major. The author has an hindex of 16, co-authored 37 publications receiving 1187 citations. Previous affiliations of Kai Zhang include The Catholic University of America & Washington University in St. Louis.
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Journal ArticleDOI
Divergent Regulation of Dihydrofolate Reductase Between Malaria Parasite and Human Host
Kai Zhang,Pradipsinh K. Rathod +1 more
TL;DR: Antifolate treatment does not relieve translational inhibition and parasites cannot replenish dead enzyme, and selectivity may also arise through previously unappreciated differences in regulation of this drug target.
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Sphingolipids are essential for differentiation but not growth in Leishmania
TL;DR: It is suggested that SL‐deficient Leishmania provide a useful biological setting for tests of essential SL enzymes in other organisms where SL perturbation is lethal.
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Redirection of sphingolipid metabolism toward de novo synthesis of ethanolamine in Leishmania
Kai Zhang,Justine M Pompey,Fong-Fu Hsu,Phillip Key,Padmavathi Bandhuvula,Julie D. Saba,John Turk,Stephen M. Beverley +7 more
TL;DR: Leishmania has undergone two major metabolic shifts: first in de‐emphasizing the metabolic roles of SLs themselves in growth, signaling, and maintenance of membrane microdomains, and second, freed of typical SL functional constraints and a lack of alternative routes to produce EtN, Leishmania redirected SL metabolism toward bulk EtN synthesis.
Journal ArticleDOI
Phospholipid and sphingolipid metabolism in Leishmania
Kai Zhang,Stephen M. Beverley +1 more
TL;DR: In Leishmania, the composition, metabolism, and function of PLs and SLs differ significantly from those in mammalian cells, and available data suggest many steps of PL/SL metabolism are critical for LeishMania viability and/or virulence, and could be a source for new drug targets.
Journal ArticleDOI
Leishmania salvage and remodelling of host sphingolipids in amastigote survival and acidocalcisome biogenesis.
Kai Zhang,Fong-Fu Hsu,David A. Scott,David A. Scott,Roberto Docampo,John Turk,Stephen M. Beverley +6 more
TL;DR: It is shown thatnull mutants defective in de novo sphingoid base synthesis (spt2–) lacked SLs but grew well and retained lipid rafts while replicating as promastigotes in vitro, and retained the ability to enter macrophages silently and inhibit activation, although as expected most parasites were destroyed.