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Drosophila melanogaster deoxyribonucleoside kinase activates gemcitabine

Knecht, Wolfgang LU ; Mikkelsen, Nils Egil ; Clausen, Anders Ranegaard LU ; Willer, Mette ; Eklund, Hans ; Gojkovic, Zoran and Piskur, Jure LU (2009) In Biochemical and Biophysical Research Communications 382(2). p.430-433
Abstract
Drosophila melanogaster multisubstrate deoxyribonucleoside kinase (Dm-dNK) can additionally sensitize human cancer cell lines towards the anti-cancer drug gemcitabine. We show that this property is based on the Dm-dNK ability to efficiently phosphorylate gemcitabine. The 2.2 angstrom resolution structure of DmdNK in complex with gemcitabine shows that the residues Tyr70 and Arg105 play a crucial role in the firm positioning of gemcitabine by extra interactions made by the fluoride atoms. This explains why gemcitabine is a good substrate for Dm-dNK(. (C) 2009 Elsevier Inc. All rights reserved.
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author
; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Structure-function relationship, Salvage pathway, Cancer, Gene-therapy, Nucleoside analogs, Deoxyribonucleoside kinase
in
Biochemical and Biophysical Research Communications
volume
382
issue
2
pages
430 - 433
publisher
Elsevier
external identifiers
  • wos:000265279300039
  • scopus:63349095879
ISSN
1090-2104
DOI
10.1016/j.bbrc.2009.03.041
language
English
LU publication?
yes
id
bf59b6d7-c510-41e2-9613-dee11d62665f (old id 1400387)
date added to LUP
2016-04-01 13:37:34
date last changed
2022-01-27 20:15:03
@article{bf59b6d7-c510-41e2-9613-dee11d62665f,
  abstract     = {{Drosophila melanogaster multisubstrate deoxyribonucleoside kinase (Dm-dNK) can additionally sensitize human cancer cell lines towards the anti-cancer drug gemcitabine. We show that this property is based on the Dm-dNK ability to efficiently phosphorylate gemcitabine. The 2.2 angstrom resolution structure of DmdNK in complex with gemcitabine shows that the residues Tyr70 and Arg105 play a crucial role in the firm positioning of gemcitabine by extra interactions made by the fluoride atoms. This explains why gemcitabine is a good substrate for Dm-dNK(. (C) 2009 Elsevier Inc. All rights reserved.}},
  author       = {{Knecht, Wolfgang and Mikkelsen, Nils Egil and Clausen, Anders Ranegaard and Willer, Mette and Eklund, Hans and Gojkovic, Zoran and Piskur, Jure}},
  issn         = {{1090-2104}},
  keywords     = {{Structure-function relationship; Salvage pathway; Cancer; Gene-therapy; Nucleoside analogs; Deoxyribonucleoside kinase}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{430--433}},
  publisher    = {{Elsevier}},
  series       = {{Biochemical and Biophysical Research Communications}},
  title        = {{Drosophila melanogaster deoxyribonucleoside kinase activates gemcitabine}},
  url          = {{http://dx.doi.org/10.1016/j.bbrc.2009.03.041}},
  doi          = {{10.1016/j.bbrc.2009.03.041}},
  volume       = {{382}},
  year         = {{2009}},
}