Source:http://linkedlifedata.com/resource/pubmed/id/15463143
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
10
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| pubmed:dateCreated |
2004-10-6
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| pubmed:abstractText |
The development of new and effective ontiprotozool drugs has been difficult because of the close metabolic relationship between protozoa and mammalian cells. In this article, Michael Riscoe, Al Ferro and john Fitchen present their hypothesis for chemotherapeutic exploitation of methylthioribose (MTR) kinase, an enzyme critical to methionine salvage in certain protozoa. They propose that analogues of MTR if properly designed, would be converted to toxic products in organisms that contain MTR kinase but not in mammalian cells, which lack this enzyme.
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| pubmed:commentsCorrections | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:status |
PubMed-not-MEDLINE
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| pubmed:month |
Oct
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| pubmed:issn |
0169-4758
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
5
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
330-3
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| pubmed:year |
1989
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| pubmed:articleTitle |
Methionine recycling as a target for antiprotozoal drug development.
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| pubmed:affiliation |
M. Riscoe and J. Fitchen are at the Medical Research Service, Veterans Administration Medical Center, Portland, OR 97207, USA.
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| pubmed:publicationType |
Journal Article
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