Stimulation of amino acid transport in Saccharomyces cerevisiae by metabolic inhibitors
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články
PubMed
357269
DOI
10.1007/bf02876682
Knihovny.cz E-zdroje
- MeSH
- adenosintrifosfát metabolismus MeSH
- aktivní transport účinky léků MeSH
- aminokyseliny metabolismus MeSH
- antimycin A farmakologie MeSH
- dicyklohexylkarbodiimid farmakologie MeSH
- jodacetamid farmakologie MeSH
- karbonylkyanid-m-chlorfenylhydrazon farmakologie MeSH
- kinetika MeSH
- leucin metabolismus MeSH
- Saccharomyces cerevisiae metabolismus MeSH
- uran farmakologie MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- adenosintrifosfát MeSH
- aminokyseliny MeSH
- antimycin A MeSH
- dicyklohexylkarbodiimid MeSH
- jodacetamid MeSH
- karbonylkyanid-m-chlorfenylhydrazon MeSH
- leucin MeSH
- uran MeSH
Inhibitors of energy metabolism (3-chlorophenylhydrazonomalononitrile, antimycin A, iodoacetamide, dicyclohexylcarbodiimide) but not of transport (uranyl ions) stimulate at low concentrations the uptake of L-leucine, L-glutamic acid, L-arginine and, to a lesser degree, of 2-aminoisobutyric acid in Saccharomyces cerevisiae. The effect is apparent only after augmenting the energy reserves of cells by preincubation with D-glucose or, more strikingly, with ethanol. It is absent in a mutant (op1) lacking the translocation system for ADP--ATP in mitochondria. The presence of two different energy reserves for amino acid transport is indicated (one in energy-poor, the other in energy-rich cells). The stimulating effect appears to be caused by a retarded degradation of the transport proteins as occurs at a lowered level of mitochondria-produced ATP.
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