The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Regulation of primary alkylsulfatase induction in Pseudomonas C12B: concentration-dependent stimulation-inhibition by exogenous UTP and sodium acetate and inhibition by 1-hexanol.

Pseudomonas C12B, an isolate from detergent-enriched soil, synthesized primary alkylsulfatase in response to sodium hexan-1-yl sulfate as the inducer. The induction of this enzyme was inhibited by exogenous 1 mM UTP but not by ATP or other nucleoside triphosphates. The uridine nucleotide was about 10-fold more effective than other uracil-related effectors and the ability of the nucleotide (0.1-1.0 mM) to inhibit induction was dependent upon the presence of added Mg2+. At concentrations less than 0.1 mM, UTP stimulated induction and the extent of this effect was also Mg2+ dependent. Marked stimulation of induction also occurred in response to low (less than or equal to 2.5 mM) concentrations of acetate, citrate, and succinate. However, only acetate inhibited induction (by 64%) at higher (20 mM) concentrations. 1-Hexanol was a more effective inhibitor. An 80% reduction in activity was recorded after exposure of cells to 5 mM 1-hexanol. At this concentration, 2-hexanol was without effect and 3-hexanol inhibited induction by 35%. Simultaneous exposure of the cells to 2,4-dinitrophenol failed to reverse hexanol- or acetate-mediated inhibition. It is suggested that 1-hexanol per se regulates alkylsylfatase induction and immediate product inhibition was proposed as a term to describe this type of inhibition.[1]

References

 
WikiGenes - Universities