Inhibitor response

Proscar (Propecia) 2.8 (0.1) b b An anabolic steroid that acts as a 5-a-ieductase inhibitor responsible for the biotransformation of testosterone to dibydrotestosterone in the skin and prostate gland. 

D. D. Nguyen, X. Huang, D. W. Greve, and M. M. Domach. Fibroblast growth and h-7 protein kinase inhibitor response monitored in microimpedance sensor arrays. Biotechnol. Bioeng., 87 138—144, 2004. 

Two agents, oseltamivir and zanamivir, are approved for the management of Influenza A and B infection. Both are potent neuraminidase inhibitors responsible for inhibiting viral replication. These agents differ in their structural compounds, enabling oseltamavir to have greater bioavailabihty and be the only oral option. There have been no reports of nephrotoxicity with the use of either agent. 

There is evidence of racial differences in antihypertensive response to ACE inhibitors. Specifically, African-Americans in general are believed to have diminished antihypertensive responses to ACE inhibitors compared with Caucasians.The frequencies of many SNPs in the renin-angiotensin system vary between African-American and white populations and may contribute to the observed racial differences in ACE inhibitor response.Indeed, most racial differences in drug response probably can be attributed to racial differences in genotype frequencies, although this is yet to be determined. 

Pharmacology and Mechanism of Action. Phenobarbital may elevate seizure threshold by decreasing postsynaptic excitation, possibly by stimulating postsynaptic GABAergic inhibitor responses. ... 

Hagashihara E, Nutahara K, Takeuchi T, Nobyukis S, Araie M, Aso Y Calcium metabolism in acidotic patients induced by carbonic anhydrase inhibitors responses to citrate. J Urol 1991 145 942-948. 

Soreq, H. and Glick, D., Novel roles for cholinesterases in stress and inhibitor responses, in Cholinesterases and Cholinesterase Inhibitors Basic, Preclinical and Clinical Aspects, Giacobini, E., ed., Martin Dunitz, Ltd., London, 47-61, 2000. 

Structural alteration in PRPP synthetase appears to underlie enzyme superactivity in each family studied in detail,Evidence to support this contention is indirect, since no precise alteration in enzyme primary structure has been demonstrated. Nevertheless, each superactive enzyme studied in partially purified or homogenous preparation has shown at least one variant property in either electrophoretic mobility, thermal stabilitysubstrate affinity, inhibitor responsiveness, or immunochemical inactivation 11 1 when compared to normal enzyme of comparable purity. Moreover, the pattern of variant properties of each aberrant enzyme has been distinct indicating that enzyme superactivity can result from a diverse array of inherited structural changes in PRPP synthetase. 

PRPP synthetases. A. Enzyme activities in dialyzed hemolysates. Sigmoidal activation is seen for both enzymes. Activity of the mutant enzyme with an increased maximal reaction velocity is, however, increased by a constant proportion at all Pi concentrations. B. Enzyme activities in undialyzed (crude) hemolysates. The mutant enzyme, deficient in inhibitor responsiveness, shows hyperbolic activation with increased activity only at Pi concentrations below 2 mM. C. Enzyme activities in partially purified erythrocyte preparations from a normal individual and the patient with the feedback-resistant PRPP synthetase studied in B. Note hyperbolic activation of the purified normal enzyme and the resulting similarity of the Pi activation curves. D. Enzyme activities in dialyzed fibroblast extracts. The mutant enzyme, with combined increased maximal reaction velocity and diminished nucleotide responsiveness, shows both hyperbolic activation and increased enzyme activity at all Pi concentrations. 

Acetolactate synthase inhibitors, response patterns from metabolic profiling, 293,294/... 

Acetyl coenzyme A carboxylase inhibitors, response patterns from metabolic profiling, 293,294/ Acylcyclohexanedione(s), synthetic transformations, 247-253 2-Acylcyclohexane-l,4-dione, synthesis, 248-249... 

The DIFICI is closely related to the Turing instability (TI) [4], In both instabilities, the homogeneous and stable state of a system composed of an activator (a species that tends to grow autocatalytically) and an inhibitor (which suppresses the growth) may lose its stability through their differential transport by a differential bulk flow in the case of the DIFICI and by differential diffusivity in the TI. The ultimate cause in both instabilities is the inherent tendency of the activator to grow locally when decoupled spatially from the inhibitor response. 

We conclude this section by noting that the essential role of differential diffusion in the Turing case is to spatially decouple the activator from the inhibitor response, releasing locally the inherent tendency of the activator to grow. 

For comparison, Figure 4c represents the Turing instability (v = 0) with the curves parameterized by the ratio of diffusion coefficients 6. It illustrates the common feature of DIFICI and TI. Identical decay rates at A = 0 and maximal growth rates (= a 11) of perturbations at A = oo demonstrate the fact that the ultimate cause of the instabilities in both cases is the local activator kinetics when it is disengaged from the inhibitor response through differential transport. 

Fig. 22.3 Consensus effects of Spd and Spm on auxin metabolism and signaling cascade. Description is same as in legends to Fig. 22.1. AFB2 auxin signaling F-box protein 2, ARFs auxin response factors, Awc/IAA indole-3-acetic acid inducible (members of Aux/IAA protein family), AuxRE auxin response cu-elements, GH3 lAA-amido synthetase, lAMTl lAA carboxyl methyl transferase 1, ILL4 lAA amidohydrolase, LAX3 like AUXl 3, PGP 10 P-glycoprotein 10 (auxin efflux carrier), PINl PIN-formed 1, PINS PIN-formed 5, TIRl transport inhibitor response 1, YUC YUCCA...

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