MgF3- presents both the correct geometry and the charge to mimic the PO3- group in flight, and so is particularly interesting to characterize as a potentially highly accurate transition state analogue (TSA). In this article, we provide a kinetic analysis of fluoride inhibition of beta-phosphoglucomutase that allows us to measure the stability constant and characteristics of the formation of the transition state analogue (MgF3-). The detailed kinetic analysis shows how a special type of TSA (MgF3-) that does not exist in solution is assembled in the active site of an enzyme.
COBISS.SI-ID: 26007001
Aflatoxin B1 reversibly inhibits cholinesterases by binding to a peripheral site of different species of cholinesterases. Electric eel enzyme was best inhibited with a binding constant of 0.35 microM. This binding prevents the entrance of substrate to the catalytic site and also decreases chemical steps of the reaction at the catalytic site. Electric eel enzyme was used to settle an amperometric biosensor. The best detection was obtained by using 0.3 mU enzyme on the electrode and 0.5mM ATCh in the solution. The limit of detection was 3 microM corresponding to 20% inhibition.
COBISS.SI-ID: 26328281
Glutathione S-transferases show peroxidase activity towards cytotoxic metabolites produced in inflammatory reactions, the main feature of rheumatoid arthritis (RA). Genetic polymorphisms modify the enzyme conjugation capacity and may be associated with the activity of RA. A genotyping approach was used to analyze polymorphisms of corresponding enzymes in 213 RA patients. It was found that the presence of certain genotype (GSTT1-0) contributed to higher disease activity in RA patients. The risk for developing highly active RA was the highest in smokers with the GSTT1-0 genotype.
COBISS.SI-ID: 25816281
We examined gene expression of estrogen-metabolizing enzymes in SDRs (17beta-HSD types 1, 2, 4, 7, 8, 12) and AKR1C3, aromatase, steroid sulfatase, estrogen sulfotransferase, and in alpha and beta estrogen receptors (ERs), in MCF-7, Ishikawa, JEG3 and liver cancer (HepG2) cells. It turned out that estradiol is synthesized by 17beta-HSD-12 and by sulfatase. In JEG3 and HepG2 cells, estradiol is formed by aromatase and 17b-HSD-1. In HepG2 cells, AKR1C3 and aromatase produce estradiol. In MCF7 and Ishikawa cells, estradiol affects ERa, while ERS are not involved in JEG3 and HepG2 cells
COBISS.SI-ID: 25142745
Textbook of up-to-date knowladge on structure and function of peptides and proteins for under- and post-graduate students in life-sciences.
COBISS.SI-ID: 26258393