Academic literature on the topic 'Fem transferases'

Abstract The ester synthesizing activity of alcohol acetyl transferase under batch fermentation conditions is subject to cyclic variations depending upon yeast growth and substrate availability. It is therefore clear that for achieving the full potential of brewing yeast to produce esters we need to conduct the fermentation at a single optimum condition.

This introductory chapter defines natural products as conditional metabolites, small molecules from secondary rather than primary metabolic pathways, noting how a few primary metabolites serve as building blocks for specific classes of up to hundreds of downstream conditional metabolites. The major classes of natural products, whose modes of biosynthesis are examined, include polyketides, ribosomal and nonribosomal peptides, isoprenoid scaffolds, purines and pyrimidines, phenylpropanoids, glycosides, and alkaloids. Three major categories of enzymes involved in complexity generation of natural product frameworks are oxygenases, S-adenosylmethionine (SAM)-dependent transferases that fragment SAM by two-electron and one-electron reaction manifolds, and pericyclases that catalyze concerted pericyclic transition states without any reaction intermediates.

Abstract Galactose metabolism involves three enzymes: galactokinase, galactose-1-phosphate uridyl transferase (GALT) and uridine diphosphate-4-epimerase (Fig. 49–1). Inborn errors of metabolism (IEM) have been described for all three enzymes. The most common inborn error in galactose metabolism is deficiency of the GALT enzyme. Its incidence in North America is approximately 1 in 60,000. Galactose levels and/or GALT activity are routinely tested in all infants by newborn screening programs. Infants with elevated galactose and/or decreased enzyme activity should be referred to a biochemical genetics program that specializes in treatment of IEM. This chapter will focus on GALT deficiency since the classical form of the disease requires lifelong dietary treatment. In classical galactosemia, the GALT enzyme is not produced and the affected individual has no enzyme activity. Neonates with untreated classical GALT deficiency present a few days after starting milk-based formula or breast milk feeding. The initial symptoms include poor feeding, vomiting, and jaundice. Failure to thrive, hepatomegaly, edema, splenomegaly, and sepsis can follow. The disease is rapidly fatal if milk feedings continue. For surviving infants, mental retardation and behavioral problems are common.