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K Skorecki

Publications and source records attributed to K Skorecki.

40 records · Page 3Linked to original sources
PubMed1984

Radiation inactivation of oligomeric enzyme systems: theoretical considerations.

Radiation inactivation has been used as a tool to explore the size, structure, and function of soluble and membrane-bound enzymes. Enzyme systems consisting of a single functional unit yield a single exponential dependence of enzyme activity on radiation dose. Complex, nonexponential, inactivation curves suggest the presence of a multiunit enzyme system. A concave-upward inactivation curve suggests the presence of multiple independent functional units of distinct size and activity that do not interact with each other. An oligomeric enzyme, consisting of n identical subunits in equilibrium with monomers, can give simple exponential decay curves or more complex inactivation curves with various degrees of upward or downward concavity, depending upon the extent of oligomer-monomer equilibration among subunits after radiation, oligomer-to-monomer size and activity ratios, and multihit requirements for oligomer inactivation. For each of these possibilities, equations for the inactivation curves are derived, calculated numerically, and discussed in qualitative terms. A systematic approach to the evaluation of complex radiation inactivation curves is proposed and limitations of the radiation inactivation method are reviewed.

Enzyme Inhibitors↗
PubMed1983

Response of the kidney to furosemide. I. Effects of salt intake and renal compensation.

We investigated the effects of varying salt intake on five factors that could affect sodium balance during furosemide (F) administration: the quantity of F reaching the renal tubules; the magnitude of the acute natriuresis; Na+ excretion in the period after the acute diuresis; diuretic tolerance; and changes in plasma aldosterone. Six normal subjects were given F (40 mg day-1) for 3 days after equilibration to Na+ intakes of 20 mmol day-1 (low salt, LS) and 270 mmol day-1 (high salt, HS). Salt intake did not modify F excretion. Salt restriction reduced the short-term natriuretic response to F, led to diuretic tolerance, and potentiated the F-induced rise in plasma aldosterone. There was a progressive diminution in the quantity of Na+ excreted per unit of F excreted during LS. In spite of this, cumulative Na+ balance was negative only during LS because of a compensatory increase in Na+ reabsorption in the period between diuretic doses. During HS, this compensation exactly matched the short-term loss of Na+ produced by F, leading to neutral Na+ balance. During LS, the acute natriuresis exceeded the daily Na+ intake, so that, despite the renal compensation, Na+ balance was negative. In conclusion, salt restriction impairs the short-term natriuretic response to F and leads to diuretic tolerance. However, homeostatic mechanisms activated by the diuretic can maintain Na+ balance even in subjects without a disease causing Na+ retention, unless dietary salt is restricted.

Adult↗
PubMedDate not supplied

Interaction of epidermal growth factor with vasoactive hormones in the regulation of phospholipase A2.

The interaction of growth factors with their receptors initiates a series of intracellular events that are of critical importance in the control of normal cell proliferation. In this regard considerable attention has focused on the coupling of phospholipase C-gamma to growth factor receptor tyrosine kinases. In contrast, the interaction of growth factors with phospholipase A2 has received less attention, most likely because the arachidonic acid release response has been considered to be an accompaniment of phospholipase C activation. Work from our laboratory using a well defined model system demonstrated a distinct coupling relationship of epidermal growth factor to phospholipase A2. This review focuses on the interaction of the epidermal growth factor receptor with phospholipases involved in both mitogenic and non-mitogenic responses and discusses their possible relation with vasoactive hormones.

Angiotensin II↗