Naomi Kraus-Friedmann

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In isolated hepatic microsomal vesicles the heavy metals Cd2+, Cu2+, and Zn2+ inhibit Ca2+ uptake and evoke a prompt efflux of Ca2+ from preloaded vesicles in a dose-dependent manner. N-Ethylmaleimide also inhibits Ca2+ uptake and causes Ca2+ release, but it is less effective in these respects than the heavy metals. Measurement of mannose-6-phosphatase(More)
A liver plasma-membrane fraction capable of Ca2+ uptake was isolated. The fraction exhibited high Na+, K+-ATPase, low glucose-6 phosphatase activity, and transported alanine in a Na+-dependent fashion. The uptake of Ca2+ was ATP-dependent; UTP, GTP, or CTP did not substitute for ATP. The presence of oxalate did not significantly alter the rate of uptake.(More)
The mechanism of action of the immunosuppressant FK506 in the liver was studied. The hypothesis was tested that FK506 exerts its effect in the liver by interacting with the ryanodine-binding Ca2+ release channel. Two types of experiments were carried out: (1) [3H]-ryanodine binding studies with isolated microsomal fractions, and (2) cytosolic-free Ca2+(More)
In this study, the binding of [3H]ryanodine to liver microsomal subfractions was investigated. The specific binding of [3H]ryanodine, as determined both by vacuum filtration and by ultracentrifugation, is to a single class of high-affinity binding sites with a Kd of 10 +/- 2.5 nM and density of 500 +/- 100 and 1200 +/- 200 fmol/mg of protein by the(More)
Regulation of free cytosolic Ca2+ level in the liver is important because of the many Ca2(+)-dependent processes in the liver, such as respiration, gluconeogenesis, glycogenolysis, cell division, etc. Free cytosolic Ca2+ levels are maintained in the unstimulated state below 1 microM. This level is maintained by an outwardly directed Ca2(+)-ATPase in the(More)
A hypothesis for the hormonal regulation of gluconeogenesis, in which increases in cytosolic free-Ca2+ levels ([Ca2+]i) play a major role, is presented. This hypothesis is based on the observation that gluconeogenic hormones evoke a common pattern of Ca2+ redistribution, resulting in increases in [Ca2+]i. Current concepts of hormonally evoked Ca2+ fluxes(More)
Glucagon and beta-adrenergic agents increase cAMP levels and stimulate Ca2+ influx in liver cells. There is no consensus as to the mechanism by which these hormones stimulate the influx of Ca2+. Using mouse retinal rod CNGCalpha cDNA probes, we cloned rat liver and skeletal muscle, and human hepatic CNGCalpha subunit sequences showing 97-100% identity with(More)
Ryanodine, a highly toxic alkaloid known to react specifically with the Ca2+ release channels in sarcoplasmic reticulum (SR), was employed to study Ca2+ sequestration in the liver. Ryanodine at a 200 microM concentration increased cytosolic free Ca2+ levels and phosphorylase a activity in isolated hepatocytes. These effects may involve microsomal Ca2+(More)
Previous studies have suggested a role for the actin cytoskeleton in hormonally evoked Ca2+ signaling in the liver. Here, we present evidence supporting a connection between filamentous actin (F-actin) organization and the ability of vasopressin and glucagon to increase cytosolic free-Ca2+ ([Ca2+]i) levels. F-actin was disrupted in hepatic cells by(More)