Subunit composition of the purified dihydropyridine binding protein from skeletal muscle.

The dihydropyridine (DHP) receptor from rabbit skeletal muscle has been characterized by affinity labeling and purification. Two procedures were used for purification: one that was a procedure modified from that of Curtis and Catterall (1984) and one that employed an anti alpha 1 monoclonal antibody (Mab) affinity column. In addition, both digitonin and CHAPS solubilizations were utilized with each purification technique.

A procedure for purification of the ryanodine receptor from skeletal muscle.

In this paper, we describe a simple and reproducible method for purifying large quantities of ryanodine receptor from skeletal muscle membranes. The procedure involves the use of ion exchange chromatography and sucrose gradient centrifugation to purify the protein which has been identified as the calcium release protein of the sarcoplasmic reticulum (Imagawa, T., Smith, J.

Characterization and properties of nine human ovarian adenocarcinoma cell lines.

Four series of cell lines have been derived from patients with ovarian adenocarcinoma. Nine cell lines have been established at one from a solid metastasis. Six lines were derived from the ascites or pleural effusion of patients with poorly differentiated adenocarcinoma: PEO1, PEO4, and PEO6 from one patient, PEA1 and PEA2 from a second, and PEO16 from a third.

Effect of sodium butyrate and other differentiation inducers on poorly differentiated human ovarian adenocarcinoma cell lines.

We have studied the effects of sodium butyrate, retinoic acid, and dimethyl sulfoxide on two human ovarian carcinoma cell lines PE04 and PE01. PE04 cells, after treatment with sodium butyrate at cytostatic doses (2-3 mM for 4 days), exhibited phenotypic changes including induction of alkaline phosphatase and determinants recognized by the monoclonal antibodies 123C3 and 123A8. These effects are not simply the result of cytostasis as they were not produced by dimethyl sulfoxide or retinoic acid.

Low affinity binding sites for 1,4-dihydropyridines in mitochondria and in guinea pig ventricular membranes.

In this paper, we describe the occurrence of both high and low affinity sites for dihydropyridines in crude membrane preparations from guinea pig ventricular tissue. The physiological significance of the low affinity site (apparent dissociation constant = 76 +/- 9 nM) is not currently known; it has, however, a binding capacity which was 300-1000 times that of the high affinity site and was resistant to heat denaturation. The magnitude of the binding to the low affinity site was affected by both the ionic strength of the medium and by the presence of divalent ions.

Dihydropyridine binding and calcium channel function in clonal rat adrenal medullary tumor cells.

We correlated the binding of the dihydropyridines, nitrendipine and PN200-110, with their pharmacological actions on voltage-dependent membrane calcium channels. Binding was studied in clonal rat adrenal medullary cells (PC12) and in plasma membranes prepared from them. Calcium currents were studied using whole cell and single channel patch clamp methods.

Atrotoxin: a specific agonist for calcium currents in heart.

A specific label for voltage-dependent calcium channels is essential for the isolation and purification of the membrane protein that constitutes the calcium channel and for a better understanding of its function. A fraction of Crotalus atrox that increases voltage-dependent calcium currents in single, dispersed guinea pig ventricular cells was isolated. In the doses used, neither sodium nor potassium currents were changed.

Effects of hypothalamic lesions on levels of plasma free fatty acids in the mallard duck.

Plasma free fatty acid (FFA) levels were measured in the mallard duck (Anas platyrhynchos) following hypothalamic lesions at various sites. The results indicate that ventromedial lesions produced hyperphagia, increased deposition of fat, and significantly elevated levels of plasma FFA. Anterior bilateral lesions resulted in aphagia, severe loss in body weight and a marked decrease in plasma FFA.