Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of variations in pH and Ca2+ on angiotensin II (A-II)-induced steroidogenesis was tested on isolated adrenal glomerulosa cell suspensions. The results show that a reduction in pH from 7.4 to 6.5 produces both a shift to the left of the A-II dose-response curve as well as an increase in maximum steroid production. In contrast, removal of Ca2+ from the incubation medium virtually abolished steroidogenesis to A-II (5 X 10(-9)M(, KCl(10mM) and ACTH (250 microU/ml). The Ca2+ antagonist D-600, however, was less effective than simple removal of Ca2+ as 10(-4) M was required to block the steroidogenic response to these same agonists. The results indicate that the response characteristics of this system to A-II resemble most closely those seen with isolated arterial smooth muscle - especially rabbit aortic strips.
Mol Cell Endocrinol 1979 Feb
PMID:Angiotensin-induced steroidogenesis in rabbit adrenal: effects of pH and calcium. 3 13

This short review summarizes some of the data concerning the regulation of adrenocortical adenylate cyclase by ACTH and other putative effectors, such as guanosine and nucleotides, divalent cations and adenosine. The available information on ACTH-sensitive adenylate cyclase of the adrenal cortex is discussed in comparison to other cyclase systems and the possible biochemical mechanisms of action of ACTH on the adrenal cortex.
Mol Cell Endocrinol 1979 Feb
PMID:The regulation of adenylate cyclase of the adrenal cortex. 3 14

Antisera to ACTH were produced in rabbits injected repeatedly at multiple intradermal sites with synthetic [Asp25, Ala26, Gly27]alphah-corticotropin-(1-28)-octacosapeptide-bovine gamma globulin conjugate (octacosapeptide is a sequence analogue of alphah1-28-ACTH). Antibodies to extracted human or porcine ACTH were detected in all of the sera 1 month after immunization. A considerable proportion of the antisera obtained from a single final bleeding 5 months after the primary immunization were suitable for sensitive radioimmunoassay. The antisera were shown to neutralize the steroidogenic activity of ACTH in an isolated rat adrenal cell bioassay system. Titres estimated from antiserum dilution curves and relative avidities from the standard curves were compared. It was possible to detect picogram amounts of ACTH in plasma-free medium with the best antisera. The method described is an effective means of producing anti-sera to the weakly immunogenic N-terminal fragment of the ACTH molecule.
Mol Cell Endocrinol 1977 Sep
PMID:Preparation and assessment of antisera to ACTH. 7 98

1. Changes in plasma concentrations of catecholamines and cortisol were measured before and after static exercise performed by the subject pushing with both legs against a strain-gauge bar. No marked changes in plasma catecholamine were observed but plasma cortisol increased after the subject pushed for 3 min at 50% of maximum force. 2. Holding a 20 kg weight for 5 min in one hand caused a rise in plasma cortisol and in plasma ACTH but no changes in growth hormone were observed.
Clin Sci Mol Med 1975 Sep
PMID:Pituitary-adrenal response to static exercise in man. 17 32

Corticosterone production by isolated rat adrenal cells in the absence of ACTH is stimulated by 20alpha-hydroxycholesterol, 22R-hydroxycholesterol and 25-hydroxycholesterol. This effect is also seen at sub-maximal ACTH concentrations. Aminoglutethimide (AGI) inhibits the stimulation caused by the three hydroxylated cholesterols. In the presence of ACTH, AGI also inhibits steroid production both under control conditions and in the presence of the sterols. The stimulation by 25-hydroxycholesterol is dose-dependent, both in the presence and absence of a sub-maximal ACTH concentration. At maximal ACTH concentrations 25-hydroxycholesterol does not give additional stimulation. Cycloheximide has no effect on corticosterone production from 25-hydroxycholesterol whether ACTH is present or not. Our results indicate that 25-hydroxycholesterol is a good substrate for the study of the cholesterol side-chain cleaving system and the mechanism of action of ACTH at the levels of the intact cell.
Mol Cell Endocrinol 1975 Nov
PMID:Studies on isolated rat adrenal cells metabolism of hydroxylated sterols. 17 94

The production of corticosterone from 25-hydroxycholesterol by isolated rat adrenal cells is inhibited by aminoglutethimide phosphate (AGI); half-maximal inhibition is obtained at ca. 10 muM. AGI also inhibits ACTH-stimulated steroid production from endogeneous substrates; here half-maximal inhibition is obtained with ca. 40 muM AGI. In the presence of ACTH + AGI, 25-hydroxycholesterol causes additive inhibition. This effect of 25-hydroxycholesterol is dose-dependent. ACTH-stimulated steroid production from endogeneous substrates is partially inhibited by 5-cholene-3 beta,24-diol. These results may just reflect substrate competition for the side-chain cleaving system or may be due to some seocndary toxic effect on the cells.
Mol Cell Endocrinol 1976 Jan
PMID:Effects of 25-hydroxycholesterol and aminoglutethimide in isolated rat adrenal cells. A model for congenital lipoid adrenal hyperplasia? 17 62

Y-1-L cells, a subline of the Y-1 functional murine adrenocortical tumor cell line, were enucleated with cytochalasin B and the response of these enucleated cells to ACTH and dibutyryl cyclic AMP (dbcAMP) was examined. Enucleated Y-1-L cells maintained a basal steroid output for at least 24 h and responded to either ACTH (10 mU/ml) or dbcAMP (1 mM) by a change from flat to rounded cell shape, and by increased steroidogenesis. The steroidogenic response of enucleated cells during the first 3 h after enucleation was highly significant and, though it decreased rapidly thereafter, it persisted to a limited degree for up to 12 h. On the other hand, the morphologic change could be induced even at 33 h after enucleation. The results of this study show that the nucleus is not required for the expression of the acute effects of ACTH or dbcAMP and that the cytoplasmic components necessary for cell 'rounding' and a steroidogenic response are stable for 36 h and 12 h, respectively.
Mol Cell Endocrinol 1976 Mar
PMID:Response to ACTH and dibutyryl cyclic AMP by enucleated adrenocortical tumor cells. 17 19

ACTH stimulated steroidogenesis and cAMP (adenosine 3',5'-monophosphate) accumulation in an adrenocortical mouse tumor cell line (clone Y1) with Kd values which differed by more than one order of magnitude (5.2 X 10(-11) M and 7 X 10(-10) M, respectively). All of the cAMP formed in response to added ACTH appeared extracellularly in 5- or 30-min incubations. ACTH, at 5 and 10 muU/ml, stimulated steroidogenesis to 25% and 40% of maximum activity; and increased the extracellular accumulation of cAMP 1.4-fold and 2.3-fold, respectively. The effects of ACTH appeared to be via an action on intracellular ATP, specific for cAMP and dependent on an ACTH-sensitive adenylate cyclase system. These observations indicate that ACTH increases cAMP accumulation in Y1 cells at virtually all steroidogenic concentrations and suggest that cAMP is an essential component of ACTH-stimulated steroidogenesis.
Mol Cell Endocrinol 1976 Mar
PMID:Steroidogenesis and extracellular cAMP accumulation in adrenal tumor cell cultures. 17 21

The effects of cholera on adrenal weight in hypophysectomized rats were investigated, in an attempt to demonstrate an ACTH-like, adrenal trophic effect of the toxin. The results suggested that the toxin probably exerts is ACTH-like action on the adrenal via adenylate cyclase. Cholera toxin was also shown to have a thermolytic action, similar to that of ACTH, probably due to stimulation of adrenal glucocorticoid secretion.
Mol Cell Endocrinol
PMID:The effects of cholera toxin on the adrenal weight in hypophysectomized rats. 18 72

In this work the kinetics of activation of the cyclic AMP-dependent protein kinase by several catecholamines and ACTH, have been studied in rat epididymal fat pads and isolated fat cells. The method of Soderling and co-workers which permits the measurement of the state of activation of the protein kinase after hormonal stimulation in adipose tissue, has been used. Kinetics experiments where norepinephrine was used showed that the results obtained with isolated cells conform to the models of Sutherland and Brostrom and co-workers. Wtih intact tissue, norepinephrine not only stimulates the protein kinase activity measured without exogenous cyclic AMP but also the total activity measured in the presence of cyclic AMP (5 X 10(-6) M); thus the effect of norepinephrine, obtained during incubation of the tissue, and that of cyclic AMP, added to the soluble fraction after incubation, were additive. This effect seems to be of the beta type because it is blocked completely by propranolol. A weak, additive but significant effect was also obtained with epinephrine and isoproterenol but not with ACTH. Neither cyclic GMP nor cyclic IMP seems implicated in this effect. It was shown that stroma vascular cells which are present in the fat pads are not involved. These results suggest that the effects of norepinephrine on the protein kinase of the fat pads cannot be completely explained by the model of Brostrom and colleagues.
Mol Cell Endocrinol 1976 Oct
PMID:Additive effects of norepinephrine and cyclic AMP on the activation of the protein kinase from adipose tissue. 18 9


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