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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Incubation of cells from a wild type strain of E. coli with 0.3 mg/ml rifampicin for 15 minutes lead to a complete inhibition of RNA synthesis measured as the uracil incorporation into the trichloroacetic acid insoluble fraction. In these rifampicin-treated cells [14C]uracil incorporation tended to decrease during a further incubation at 37 degrees. Addition of cyclic AMP increased the inactivation of the system responsible for [14C]uracil uptake. The cyclic nucleotide effect seems to be specific since ATP or 5'AMP did not increase such inactivation.
Mol Cell Biochem 1977 Jul 05
PMID:Influence of cyclic 3',5'-adenosine monophosphate on uracil uptake by rifampicin treated Escherichia coli cells. 19 84

A somatic cell genetic approach was used to study the role of cyclic nucleotides in adrenal steroidogenesis. 8-Bromoadenosine 3',5'-monophosphate (8BrcAMP) stimulated steroidogenesis (K'd=0.1 mM) in cultured mouse adrenocortical tumor cells (Clone Y1). In addition, 8BrcAMP inhibited Y1 cell growth and caused Y1 cell monolayers to assume a rounded morphology. As a consequence, 8BrcAMP (at concentrations greater than or equal to 0.4 mM) reduced the relative plating efficiency of Y1 cells to less than 10(-5). Y1 cells were mutagenized with ethyl methanesulfonate (300 microgram/ml) and grown in the presence of 0.4 mM 8BrcAMP. A surviving colony (8BrcAMPr-1) was shown to be resistant to growth inhibition (relative plating efficiency at 1.0 mM 8BrcAMP=50 percent)) and to morphological changes induced by 8BrcAMP. 8BrcAMPr-1 cells had diminished steroidogenic responses to cyclic nucleotides and to ACTH (less than or equal to 33 percent of maximum). In 8BrcAMP(R)-1 cells, adenylate cyclase activity remained responsive to ACTH, and cyclic AMP phosphodiesterase activity was not increased. These data suggest that 8BrcAMPr-1 cells are defective at a point common to cyclic AMP action on growth, morphology and steroidogenesis. The associated decrease in responsiveness of the steroidogenic pathway to ACTH suggests that ACTH-regulated steroidogenesis is via a cyclic nucleotide-mediated mechanism.
Mol Cell Endocrinol 1977 Aug
PMID:Isolation of mutant adrenocortical tumor cells resistant to cyclic nucleotides. 20 May 6

Several characteristics of the binding of insulin and glucagon to human circulating mononuclear leukocytes have been studied. Functional analysis (latex bead ingestion) revealed that cell mixtures, as prepared according to Boyum and used generally in studies of insulin resistance in humans, consist of 20-29% phagocytic monocytes, with the remainder being lymphocytes. Partial separation of monocytes from lymphocytes on columns of Sephadex G-10, followed by correlation of insulin binding with cell type, confirms that the monocyte is the binding species. Insulin influenced neither glucose uptake nor the further conversion of glucose to lipids and CO2 by the leukocytes. The transport of alpha-aminoisobutyrate, a nonmetabolizable amino acid, into these cells was also unaffected by insulin. Monocyte/lymphocyte mixtures specifically bound glucagon and prostaglandin E1. At physiological concentrations of these hormones, steady states were reached in 15 min and 45 min, respectively. In contrast to the 8-10-fold increases in cellular cyclic AMP produced by prostaglandins, the effect of glucagon was very small but apparently real. Under appropriate preincubation conditions, sodium azide and iodoacetamide inhibited phagocytosis and insulin binding in parallel. The binding of glucagon was unaffected by these agents. Although both antimycin A and actinomycin D inhibited phagocytosis of the monocytes, only the former inhibited insulin binding; there was only a slight effect on glucagon binding. We would conclude that the binding of insulin to human circulating monocytes, although reflective of insulin resistance in diabetes mellitus and obesity, may not be to traditional receptors. In contrast, the binding of glucagon to lymphocyte/monocyte mixtures may be to function-linked receptors.
Mol Cell Endocrinol 1977 Oct
PMID:Hormone receptors: VI. On the nature of the binding of glucagon and insulin to human circulating mononuclear leukocytes. 20 May 11

1. The effect of extracellular volume expansion (ECVE) on renal production of cyclic AMP was evaluated in 19 thyroparathyroidectomized dogs. ECVE was produced by the infusion of Ringer bicarbonate solution at a rate of 2 ml min-1 kg-1 body weight; cyclic AMP was measured in plasma obtained from the aorta and renal vein and in the urine. 2. During the natriuresis of ECVE urinary excretion of cyclic AMP, the clearance of cyclic AMP, net nephrogenous cyclic AMP added both to urine and to the renal vein and hence total nephrogenous cyclic AMP increased significantly. 3. This rise in net production of cyclic AMP and a significant natriuresis by the kidney persisted for 60--90 min after discontinuation of active ECVE and return of renal plasma flow to normal. 4. The results support the notion that an increase in the production of cyclic AMP by the kidney may play a role in the natriuresis of ECVE.
Clin Sci Mol Med 1977 Dec
PMID:Role of cyclic AMP in the natriuresis of extracellular fluid volume expansion in the dog. 20 23

The release of 131I-labeled thyroxine (T4) from isolated hog thyroid cells was increased 1.5--2-fold by thyrotropin (TSH). Dibutyryl cyclic AMP failed to reproduce this TSH action. In this in vitro system another cell activity, T4 synthesis, was stimulated in an essentially identical fashion by TSH and dibutyryl cyclic AMP (time course of action, dose-response relationship). 3-Isobutyl-1-methylxanthine (IBMX), 0.5 mM, did not alter the basal [131I]T4 release whereas it enhanced the [131I]T4 synthesis. TSH, 60 MU/ml, increased the intracellular cyclic AMP concentration 3-4-fold. Chlorpromazine (5 X 10(-4)M) abolished the TSH stimulation of cyclic AMP accumulation but did not alter the TSH-induced increase in [131I]T4 secretion. It is concluded that the TSH action on [131I]T4 secretion by isolated thyroid cells is not mediated by the adenylate cyclase-cylic AMP system.
Mol Cell Endocrinol 1977 Nov
PMID:Thyroxine secretion by isolated hog thyroid cells: a cyclic AMP independent pathway. 20 15

Calcium salts were found to replace ACTH in inducing steroidogenesis in isolated adrenocortical cells from rats. This Ca-specific stimulation occurred when the cation was presented to the cells in the presence of phosphate and carbonate as a counter-ions under conditions which favoured the formation of colloidal calcium. Colloid generation and stabilization was facilitated by the use of calcium buffers and gelatin. Stable soluble or sparingly soluble calcium complexes were inactive. The preparation of cells and metastable calcium solutions is described in detail. The Ca trigger was sensitive to Ca deprivation or inhibitors of Ca transport and could be replced by Sr. The relative role of Ca and cyclic AMP as second messengers is discussed.
Mol Cell Endocrinol 1978 Jan
PMID:Steroidogenesis in isolated adrenal cells: excitation by calcium. 20

The synthesis of the four enzymes of the deo operon in Escherichia coli is known from in vivo experiments to be subject to a double negative control, exerted by the products of the cytR and deoR genes. A DNA-directed in vitro protein synthesizing system makes the deo enzymes (exemplified by thymidine phosphorylase) in agreement with in vivo results. Enzyme synthesis is stimulated by cyclic AMP and repressed by the cytR and deoR gene products. Repression by the cytR repressor is reversed by cytidine or adenosine in the presence of cyclic AMP, while repression by the deoR repressor is reversed by deoxyribose-5-phosphate. Assays for the presence of the cytR and deoR repressors were established by use of S-30 extracts prepared from the regulatory mutants. Dissociation constants for repressor-operator binding as well as for repressor-inducer interactions have been estimated from the results.
Mol Gen Genet 1978 Feb 16
PMID:Regulation of the deo operon in Escherichia coli: the double negative control of the deo operon by the cytR and deoR repressors in a DNA directed in vitro system. 20 61

The rapid isolation of high yields of parenchymal cells from chicken liver is described. Stringent tests of viability show that the isolated hepatocytes are both structurally and metabolically similar to those in intact liver. During incubation viability decreased and the significance of this change on the interpretation of metabolic experiments is discussed. Lactate was a much more effective gluconeogenic precursor than pyruvate even in the presence of additional reducing equivalents. Hepatocytes isolated from fed chickens produced glucose from glycogen degradation. Glycogenolysis was stimulated by glucagon, dibutyryl cyclic AMP and adrenaline. Half maximal glucagon effects were elicited by physiological concentrations of the hormone. Glucagon and dibutyryl cyclic AMP stimulated glucagon, dibutyryl cyclic AMP and adrenaline their action was not additive to that of adrenaline.
Mol Cell Biochem 1978 Apr 11
PMID:The use of viable hepatocytes to study the hormonal control of glycogenolysis in the chicken. 20 19

Based on previous studies which have revealed that glucose 1,6-bisphosphate (Glc-1,6-P2) is a potent inhibitor of muscle hexokinase and an activator (deinhibitor) of phosphofructokinase and phosphoglucomutase, the effect of epinephrine on the levels of this regulator in rat diaphragm muscle was investigated. It was found that epinephrine caused an increase in diaphragm Glc-1,6-P2 levels, accompanied by a reduction in the activity of hexokinase and an activation (deinhibition) of phosphofructokinase and phosphoglucomutase. N6-2'-O-dibutyryl cyclic AMP was able to mimic all these effects of epinephrine. The concentration of glucose-6-phosphate was not changed by epinephrine, under conditions in which the hormone produced an increase in cyclic AMP and Glc-1,6-P2 levels and the concomitant decrease in hexokinase activity. It was also shown that Glc-1,6-P, in the concentration range found after epinephrine, inhibited the diaphragm hexokinase and deinhibited phosphoglucomutase. These results may suggest a mechanism of epinephrine action by which the activities of hexokinase, phosphoglucomutase and phosphofructokinase, through the action of Glc-1,6-P2, are synchronized with the cyclic AMP-mediated activation of glycogen phosphorylase, to achieve an increase in total glycogenolysis and glycolysis and a concomitant reduction in glucose utilization by the muscle.
Mol Cell Endocrinol 1978 Apr
PMID:The effect of epinephrine and dibutyryl cyclic AMP on glucose 1,6-bisphosphate levels and the activities of hexokinase, phosphofructokinase and phosphoglucomutase in the isolated rat diaphragm. 20 4

The catalytic groups, involved in aminoacyl-tRNA formation remain unknown. The isolation and identification of an active covalent complex between the enzyme and substrate is an essential step in understanding the reaction mechanism. We identified and isolated the covalent complex of tryptophanyl-tRNA synthetase (EC 6.1.1.2) and tryptophane which was able to aminoacylate the tRNATrp in the absence of ATP. In beef pancreas tryptophanyl-tRNA synthetase preparations, isolated by the previously described method, a tightly bound tryptophan was revealed which could not be removed by charcoal treatment, by gel-filtration and by replacement with the excess of typtamine, a competitive inhibitor of tryptophane. This tightly bound tryptophane is able to exchange rapidly and specifically with radioactive tryptophane allowing to obtain [14C]tryptophane-tryptophanyl-tRNA synthetase complex. After the reaction of this complex with NH2OH at neutral pH tryptophanyl hydroxamate is formed proving the activated state of the tryptophane in the initial complex with the enzyme. No nucleotide impurites were noticed in the enzyme preparation; the complex is stable at denaturation. A conclusion is made that the tryptophanyl-tRNA synthetase isolated by our method is a tryptophanyl-enzyme. The tryptophanyl residue could be specifically transferred to tRNATrp in the absence of other substrates of the reaction, the efficiency of the transfer does not exceed 25%. The content of the covalently bound tryptophane never exceeds 1 mole per mole of the dimeric enzyme. The total content of tryptophane in the forms of tryptophanyl-enzyme and tryptophanyl adenylate enzyme complex equals 2 moles per mole of the enzyme. The tryptophanyl-enzyme is destroyed during incubation with AMP or with pyrophosphate. The role of the tryptophanyl-enzyme as a possible intermediate in the course of aminoacylation of tRNATrp is discussed.
Mol Biol (Mosk)
PMID:[Tryptophanyl tRNA synthetase: isolation and characteristics of the tryptophanyl-enzyme]. 20 77


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