Mechanism of hydroxylamine-induced inhibition of β-galactosidase synthesis in Escherichia coli
30 Nov 1967-Biochemical and Biophysical Research Communications (Academic Press)-Vol. 29, Iss: 4, pp 463-468
TL;DR: It is demonstrated that in some strains, the HA effect involves catabolite repression in addition to interference with translation of the specific m-RNA, and the use of HA as a specific inhibitor of chain initiation is thus limited in such strains.
About: This article is published in Biochemical and Biophysical Research Communications.The article was published on 1967-11-30. It has received 4 citations till now. The article focuses on the topics: Catabolite repression & Hydroxylamine.
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TL;DR: This chapter focuses on three devices: catabolite repression, transient repression, and catabolites inhibition, which regulate the utilization of many carbohydrates, which influences many aspects of microbial growth and metabolism.
Abstract: Publisher Summary This chapter focuses on three devices: catabolite repression, transient repression, and catabolite inhibition, which regulate the utilization of many carbohydrates. Catabolite repression is a reduction in the rate of synthesis of certain enzymes, particularly those of degradative metabolism, in the presence of glucose or other readily metabolized carbon sources. Catabolite inhibition is a control exerted by glucose on enzyme activity rather than on enzyme formation, analogous to feedback inhibition in biosynthetic pathways. Catabolite repression influences many aspects of microbial growth and metabolism. In addition to the well known repressions of carbohydrate utilization and amino-acid degradation in bacteria and yeast, catabolite repression affects the formation of enzymes that function in the tricarboxylic acid cycle, glyoxylate cycle, fatty acid degradation, carbon dioxide fixation, and the respiratory chain. In higher organisms, catabolite repression has been observed in sugar cane, rats, and man. The question of whether catabolite repression acts to inhibit the transcription of DNA into m-RNA or to inhibit translation of messenger into protein has received conflicting answers. Catabolite repression is a control system that usually affects catabolic enzymes. If catabolite repression and transient repression are not mediated by the specific apo-repressor of each operon, there must be another protein that recognizes the low molecular-weight effector. The significance of a control mechanism, which influences the activity as opposed to the concentration of a carbohydrate-metabolizing enzyme is readily appreciated because bacteria have a limited ability to change enzyme concentrations.
163 citations
TL;DR: Based on the activities of BPAF, BPF, BPA and MBP, the XenoScreen XL YES/YAS assay gives comparable results to the (anti)estrogenic or (anti-androgenic assays that are reported in the literature.
56 citations
TL;DR: Iptakalim has exerted protective effects against hypertensive damage to target organs in rats and improves endothelial dysfunction associated with cardiovascular diseases by selective activation of the SUR2B/Kir6.1 subtype of KATP channels expressed in the endothelium.
Abstract: Hypertension is the most common cardiovascular disease. The discovery of the antihypertensive action of adenosine triphosphate-sensitive potassium (K(ATP)) channel openers was a significant advance in the treatment of hypertension. Iptakalim is a novel K(ATP) channel opener with a unique chemical structure that differs from other K(ATP) openers. Among the 3 different subtypes of K(ATP) channels heterologously expressed in human embryonic kidney cells and Xenopus oocytes, iptakalim exhibits significant selectivity for SUR2B/Kir6.1 channels, mild effects on SUR2A/Kir6.2 channels, and fails to open SUR1/Kir6.2 channels. Iptakalim is a more potent activator of the SUR2B/Kir6.1 subtype of K(ATP) channels than diazoxide and pinacidil, the 2 most commonly studied K(ATP) channel openers. Iptakalim selectively produces arteriolar vasodilation with essentially no effect on the capacitance vessels. It can preferentially relax arterioles and small arteries, without affecting large arteries. Furthermore, iptakalim strongly lowers the blood pressure of hypertensive rodents and humans but has little effect on normotensive rodents and humans. Selective antihypertensive action is not observed with pinacidil or diazoxide and may be due to the high selectivity of iptakalim for the SUR2B/Kir6.1 subtype of K(ATP) channels, as well as its selective relaxation of resistance vessels. In pulmonary arterial smooth muscle cells, iptakalim inhibits the increase of cytoplasmic free Ca2+ concentration, as well as cell proliferation induced by endothelin-1. Furthermore, iptakalim has exerted protective effects against hypertensive damage to target organs in rats and improves endothelial dysfunction associated with cardiovascular diseases by selective activation of the SUR2B/Kir6.1 subtype of K(ATP) channels expressed in the endothelium. Clinical trials of iptakalim in the treatment of mild-moderate hypertension have been completed in China. In additional to strong antihypertensive efficacy, iptakalim seems to have a favorable safety and tolerability profile. Iptakalim is a promising new generation antihypertensive drug.
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TL;DR: It was found that high levels of tryptophan overcame by 40% the repression caused by glucose, and the stimulatory effect of glucose on tryPTophan synthetase formation in E. coli 9723E could be duplicated by indole-3-propionic acid.
Abstract: Freundlich, Martin (University of Minnesota, Minneapolis) and Herman C. Lichstein. Tryptophanase-tryptophan synthetase systems in Escherichia coli. II. Effect of glucose. J. Bacteriol. 84:988-995. 1962.-The effect of glucose and other compounds on the formation of tryptophanase and tryptophan synthetase in Escherichia coli was examined. Although most of these compounds were potent inhibitors of the synthesis of tryptophanase, they invariably increased the formation of tryptophan synthetase. The severity of tryptophanase inhibition depended upon the degree of utilization of the compound by the growing bacterial cells. It was found that high levels of tryptophan overcame by 40% the repression caused by glucose. The stimulatory effect of glucose on tryptophan synthetase formation in E. coli 9723E could be duplicated by indole-3-propionic acid. A study of the amino acid pool of E. coli 9723E revealed no free tryptophan in cells harvested from the basal medium containing glucose. In contrast, cells grown in the absence of glucose possessed a measurable amount of this amino acid. The possible mechanisms of the effect of glucose and related compounds on tryptophanase and tryptophan synthetase formation, as well as the relationship of these effects to the metabolic control of tryptophan metabolism, are discussed.
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