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

A multicopy plasmid containing the Escherichia coli fur gene was introduced into Pseudomonas aeruginosa strain PA103C. This strain contains a toxA-lacZ fusion integrated into its chromosome at the toxA locus. Beta-galactosidase synthesis in this strain is regulated by iron, as is seen for exotoxin A production. Beta-galactosidase synthesis and exotoxin A production in PA103C containing multiple copies of E. coli fur was still repressed in low iron conditions. The transcription of regA, a positive regulator of toxA, was also found to be inhibited by multiple copies of the E. coli fur gene. In addition, the ability of PA103C containing multiple copies of E. coli fur to produce protease was greatly reduced relative to PA103C containing a vector control. A polyclonal rabbit serum containing antibodies that recognize E. coli Fur was used to screen whole-cell extracts from Vibrio cholerae, Shigella flexneri, Salmonella typhimurium and Pseudomonas aeruginosa. All strains tested expressed a protein that was specifically recognized by the anti-Fur serum. These results and those described above suggest that Fur structure and function are conserved in a variety of distinct bacterial genera and that at least some of these different genera use this regulatory protein to control genes encoding virulence factors.
Mol Microbiol 1991 Nov
PMID:Regulation of toxA and regA by the Escherichia coli fur gene and identification of a Fur homologue in Pseudomonas aeruginosa PA103 and PA01. 177 68

Vibrio cholerae is known to secrete DNase(s) into the extracellular environment. These proteins have been thought to be responsible for the difficulties in transforming this organism. In this work we demonstrate that the dns and xds genes differ and that their products are solely responsible for the extracellular DNase activity. By site-directed mutagenesis, strains have been constructed which are mutant in one or both genes. These strains have been assessed for their ability to be transformed with plasmid DNA and for their virulence in the infant mouse cholera model. DNase-deficient mutants can be readily transformed and the product of dns appears to be the more significant barrier. No effect on virulence was observed with the mutants.
Mol Microbiol 1991 Oct
PMID:Distinguishing between the extracellular DNases of Vibrio cholerae and development of a transformation system. 179 65

Senescence in primary cultures of mammalian cells is characterised by cessation of growth after a number of cell divisions; this may be associated with loss of some differentiated functions. Recent studies on bovine adrenocortical cells have suggested that expression of simian virus-40 (SV40) early region in these cells may prevent phenotypic losses due to senescence. We report here data on growth and differentiated function of two human thyrocyte cell lines (SGHTL-34 and -45) generated by the transfection of primary thyrocytes with the plasmid pSV3neo which contains the SV40 early region. Growth was assessed by fluorometric DNA estimations and calculation of cell population doubling time; function was assessed by binding studies using 125I-bovine thyrotrophin (TSH) and measurement of cyclic adenosine 3',5'-monophosphate (cAMP) response to stimulation with TSH, forskolin and cholera toxin. After 3-12 months in stable culture there was a gradual increase in the doubling time of both cell lines over a 3-month period (SGHTL-34 cells, early 34.5 +/- 4.5 h, late 301 +/- 111.6 h; SGHTL-45 cells, early 53.4 +/- 4.4 h, late 148.3 +/- 26.3 h; mean +/- SEM). Scatchard analysis demonstrated a loss of the high affinity TSH receptor over the same time period. The increase in cAMP in response to 1000 microU/ml TSH declined until the cells became unresponsive (SGHTL-34 early, cAMP 10.3 +/- 0.7 pmol/well; late, cAMP -0.4 +/- 0.3 pmol/well; SGHTL-45 early, cAMP 11.3 +/- 1.1 pmol/well, late, cAMP 0.3 +/- 0.1 pmol/well). The cAMP responses to forskolin and cholera toxin were unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Cell Endocrinol 1991 Dec
PMID:Effects of ageing on the growth and differentiated function of transfected human thyrocytes. 179 5

Five ADP-ribosylating bacterial toxins, pertussis toxin, cholera toxin, diphtheria toxin, Escherichia LT toxin and Pseudomonas exotoxin A, show significant homology in selected segments of their sequence. Site-directed mutagenesis and chemical modification of residues within these regions cause loss of catalytic activity and of NAD binding. On the basis of these results and of molecular modelling based on the three-dimensional structure of exotoxin A, the geometry of an NAD binding site common to all the toxins is deduced and described in the paper. For diphtheria toxin, sequence similarity with exotoxin A is such that its preliminary structure can be computed by molecular modelling, whereas for the other toxins similarity appears to be restricted to the NAD binding site. Moreover, an analysis of molecular fitting of the NAD molecule into its binding cavity suggests a new model for the conformation of the bound NAD that better accounts for all available experimental information.
Mol Microbiol 1991 Jan
PMID:Computer modelling of the NAD binding site of ADP-ribosylating toxins: active-site structure and mechanism of NAD binding. 190 17

We have investigated the possible role of guanine nucleotide-binding proteins in the process of antigen-induced exocytosis in a cultured rat mast cell line, RBL-2H3 cells. The mRNAs for the alpha subunits of the guanine nucleotide-binding proteins G alpha S (short and long forms), G alpha i-2, G alpha i-3, and G alpha Z were detected by hybridization with G alpha-specific oligonucleotide probes. The corresponding proteins were identified in membranes of RBL-2H3 cells on the basis of size, immunoreactivity with specific antibodies, and their ability to serve as substrates for ADP-ribosylation by cholera toxin or pertussis toxin. Treatment of cells with as little as 10(-9) to 10(-7) M dexamethasone markedly decreased the amount of G alpha Z mRNA and membrane G alpha Z, as well as the responsiveness of the cells to antigen stimulation. In the same cells, the exposure to dexamethasone caused an increase in the amounts of certain other G alpha subunits, particularly G alpha i-3, and in the responsiveness of the cells to an adenosine analog, N(ethylcarboxamido)-adenosine. Because of the apparent decrease in G alpha Z mRNA and protein in dexamethasone-treated cells and the fact that neither cholera toxin nor pertussis toxin inhibits the stimulatory signals to antigen [J. Biol. Chem. 265:745-753 (1990)], we suggest that G alpha Z is a potential candidate for regulating the early signals in antigen-stimulated RBL-2H3 cells.
Mol Pharmacol 1991 Oct
PMID:GTP-binding protein G alpha Z: its down-regulation by dexamethasone and its credentials as a mediator of antigen-induced responses in RBL-2H3 cells. 192 83

The uptake of L-[14C]glycine and the activities of intracellular marker enzymes of enterocytes were studied in ligated small intestinal segments of rabbits during experimental cholera induced by intra-intestinal injection of pure cholera toxin (CT). No significant difference was observed in the active uptake of L-[14C]glycine between the CT-injected small intestinal segments and the saline-injected control segments, indicating that there is an intact active transport system for intestinal absorption of L-[14C]glycine during experimental cholera in rabbits. Apart from a significant increase in the activity of a brush border marker enzyme (alkaline phosphatase), there was no significant difference between the activities of marker enzymes for lysosomes (acid phosphate), microsomes (glucose-6-phosphatase), mitochondria (succinate dehydrogenase), and a cytosol enzyme (proteinase) in mucosal homogenates of CT-injected small intestinal segments compared to controls. The finding of an intact mitochondrial marker enzyme together with intact L-[14C]glycine absorption provides a scientific basis for considering the use of glycine and other monoamino monocarboxylic amino acids in "improved" oral rehydration solutions for the treatment of acute diarrhea, including cholera.
Mol Biol Med 1991 Feb
PMID:Effect of cholera toxin on L-[14C]glycine uptake and intestinal cell enzymes in rabbit. 194 84

Oligonucleotide-directed mutagenesis of ctxB was used to produce mutants of cholera toxin B subunit (CT-B) altered at residues Cys-9, Gly-33, Lys-34, Arg-35, Cys-86 and Trp-88. Mutants were identified phenotypically by radial passive immune haemolysis assays and genotypically by colony hybridization with specific oligonucleotide probes. Mutant CT-B polypeptides were characterized for immunoreactivity, binding to ganglioside GM1, ability to associate with the A subunit, ability to form holotoxin, and biological activity. Amino acid substitutions that caused decreased binding of mutant CT-B to ganglioside GM1 and abolished toxicity included negatively charged or large hydrophobic residues for Gly-33 and negatively or positively charged residues for Trp-88. Substitution of lysine or arginine for Gly-33 did not affect immunoreactivity or GM1-binding activity of CT-B but abolished or reduced toxicity of the mutant holotoxins, respectively. Substitutions of Glu or Asp for Arg-35 interfered with formation of holotoxin, but none of the observed substitutions for Lys-34 or Arg-35 affected binding of CT-B to GM1. The Cys-9, Cys-86 and Trp-88 residues were important for establishing or maintaining the native conformation of CT-B or protecting the CT-B polypeptide from rapid degradation in vivo.
Mol Microbiol 1991 Jul
PMID:Analysis of structure and function of the B subunit of cholera toxin by the use of site-directed mutagenesis. 194 8

Sertoli cell produces several biological factors that modulate Leydig cell steroidogenic function by either stimulating or inhibiting its testosterone production. We have evaluated the effect of an inhibitory factor in the spent media of a Sertoli clonal cell line (TM4) which inhibits Leydig cell steroidogenesis. The presence of such an inhibitory factor in TM4 media was bioassayed using Percoll purified Leydig cells isolated from adult rats with purity of greater than 95%. TM4 media inhibited both human chorionic gonadotropin (hCG)-stimulated testosterone and cAMP production by purified Leydig cells dose-dependently but had no apparent effect on 8-bromo-cAMP- and forskolin-stimulated testosterone production. Also it did not interfere with the binding of [125I]hCG to Leydig cells. TM4 media inhibited cholera toxin-stimulated testosterone production as well as forskolin- and cholera toxin-stimulated cAMP production. The mechanism of action of this factor in TM4 media appears to be different from transforming growth factor (TGF-beta) which inhibited both 8-bromo-cAMP- and forskolin-stimulated testosterone production and inhibited the binding of [125I]hCG binding to Leydig cells. The inhibitory factor contained in TM4 media has been partially purified by sequential preparative anion exchange and C-18 reversed-phase high-performance liquid chromatography. In summary, the Sertoli TM4 cell line produces at least one potent inhibitory factor which decreases the responsiveness of purified Leydig cells to hCG stimulation with a dramatically different mechanism from other currently known Leydig cell inhibitory factors; this protein may serve as a valuable tool to study testicular paracrine regulation.
Mol Cell Endocrinol 1991 Sep
PMID:Identification of an inhibitory factor from a Sertoli clonal cell line (TM4) that modulates adult rat Leydig cell steroidogenesis. 195 71

This study aims to elucidate gene expression of laminin and its role in expansion of the blastocyst during mouse early embryo-genesis. The gene expression of laminin, in particular the B1 subunit and the synthesis of laminin polypeptides, was examined during the expansion of blastocyst by a RNA-blot hybridization with 32P-labeled laminin B1 cDNA and immunoprecipitation followed by a SDS-PAGE, respectively. Laminin B1 transcript was actively expressed in the blastocyst stage of embryos. The gene expression of laminin B1 and the synthesis of laminin protein were also increased when blastocyst was expanded. Treatments of cAMP analogue, isobutylmethylxanthine, forskolin, and cholera toxin, which are known to stimulate the blastocyst expansion, increased laminin B1 transcript levels and synthesis of laminin polypeptides. Treatment with retinoic acid, a known regulator of laminin gene expression, not only increased the gene expression of laminin but stimulated the blastocoel expansion without a significant increase in intracellular cAMP levels. These results indicate that laminin gene expression may play an important role in the process of blastocyst expansion in the mouse preimplantation embryos.
Mol Reprod Dev 1990 Nov
PMID:Regulation of laminin gene expression in the expansion of mouse blastocysts. 196 57

We examined the effect of GM1-ganglioside in combination with cholera toxin B, and synthetic alpha-sialyl cholesterol (alpha-SC) on neutral amino acid (tritiated alpha-aminoisobutyric acid, [3H]AIB) uptake, protein synthesis [( 3H]leucine incorporation), and Na+,K(+)-ATPase activity in isolated superior cervical ganglia (SCG) and nodose ganglia (NG) from adult rats after aerobic incubation, usually for 2 h at 37 degrees C in vitro. Cholera toxin B, that specifically masks the oligosaccharide chain of GM1-ganglioside, antagonized the GM1-induced changes in [3H]AIB uptake, [3H]leucine incorporation, and Na+,K(+)-ATPase activity almost completely in SCG, but partially in NG. Although cholesterol itself had little effect on either [3H]AIB uptake and Na+,K(+)-ATPase activity both in SCG and NG, alpha-SC caused considerable reduction of both amino acid uptake and the transport enzyme activity in each ganglia. However, cholesterol was more effective than alpha-SC in decreasing [3H]leucine incorporation in either ganglia. Whereas addition of EGTA markedly reduced either GM1-induced or alpha-SC-induced change in [3H]leucine incorporation into acid-insoluble fraction in both SCG and NG, application of Ca2+ ionophore produced considerable recovery of the protein synthesis from the inhibited level by Ca2(+)-deprivation. ATP and creatine phosphate contents in SCG were elevated by the presence of GM1 or alpha-SC, whereas [3H]AIB uptake and Na+,K(+)-ATPase activity were inhibited, suggesting that utilization for membrane transport was diminished as a result of GM1- or alpha-SC-induced decrease of ATPase activity.
Mol Chem Neuropathol
PMID:Effects of GM1-ganglioside and alpha-sialyl cholesterol on amino acid uptake, protein synthesis, and Na+,K(+)-ATPase activity in superior cervical and nodose ganglia excised from adult rats. 196 79


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