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

Cell kinetic studies on cultured human epidermal cells have indicated that cycling basal cells may be divided into at least two subpopulations that seem to differ with respect to the rate of DNA replication. The present study was undertaken in order to elucidate the biological significance of these subpopulations. The proliferation characteristics of cultured basal cells were changed by the addition of epidermal growth factor (EGF) and cholera toxin to the culture medium. It was shown that EGF and cholera toxin stimulated the growth of human epidermal cells in culture. Simultaneously, the terminal differentiation of the cells was inhibited resulting in a reduced multilayering and a reduced formation of the cornified envelope. However, only minor differences in the protein synthesis pattern were observed between cultures maintained in the presence or absence of the growth stimulators. The effect of EGF and cholera toxin on the basal cell subpopulations was investigated after 3H-thymidine labelling followed by cell sorting and autoradiography. In the presence of EGF and cholera toxin dramatic changes were induced in the labelling pattern of sorted S-phase cells indicating significant alterations in the balance between the subpopulations of cycling basal cells. Our results with these substances are in accord with the hypothesis that the observed cell kinetic subpopulations may be related to regeneration or early events in the differentiation process of the keratinocyte.
Virchows Arch B Cell Pathol Incl Mol Pathol 1985
PMID:Changes in basal cell subpopulations and tissue differentiation in human epidermal cultures treated with epidermal growth factor and cholera toxin. 241 7

The purpose of this study was to determine the role of cAMP in the growth of FRTL and FRTL5 cells, 2 continuous cultured thyroid lines. TSH, at concentrations similar to those reported to induce growth in primary dog thyroid cultures, played an essential role for growth. Stimulators of adenylate cyclase, cholera toxin and forskolin, and cAMP analogues, dibutyryl cAMP and 8-bromo cAMP, mimicked the effect of TSH in both groups of cultured cells. The present data confirm the role of TSH in controlling growth of both cell lines and suggest that cAMP is an essential intracellular mediator of TSH action.
Mol Cell Endocrinol 1986 Mar
PMID:Control of growth in cultured rat thyroid cells. 242 Jun 57

In the design of the synthetic antigens and synthetic vaccines, primary consideration should be given to the choice of the carrier. Since small peptides which are being used as the relevant antigenic determinants are likely to be poor immunogens as such, the augmentation of their immunogenic capacity by the carrier or any other means is crucial for the induction of immunity. In the present study, we explored several approaches for the enhancement of the immune response towards synthetic peptides derived from the B-subunit of cholera toxin. The results indicate that the use of tetanus toxoid as a macromolecular carrier, polymerization of the peptide without any external carrier and the conjugation of dipalmityl side chain had comparable effects in enhancing the immune response to several synthetic peptides. This effect was manifested both at the level of antibodies produced and in their capacity to neutralize the biological activity of the cholera toxin. Prior exposure to the carrier resulted in a dose-dependent suppression against the synthetic epitope attached to it.
Mol Immunol 1985 Dec
PMID:Effect of carrier on the immunogenic capacity of synthetic cholera vaccine. 242 Nov 53

Upon first exposure, synthetic human growth hormone-releasing factor (GRF) and prostaglandin E2 (PGE2) cause a rapid and marked stimulation of cyclic AMP accumulation and GH release in rat adenohypophysial cells in primary culture. However, a marked attenuation of these responses occurs following previous incubation with the 2 compounds. A 50% desensitization of the cyclic AMP and GH responses is observed after 100 and 150 min of preincubation with 300 nM GRF, respectively. After a prior exposure to 3 microM PGE2, a 50% maximal decrease of the cyclic AMP and GH responsiveness to a subsequent 3 h incubation with PGE2 is obtained at 90 and 120 min, respectively. Following preincubation with GRF, a loss of responsiveness of the cyclic AMP and GH responses is also observed after heterologous stimulation with PGE2. A similar heterologous desensitization to the action of GRF is observed following pretreatment with PGE2. The desensitizing action of GRF on the cyclic AMP and GH responses is obtained at respective IC50 values of 2 and 7 nM for both the homologous and heterologous responses. The sensitivity of the desensitizing effect of GRF (7 nM) is thus identical to that of its stimulatory action on GH release (6.2 nM). The desensitization to GRF, in analogy to that to PGE2, is mainly due to a decrease in the maximal action of GRF. Although GH cell content is decreased by previous exposure to GRF and/or PGE2, the ability of forskolin, cholera toxin, 8-bromo 3',5'-adenosine cyclic monophosphate and 3-isobutyl-1-methylxanthine to stimulate GH release remains unchanged in cells pretreated with these compounds, thus indicating that the loss of responsiveness to GRF and PGE2 is not due to a depletion of the releasable pool of GH. On the other hand, nifedipine, a potent calcium channel antagonist, completely abolishes the stimulatory effect of GRF on GH release while not affecting basal and GRF- or PGE2-induced cyclic AMP accumulation. Preincubation with nifedipine has no influence on the desensitizing effect of GRF or PGE2 on either the cyclic AMP or GH responses to the same stimuli. In addition to showing the cross-desensitization by GRF and PGE2, the present results strongly suggest that the desensitization does not result from a depletion of the GH releasable pool but most likely results from a down-regulation and/or an impairment of coupling of a component of the adenylate cyclase system independent from calcium uptake.
Mol Cell Endocrinol 1986 Jun
PMID:Characteristics of the desensitization of growth hormone and cyclic AMP responses to growth hormone-releasing factor and prostaglandin E2 in rat anterior pituitary cells in culture. 242 97

The mutations oagM and oagR affecting the synthesis of somatic O-antigen have been localized on the chromosome of Vibrio cholerae El Jor and classic biotypes by conjugational crosses between different donor and recipient strains. The mutations are localized in the vicinity of the arg marker in both classic and El Tor biotypes of Vibrio cholerae.
Mol Gen Mikrobiol Virusol 1985 Oct
PMID:[Genetic analysis of mutations affecting the synthesis of somatic O-antigen of Vibrio cholerae]. 243 16

Ecdysteroid-producing Y-organs from the crab Cancer antennarius were shown to possess enzyme activity that was stimulated in vitro by addition of Ca2+, phosphatidylserine, or the protein kinase C activator, phorbol 12-myristate 13-acetate (PMA; ED50, 4 nM). In the presence of calcium and phosphatidylserine, PMA increased protein kinase C activity dose-dependently to a maximum 4-fold increase at 100 nM PMA. Stimulated protein kinase C activity was unaffected by calmodulin (100 nM) but was inhibited by 100 nM trifluoperazine. Pretreatment of cultured Y-organ segments with PMA elevated basal protein kinase C activity, whereas molt-inhibiting hormone (MIH) and calcium ionophore A23187 did not affect activity. PMA (1-100 nM) increased Y-organ steroidogenesis dose-dependently and alleviated suppression due to MIH or lysine vasopressin; PMA effects on steroidogenesis became evident after 2 h of incubation. Another phorbol activator of protein kinase C (phorbol 12, 13-dibutyrate) and a permeable synthetic diacylglycerol (1-oleoyl-2-acetyl-glycerol) stimulated ecdysteroidogenesis while an inactive phorbol (4 alpha-phorbol 12,13-didecanoate) and diolein were ineffective. The inhibitory effects on steroidogenesis of cholera toxin, forskolin, dibutyryl cAMP, and 3-isobutyl-1-methylxanthine were countered by PMA, but PMA did not alter basal or peptide hormone-stimulated Y-organ cAMP levels. Stimulatory effects on steroidogenesis of PMA and of A23187 were not additive, and PMA did not alter inhibition caused by lanthanum (calcium channel blocker) or trifluoperazine (calmodulin inhibitor). PMA increased the incorporation of [3H]leucine into Y-organ protein by 112%, and countered the suppressive effect of MIH on protein synthesis; PMA did not affect RNA synthesis. When Y-organs were suppressed with cycloheximide, PMA was unable to stimulate steroidogenesis. Actinomycin D alone had no effect on steroidogenesis but prevented stimulation by PMA. The results indicate that Y-organs contain protein kinase C activity which stimulates ecdysteroid production and protein synthesis by a mechanism not directly interactive with the cAMP or Ca2+-calmodulin systems.
Mol Cell Endocrinol 1987 Feb
PMID:Demonstration of protein kinase C activity in crustacean Y-organs, and partial definition of its role in regulation of ecdysteroidogenesis. 243 89

Fusion proteins comprising the amino-terminal 99 amino acids of the bacteriophage MS2 replicase and various portions of OmpV a major outer membrane protein of Vibrio cholerae were expressed in Escherichia coli K12. These fusions were expressed under the control of the PL promoter of bacteriophage lambda, and expression was controlled using a cIts repressor. Fusions occurring within the secretory signal sequence of OmpV gave rise to the production of mature OmpV. The efficiency, however, decreased with progressive deletion of the signal sequence within the fusions. The reactivity of various OmpV fusions with antisera raised against purified OmpV and whole bacteria demonstrated the existence of two antigenic domains: one present in the denatured form and another in the membrane-associated form of OmpV. These domains correspond to markedly hydrophilic regions of the protein as would be predicted for surface-exposed epitopes.
Mol Gen Genet 1986 Dec
PMID:Serological properties and processing in Escherichia coli K12 of OmpV fusion proteins of Vibrio cholerae. 243 27

Exposure of human decidual cells for 0.5 h to dibutyryl cAMP, isobutyl-methylxanthine (IBMX), cholera toxin or forskolin caused a dose-dependent inhibition of prolactin release with maximal inhibition by each agent of 50-60%. Dibutyryl cAMP (5 mM), IBMX (0.5 mM), and cholera toxin (10 micrograms/ml) also inhibited prolactin synthesis to the same extent as prolactin release. Dibutyryl cAMP, IBMX, and cholera toxin, however, had no effect on the release of 35S-methionyl-prolactin from decidual cells preincubated for 24 h in medium with 35S-methionine. These agents, however, had no effects on the synthesis or release of TCA-precipitable 35S-decidual proteins and did not cause the degradation of intracellular or released prolactin. The demonstration that agents which increase intracellular cAMP levels inhibit the synthesis and release of decidual prolactin strongly implicates cAMP as a second messenger in the regulation of the synthesis and release of the hormone. The inhibitory effect of cAMP on prolactin release appears to be on the release from a rapidly releasable, newly synthesized intracellular prolactin pool.
Mol Cell Endocrinol 1987 Mar
PMID:Cyclic AMP inhibits the synthesis and release of prolactin from human decidual cells. 243 70

1,25-Dihydroxyvitamin D3 [1,25-(OH)2D3] regulates the synthesis of bone gamma-carboxyglutamic acid (Gla) protein (BGP) by osteoblastic cells. In this study we examined the effect of cAMP, alone and in combination with 1,25-(OH)2D3, on the regulation of BGP mRNA levels in ROS 17/2 rat osteosarcoma cells. Elevation of intracellular cAMP levels by cAMP analogs or by isobutylmethylxanthine (IBMX), forskolin, or PTH, resulted in increased BGP mRNA levels and BGP secretion after 1 day of treatment. The effects of these agents were additive with 1,25-(OH)2D3 in stimulating BGP gene expression. After 4 days of treatment, pertussis toxin (PT) and 1,25-(OH)2D3 were synergistic in stimulating BGP mRNA, and the effect of PT could be mimicked by (Bu)2cAMP, IBMX, forskolin, cholera toxin, and to a lesser extent by PTH. The effect of 1-day treatment with cAMP alone and the synergistic effect with 1,25-(OH)2D3 on the stimulation of BGP mRNA were dependent on cell density, while basal and 1,25-(OH)2D3-stimulated synthesis were not. Cyclic AMP inhibited ROS 17/2 cell growth after 1 day of treatment, an effect that was also dependent on initial cell density. After 4 days of treatment, 1,25-(OH)2D3, cAMP, and PT all demonstrated inhibition of cell growth. When cells were treated with actinomycin D, both 1,25-(OH)2D3 and cAMP stimulation of BGP mRNA were blocked. In addition, neither agent was effective in enhancing BGP mRNA stability when prestimulated cells were exposed to actinomycin D.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Endocrinol 1989 Jan
PMID:Bone Gla protein messenger ribonucleic acid is regulated by both 1,25-dihydroxyvitamin D3 and 3',5'-cyclic adenosine monophosphate in rat osteosarcoma cells. 246 56

The secretagogue effects of prolactin (PRL) and of various agents acting on cAMP levels, forskolin, cholera toxin and iloprost (a stable analogue of prostaglandin I2) have been assessed in lactating doe mammary gland fragments in vitro. Forskolin (10 microM), cholera toxin (1 microgram/ml) and iloprost (10 mM) stimulated milk casein secretion. The effects of forskolin (10 microM) and cholera toxin (1 microgram/ml) were potentiated by PRL (10 micrograms/ml). Conversely, the action of iloprost (10 microM) was not amplified by PRL (10 micrograms/ml). Forskolin (10 microM) and cholera toxin (1 microgram/ml) stimulated the intracellular accumulation of cAMP. Neither PRL nor iloprost, at concentrations which stimulated casein secretion, modified the accumulation of cAMP. These results demonstrate that PRL does not act directly by any increase in intracellular cAMP levels. However, stimulating effects of forskolin and cholera toxin on casein secretion and intracellular cAMP levels suggest that various transduction signals are effective in the mammary cells.
Mol Cell Endocrinol 1989 Aug
PMID:The actions of forskolin, cholera toxin and iloprost on casein secretion by lactating doe mammary glands. 247 50


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