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 a single injection of estradiol benzoate upon the activity of 17 alpha-hydroxylase and C17,20-lyase in the ovaries of hypophysectomized immature rats was investigated. Tritiated H2O from 17 alpha-[3H]progesterone and 14CH3COOH from 21-[14C]progesterone were the products measured to evaluate the hydroxylase and lyase activities respectively. Estradiol (E2) had no direct effect upon the activity of the enzymes in vitro even when present at twice the concentration of the substrate. However, when given in vivo, E2 reduced the activity of both enzymes. The ratio of the activities remained constant supporting the contention that both enzyme activities reside in one cytochrome P-450. Cycloheximide attenuated, but did not prevent, the reduction obtained with estrogen. Enzyme activities were reduced by E2 to a slightly lesser degree when the ovaries had been exposed in vivo to exogenous gonadotropin for 72 h. The results indicate that 17 alpha-hydroxylase and C17,20-lyase activities decrease when large doses of E2 are administered in vivo, that this effect is not directly on the enzymes, and that at least a part of this effect involves macromolecular synthesis.
Mol Cell Endocrinol 1984 May
PMID:The in vitro and in vivo effect of estradiol upon the 17 alpha-hydroxylase and C17,20-lyase activity in the ovaries of immature hypophysectomized rats. 661 May 82

Tissue slices or dispersed cells of bovine parathyroid gland were incubated with [3H]leucine to label the intracellular proteins and then tested for their secretory response to isoproterenol and cycloheximide at different calcium concentrations. Secretion of the newly synthesized as well as the older PTH and SP-I was stimulated by isoproterenol at all calcium levels tested, even when it was maximally enhanced by low calcium. Cycloheximide interfered with neither the secretory process nor the secretory response to different stimuli, but decreased the amount of PTH and SP-I secreted. We conclude that the inhibitor decreased the secretion by reducing the supply of PTH and SP-I. Calculations derived from the data reveal that, under most secretory conditions, newly synthesized PTH contributed a major portion of the total hormone secretion in bovine parathyroid cells.
Mol Cell Endocrinol 1983 Dec
PMID:Effects of isoproterenol and cycloheximide on parathyroid secretion. 665 70

Normal female and ovariectomized rats were infused into the 3rd ventricle with [3H]glycine or [3H]alanine. Some rats were pretreated with cycloheximide. Hypothalamus, anterior pituitary and fragments of cortex were excised, homogenized, extracted and treated with specific antiserum to GnRH, bound to Sepharose. The radioactivity of immuno-absorbed products was counted either immediately of after extraction and thin-layer chromatography by using two different solvent systems. With the two systems, the location of the immuno-absorbed radioactivity always coincided with the spot of synthetic GnRH. Our results show that [3H]glycine was incorporated, as a function of time, into GnRH isolated from rat hypothalami. The amount was incorporated, as a function of time, into GnRH isolated from rat hypothalami. The amount of radioactivity incorporated into hypothalami from diestrous-I rats was similar to that of ovariectomized rats and twice as high as in late proestrous rats. Only minute amounts of radioactivity were incorporated into the immuno-absorbed product. Cycloheximide inhibited incorporation of [3H]glycine into the immuno-absorbed product to the same extent as its incorporation into the total protein from the hypothalamus. Our experimental results support the hypothesis of ribosomal mechanisms being involved in the biosynthesis of GnRH. They also suggest that the rate of accumulation of newly synthesized labeled GnRH is of the same order in the hypothalamus of ovariectomized rats as in diestrous-I rats.
Mol Cell Endocrinol 1982 Feb
PMID:Biosynthesis, in vivo, of gonadotropin-releasing hormone in the hypothalamus of normal and ovariectomized female rats. 703 55

When the levels of three common yeast proteinases in exponentially growing cells of mutants blocked in different repair pathways are compared to that of isogenic wild-type cells, it can be seen that the level of proteinase B is enhanced in the mutants whereas the levels of leucin aminopeptidase (Leu.AP) and lysine aminopeptidase (Lys.AP) are similar in all strains. As in its corresponding wild type, the level of proteinase B activity is further enhanced after UV-irradiation in a mutant blocked in excision-repair (rad1-3). In contrast, following the same treatment the level of proteinase B remains almost constant in a mutant blocked in a general error-prone repair system (rad6-1) and in a mutant defective in a more specific mutagenic repair pathway (pso2-1). Cycloheximide, an inhibitor of protein synthesis, blocks the post-UV enhancement in proteinase B activity observed in rad1-3 indicating that, as in the wild-type cells, an inducible process is involved. The levels of Lys.AP and Leu.AP are, respectively, either unaffected or only moderately increased following UV-treatment of the repair defective mutants, as in wild-type strains. It is obvious that the induction of protease B activity following UV-treatment in Saccharomyces cannot be equated to the induction of the recA protein in Escherichia coli. However the correlation found between the block in mutagenic repair and the lack of UV-induction of protease B activity leads to questions on the possible role of certain protease activities in mutagenic repair in eucaryotic cells.
Mol Gen Genet 1982
PMID:Proteolytic activities in yeast after UV irradiation. II. Variation in proteinase levels in mutants blocked in DNA-repair pathways. 704 85

Rat liver chromatin-bound RNA polymerase II could be differentially solubilized into two distinct populations, loosely and tightly bound enzymes, by a simple method. By this method the recovery of the solubilized enzyme from the chromatin fraction could be increased considerably as compared with the procedure of Yu (1). The two chromatin-bound enzymes had different properties: (a) Loosely bound enzyme was easily extractable from chromatin with relatively mild ionic condition (0.5 M NaCl); the tightly bound enzyme had to be solubilized by more drastic conditions such as sonication or nuclease treatment. (b) Loosely bound enzyme could not efficiently transcribe the chromatin template, but the tightly bound enzyme was active toward the same template. The latter enzyme is involved in the tight complex with the RNA synthesis activating factors. (c) Cycloheximide treatment in vivo suggests that the two enzymes have different turn-over rates. Therefore, with this simple solubilization method the functionally different two chromatin-bound RNA polymerase II activities can be estimated.
Mol Biol Rep 1982 Apr 16
PMID:A simple solubilization method for loosely and tightly chromatin-bound RNA polymerase II from rat liver nuclei. 712 57

Rats were treated with non-lethal doses of alpha-amanitin or cycloheximide. Nuclei were prepared and the particles carrying heterogeneous nuclear RNA (30--40 S-particles) isolated by density gradient centrifugation. In the case of alpha-amanitin the yield of particles was reduced to about 45%. Cycloheximide affected the composition of proteins associated with the nuclear RNA. In particular, the concentration of a 110 000 molecular weight protein as determined by sodium dodecylsulfate gel electrophoresis was reduced to 20--30% after 2 h and then increased to 150--180% of the control before it approached the normal level after 30 h. Possible mechanisms underlying these changes are discussed.
Mol Biol Rep 1980 Mar 31
PMID:Composition of hnRNA-associated proteins in rat liver is specifically altered after cycloheximide treatment. 739 26

The kinetic properties of glucocorticoid and catecholamine stimulation of amino acid transport in freshly isolated rat hepatocytes were investigated. In the basal state (i.e., with hepatocytes incubated for 2 h in the absence of glucocorticoid or catecholamine), the saturable transport of alpha-aminoisobutyric acid (AIB) was accounted for mainly by a low-affinity component (Km for AIB approximately 5 mM). Hepatocyte exposure to cortisol (or dexamethasone), or to epinephrine for isoproterenol), for 2 h resulted in a 3- to 4-fold increase in the Vmax of a high-affinity component (Km for AIB approximately 1 mM) which was only weakly expressed in the basal state. Neither glucocorticoids nor catecholamines exerted a detectable effect on the low-affinity transport component. Cycloheximide prevented the emergence of the high-affinity component in hepatocytes exposed to dexamethasone or epinephrine. The results suggest that the stmulatory effect of glucocorticoids and catecholamines on amino acid transport in hepatocytes results from the synthesis of a high-affinity transport component.
Mol Cell Endocrinol 1980 Sep
PMID:Glucocorticoid and catecholamine stimulation of amino acid transport in rat hepatocytes. Synthesis of a high-affinity component. 740 5

The kinetics of secretion of proteins by Leishmania braziliensis was followed by incorporation of [3H]leucine into macromolecules produced by the cells which are released into the growth medium. About 10% of the total protein synthesized by actively growing cells is secreted. Cycloheximide (100 microgram/ml) and puromycin (0.5 mM) inhibited the incorporation of labelled leucine by 85 and 99%, respectively. The secreted proteins do not seem to result from cell lysis since, first, the kinetics of production are linear and, secondly, less than 1% of thymidine or uridine incorporated by the cells is found in the medium. Cells grown with [3H]leucine and then transferred to fresh medium show two phases of secretion. During the first six hours, it is slow and reaches a plateau. The release increases about ten-fold during the next six hours. An analysis of the secreted material showed that following precipitation with methanol and sodium acetate, three isotopically labelled peaks were eluted from Sephadex G-120-150. The first of these, containing 50% of the radioactivity, did not react with anti-leishmanial serum, while the last two did. Since the last two fractions could be labelled with [3H]glucosamine as well as [3H]leucine it is suggested that they are glycoprotein in nature and are similar to the products released by other species of Leishmania.
Mol Biochem Parasitol 1980 Jun
PMID:Production and secretion of Leishmania braziliensis proteins. 744 14

Induction of HSP70 heat shock genes by light has been demonstrated in Chlamydomonas. Our aim was to establish whether this induction by light is mediated by the heat stress sensing pathway or by an independent signal chain. Inhibitors of cytoplasmic protein synthesis revealed an initial difference. Cycloheximide and other inhibitors of protein synthesis prevented HSP70A induction upon illumination but not during heat stress. Analysis of HSP70A induction in cells that had differentiated into gametes revealed a second difference. While heat shock resulted in elevated HSP70A mRNA levels, light was no longer able to serve as an inducer in gametes. To identify the regulatory sequences that mediate the response of the HSP70A gene to either heat stress or light we introduced a series of progressive 5' truncations into its promoter sequence. Analyses of the levels of mRNA transcribed from these deletion constructs showed that in most of them the responses to heat shock and light were similar, suggesting that light induction is mediated by a light-activated heat shock factor. However, we show that the HSP70A promoter also contains cis-acting sequences involved in light induction that do not participate in induction by heat stress. Together, these results provide evidence for a regulation of HSP70A gene expression by light through a heat shock-independent signal pathway.
Mol Gen Genet 1995 Oct 25
PMID:Heat shock and light activation of a Chlamydomonas HSP70 gene are mediated by independent regulatory pathways. 747 76

Astrocytes are immunoactive cells in brain and have been implicated in the defense mechanism in response to external injury. Previous studies using cultured glial cells indicated the ability of astrocytes to respond to bacteria endotoxin and cytokines, resulting in the release of phospholipase A2. In this study, we examined the interactive effects of lipopolysaccharides (LPS), interleukin 1 beta (IL-1 beta) and tumor necrosis factor (TNF alpha) to stimulate phospholipase A2 (PLA2) in an immortalized astrocyte cell line (DITNC) with many properties of type I astrocytes. Northern blot analysis using oligonucleotide probes derived from the cDNA encoding the rat spleen group II PLA2 indicated the ability of DITNC cells to respond to all three factors in the induction of gene expression and the release of PLA2. After an initial lag time of 2 h, PLA2 release was proportional to time, reaching a plateau by 12 h. This event occurred at a time period preceding any signs of cell death. Cycloheximide at 1.25 microM completely inhibited cytokine-induced PLA2 release. When suboptimal amounts of TNF alpha were added to the DITNC culture together with IL-1 beta or LPS, a synergistic increase in the induction of PLA2 release could be observed. On the other hand, combination of IL-1 beta and LPS resulted only in an additive increase in PLA2 release. Antibodies to IL-1 beta and TNF alpha completely neutralized the effects of these two agents on PLA2 release. However, neither antibody was able to inhibit the PLA2 release induced by LPS, suggesting that the effect of LPS was not complicated by the release of IL-1 beta or TNF alpha. Taken together, results show that the immortalized astrocyte cell line (DITNC) can be used for studies to elucidate the molecular mechanism underlying the cytokine signaling cascade and subsequent induction of PLA2 synthesis.
Mol Chem Neuropathol 1995 May
PMID:Stimulation of group II phospholipase A2 mRNA expression and release in an immortalized astrocyte cell line (DITNC) by LPS, TNF alpha, and IL-1 beta. Interactive effects. 754 15


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