Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of the mitochondrial benzodiazepine receptor gene was assayed by a semi-quantitative non-radioactive reverse transcriptase polymerase chain reaction (RT-PCR) assay. The level of amplified mitochondrial benzodiazepine receptor mRNA was expressed as a ratio of either glyceraldehyde-3-phosphate dehydrogenase (GAPDH) or beta-actin mRNA co-amplified in the same RT-PCR assay. The relative amounts of mitochondrial benzodiazepine receptor RNA in several rat tissues were found to be similar to the previously reported relative amount of mitochondrial benzodiazepine receptor binding sites. The level of these binding sites has also been reported to be altered by stress stimuli. In this study we specifically measured the effect of stress on the mRNA levels of the mitochondrial benzodiazepine receptor as an alternative method to the binding assay in an attempt to understand the mechanism by which stress alters binding. Sprague-Dawley male rats were either forced to swim for 15 min in 18 degrees C water or restrained in a plastic cylinder for 45 min either once, or twice daily for 7 days. Neither the swim stress, nor acute or chronic restraint stress, caused a measurable statistically significant relative change in mitochondrial benzodiazepine receptor mRNA in the adrenal gland, kidney, testis and olfactory bulb. However, daily treatment of rats for 7 days with 4 mg/kg of dexamethasone caused a significant decrease in mitochondrial benzodiazepine receptor gene expression in adrenal glands. This finding and the measurement of the relative levels of mitochondrial benzodiazepine receptor mRNA in the various tissues indicate that mitochondrial benzodiazepine receptor density is regulated to some extent at the gene expression level. However, the lack of detectable stress-induced changes in mRNA levels for this receptor seem to indicate that either mRNA changes were below detectable levels or that other mechanisms may be involved in the previously reported stress-induced changes of mitochondrial benzodiazepine receptor density. Because the focus of this work was on the regulation of mitochondrial benzodiazepine receptor gene expression, ligand binding studies to determine changes in receptor densities were not performed.
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PMID:Dexamethasone, but not stress, induce measurable changes of mitochondrial benzodiazepine receptor mRNA levels in rats. 927 84

Intraperitoneal injection of 500 microg poly I:C/fish into Atlantic salmon parr in freshwater and post-smolts and growers in seawater (all at 11 degrees C) induced enhanced expression of Mx mRNA in liver tissue 24 h post-injection. The level of Mx transcripts peaked at day 3 (Mx:beta-actin ratio of about 0.8) and the response disappeared by day 7. In post-smolts, mortalities occurred up to day 14 post-injection, which was dose-dependent. Histological examination of tissues revealed severe pathological changes in the liver of poly I:C injected post-smolts resulting from apoptosis and necrosis of hepatocytes. All other organs appeared histologically normal. Levels of Mx mRNA expression on day 3 post-injection were similar for fish with normal and pathological livers. In untreated or control fish injected with PBS, low levels of Mx transcripts (Mx:beta-actin ratio about 0.1) were sometimes detectable in parr but not in growers. Constitutive Mx expression was variable in post-smolts. Some populations had no detectable transcripts while in others moderate ratios (about 0.3) were detectable over a 3-week period of sampling. Poly I:C administered to parr by bath or orally did not induce upregulation of Mx expression.
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PMID:Poly I:C-induced Mx responses in Atlantic salmon parr, post-smolts and growers. 1527 4

Amnesic shellfish poisoning toxin domoic acid (DA) is a marine neurotoxin that accumulates in fish and shellfish, and has been implicated to be involved in human and marine wildlife mortality. The transcriptional responses of cytochrome P-450 1A (CYP1A), glutathione S-transferase alpha (GSTA), glutathione S-transferase rho (GSTR), heat shock protein 70 (HSP70), and Na(+)/K(+)-ATPase alpha 1 (ATP1A1) in the liver of rabbitfish (Siganus oramin) intracoelomically injected with DA, were investigated. Experimental fish were administered with one injection of DA (2 microg/g wet weight) or PBS as control. After 24 h, fish were killed and hepatic RNA was isolated. Partial cDNA of rabbitfish CYP1A, GSTA, GSTR, HSP70, ATP1A1, and beta-actin were obtained by PCR using degenerate primers. Using beta-actin as an external control, the relative liver CYP1A, GSTA, GSTR, HSP70, and ATP1A1 mRNA abundance of rabbitfish were determined by semi-quantitative RT-PCR within the exponential phase. The ratio CYP1A/beta-actin mRNA (%) of exposure group was determined to be 148.92+/-12.69, whereas the ratio of control group was 82.3+/-8.35, indicating that CYP1A was induced significantly in rabbitfish following DA exposure (P<0.05). Although the expressions of GSTA, HSP70, and ATP1A1 tended to increase and GSTR tended to decrease, no significant changes were found (P>0.05). The induction of hepatic CYP1A in response to DA suggests a potential role for fish phase I xenobiotic metabolizing enzyme in DA metabolism.
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PMID:Transcriptional responses of xenobiotic metabolizing enzymes, HSP70 and Na+/K+ -ATPase in the liver of rabbitfish (Siganus oramin) intracoelomically injected with amnesic shellfish poisoning toxin. 1821 93

CpG-oligodeoxynucleotides (CpG-ODN) are potent stimulators of the innate immune system. They promote a Th1-biased immune response with antineoplastic potential. We recently demonstrated antitumoral effects of CpG-ODN in murine transitional cell carcinoma (TCC) models. The purpose of the present work was to more precisely define the immunological nature of this immunotherapeutic approach to TCC.MB-49 TCC was established in female C57/Bl6 mice by intravesical tumor cell instillation after poly-L-lysine conditioning of the bladder (day 0) as described previously. Three groups of six mice were treated: intravesical instillation of 50 microl PBS on days 1, 3, 5, and 7 (group 1, untreated control); 10 nmol CpG 1668 on days 1, 3, 5, and 7 (group 2); and 10 nmol GpC 1668 on days 1, 3, 5, and 7 (group 3). Six native bladders served as no-treatment/no-tumor controls (group 4). Mice were sacrificed on day 11; bladders and draining lymph nodes were removed, and mRNA was prepared for quantitative real-time polymerase chain reaction. Samples were analyzed on a Bio-Rad iCycler for IL 10, TGF-beta, IL 12, and IFNgamma expression; threshold values were compared to beta-actin as housekeeping gene.Tumor take was 100%. Three animals in group 1 had to be sacrificed in advance due to rapid tumor progression. Relative cytokine expression was comparable in groups 1 and 4. IL-10, IL-12, TGF-beta, and IFNgamma were overexpressed in groups 2 and 3. CpG-ODN treatment of murine TCC results in overexpression of both classic Th1 cytokines (IL 12 and IFNgamma) and the Th2 marker IL 10. TGF-beta expression is increased as well. These phenomena are not induced by the growing TCC but by CpG-ODN therapy. They are accompanied by an objective clinical response, as we were able to show recently. Immunostimulatory DNA holds promise to be a novel therapeutic agent in TCC.
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PMID:[Immunostimulatory CpG oligodeoxynucleotides (CpG-ODN) in an orthotopic murine transitional cell carcinoma (TCC) model. Effect on local cytokine expression]. 1867 50