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Effect of opioids on Ca2+/cAMP responsive element binding protein

100%
Bilecki W., Przewlocki P. R., Przewlocki R.
Acta Neurobiologiae Experimentalis
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2000
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vol. 60
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issue 4
557-567
EN
Ca2+/cAMP response element binding protein (CREB) is an important factor linking the opioid-regulated secondary messenger systems to alterations in gene expression. Opioids regulate CREB level, its phosphorylation and binding to its corresponding response element in the promoters of several genes implicated in drug addiction. CREB mediates the action of opioids on the expression of several genes in brain regions responsible for drug-seeking behavior and manifestation of signs of dependence. Moreover, alterations in CREB level can affect the rewarding properties of morphine and regulate the self-administration of cocaine. At the cellular level CREB acts as convergence point for different cellular pathways. Opioids affect two different intracellular mediator systems: inhibitory - connected with cAMP, and stimulatory - involving calcium and the PKC pathway. Both can affect CREB but in different phases of opiate action. The presence of this biphasic mechanism can explain the phenomenon of the induction of some CRE-controlled genes after both acute and chronic morphine administration. Cellular studies also highlight the relevance of other ATF/CREB family members which can affect Ca2+/cAMP response element (CRE) controlled transcription as well as other transcription factors which make the opioid induction longer lasting.
2

Regulation of proenkephalin gene expression by transcription factors Fos and CREB: an antisense oligonucleotide approach

88%
Ziolkowska B., Przewlocka B., Bilecki W., Machelska H., Przewlocki R.
Biotechnologia
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1996
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issue 4
167-172
EN
The present study investigated the effects of antisense oligonucleotides (AS ODNs) against c-fos and CREB m RNA in two models of the proenkephalin (PENK) gene induction.AS ODNs to both c-fos and CREB mRNA markedly reduced induction of the PENK gene in the rat hippocampus in vivo during seizures produced by kainic acid (KA).In contrast, in an in vitro model of the PENK gene induction by noradrenaline and dexamothasone in C6 glioma cells, the AS ODN to c-fos was without effect, whereas the AS ODN to CREB reduced the increase in the PENK mRNA level.The obtained results suggest that the transcription factors Fos and CREB may mediate induction of the PENK gene in the hippocampus, while induction of this gene in C6 glioma is mediated by CREB rather than Fos.
3

Antisense oligonucleotides against inducible nitric oxide synthase reduce No production in RAW 264.7 cells

88%
Bilecki W., Okruszek A., Kwinkowski M., Sanak M., Przewlocki R.
Biotechnologia
|
1996
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issue 4
173-182
EN
Several oligodeoxyribonucleotides in a nuclease-resistant phosphorothioate form targeted to iNOS mRNA were tested in RAW 264,7 cells as potential antisense inhibitors.Antisense S-ODNs inhibited iNOS activity in a time- and dose-depended manner.Application of Lipofectin agent, which itself had no significant effect, greatly increased antisense activity.Decreased levels of the target mRNA, as demonstrated by reverse transcriptase -polymerase chain reaction (RT-PCR), suggest tha RNase H mediated mechanism.
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