C-Jun activation of the DYNCRE3 site in the prodynorphin promoter

Messersmith, Donna J.; Kim, D.J.; Gu, Jianxin; Dubner, Ronald; Iadarola, Michael J.

doi:10.1016/0169-328x(96)00029-0

Cited by 24 publications

(12 citation statements)

References 19 publications

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“…The fact that a dbcAMP-induced increase in ppN/OFQ mRNA is not seen when using a reporter vector could either be because the required DNA binding element needed for dbcAMP-induction is not found within the proximal 1.3 kb of promoter, or else the chromatin required for functioning of this transcription factor is not sufficient in the artificial environment of the pGL3 plasmid. In the preprodynorphin promoter, CRE sites found 1.4 kb and further upstream are required for a cAMP-induced increase in transcription (Cole et al, 1995;Messersmith et al, 1996). Nevertheless, two lines of evidence suggest that the second possibility is likely the correct one.…”

Section: Discussionmentioning

confidence: 92%

Regulation of the prepronociceptin gene and its effect on neuronal differentiation

Zaveri

Waleh

Toll

2006

Gene

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Section: Discussionmentioning

confidence: 92%

Regulation of the prepronociceptin gene and its effect on neuronal differentiation

Zaveri

Waleh

Toll

2006

Gene

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“…We also measured the effects of acute and chronic METH administration on preprotachykinin (Tac1) (Almeida et al, 2004) and prodynorphin (Pdyn) (Schwarzer, 2009) mRNA levels because of their reported acute induction by METH (Bannon et al, 1987; Wang et al, 1995) and because of the presence of AP1/CRE binding sites on their promoters (Calin-Jageman et al, 2006; Messersmith et al, 1996). Figure 6a shows that the acute METH injection caused significant increases in Tac1 (~1.5-fold, p < 0.0267).…”

Section: Resultsmentioning

confidence: 99%

Chronic methamphetamine exposure suppresses the striatal expression of members of multiple families of immediate early genes (IEGs) in the rat: normalization by an acute methamphetamine injection

et al. 2011

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Rationale Repeated injections of cocaine cause blunted responses to acute cocaine challenge-induced increases in the expression of immediate early genes (IEGs). Objectives The aim of this study was to test if chronic methamphetamine (METH) exposure might cause similar blunting of acute METH-induced increases in IEG expression. Results Repeated saline or METH injections were given to rats over 14 days. After one day of withdrawal, they received a single injection of saline or METH (5 mg/kg). Acute injection of METH increased c-fos, fosB, fra2, junB, Egr1-3, Nr4a1 (Nur77), and Nr4a3 (Nor-1) mRNA levels in the striatum of saline-pretreated rats. Chronic METH treatment alone reduced the expression of AP1, Erg1-3, and Nr4a1 transcription factors below control levels. Acute METH challenge normalized these values in METH-pretreated rats. Unexpectedly, acute METH challenge to METH-pretreated animals caused further decreases in Nr4a2 (Nurr1) mRNA levels. In contrast, the METH challenge caused significant but blunted increases in Nr4a3 and Arc expression in METH-pretreated rats. There were also chronic METH-associated decreases in the expression of cAMP responsive element binding protein (CREB) which modulates IEG expression via activation of the cAMP/PKA/CREB signal transduction pathway. Chronic METH exposure also caused significant decreases in preprotachykinin, but not in prodynorphin, mRNA levels. Conclusions These results support the accumulated evidence that chronic administration of psychostimulants is associated with blunting of their acute stimulatory effects on IEG expression. The METH-induced renormalization of the expression of several IEGs in rats chronically exposed to METH hints to a potential molecular explanation for the recurrent self-administration of the drug by human addicts.

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“…These elements function as CREs (DynCRE1, -2, and -3), and binding to CREB results in repression of AP-1-mediated prodynorphin transactivation (8). The mechanism for this transrepression is not known, although competition by different nuclear complexes at the DynCRE3 element could be a possibility, since it has been shown that DynCRE3 also binds AP-1 nuclear complexes and through this interaction transactivates the prodynorphin gene (8,29,30). In the proximal promoter region, close to the transcription start site, a noncanonical AP-1 site (ncDynAP-1) and a CRE-like element (DynCRE4) are present (11,33).…”

mentioning

confidence: 99%

Protein Kinase A-Dependent Derepression of the Human Prodynorphin Gene via Differential Binding to an Intragenic Silencer Element

Carrión

Mellström

Naranjo

1998

Molecular and Cellular Biology

119

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Induction of the prodynorphin gene has been implicated in medium and long-term adaptation during memory acquisition and pain. By 5 deletion mapping and site-directed mutagenesis of the human prodynorphin promoter, we demonstrate that both basal transcription and protein kinase A (PKA)-induced transcription in NB69 and SK-N-MC human neuroblastoma cells are regulated by the GAGTCAAGG sequence centered at position ؉40 in the 5 untranslated region of the gene (named the DRE, for downstream regulatory element). The DRE repressed basal transcription in an orientation-independent and cell-specific manner when placed downstream from the heterologous thymidine kinase promoter. Southwestern blotting and UV cross-linking experiments with nuclear extracts from human neuroblastoma cells or human brain revealed a protein complex of approximately 110 kDa that specifically bound to the DRE. Forskolin treatment reduced binding to the DRE, and the time course paralleled that for an increase in prodynorphin gene expression. Our results suggest that under basal conditions, expression of the prodynorphin gene is repressed by occupancy of the DRE site. Upon PKA stimulation, binding to the DRE is reduced and transcription increases. We propose a model for human prodynorphin activation through PKA-dependent derepression at the DRE site.

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C-Jun activation of the DYNCRE3 site in the prodynorphin promoter

Cited by 24 publications

References 19 publications

Regulation of the prepronociceptin gene and its effect on neuronal differentiation

Regulation of the prepronociceptin gene and its effect on neuronal differentiation

Chronic methamphetamine exposure suppresses the striatal expression of members of multiple families of immediate early genes (IEGs) in the rat: normalization by an acute methamphetamine injection

Protein Kinase A-Dependent Derepression of the Human Prodynorphin Gene via Differential Binding to an Intragenic Silencer Element

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