Basal and Inducible Transcriptional Activity of an Upstream AP-1/CRE Element (DYNCRE3)in the Prodynorphin Promoter

Messersmith, Donna J.; Gu, Jianxin; Dubner, Ronald; Douglass, James; Iadarola, Michael J.

doi:10.1006/mcne.1994.1028

Cited by 39 publications

(25 citation statements)

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“…Those conditions which lead to elevated dynorphin expression would be expected to have the potential to down-regulate the proliferation and migration of the granule cells during this critical step. While current evidence suggests that dynorphin expression is constitutive in the nervous sytem, there is evidence that preprodynorphin mRNA expression is inducible through cAMP responsive elements in the preprodynorphin promoter (Messersmith et al 1994). Furthermore, there is evidence inflammatory responses in the periphery are accompanied by an accumulation of dynorphin A at both the inflammatory site and in the spinal cord (Hassan et al 1992;Ruda et al 1988), and interleukin 1 induces the production of dynorphin A at sites of inflammation (Schafer, Carter, & Stein 1994).…”

Section: Discussionmentioning

confidence: 99%

Bi-directional heterologous desensitization between the major HIV-1 co-receptor CXCR4 and the κ-opioid receptor

Finley

Chen

Bardi

et al. 2008

Journal of Neuroimmunology

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We previously characterized multiple interactions between chemokine and opioid G-protein coupled receptors (GPCR), and we found both µ and δ-opioid receptors cross-desensitize CCR1, CCR2, CCR5, but not CXCR4. Here we report that the κ-opioid receptor (KOR) is able to cross-desensitize CXCR4, and this phenomenon is bi-directional. Chemotactic responses by KOR activation are diminished with prior activation of CXCR4. Additionally, calcium mobilization assays show these cross-desensitization processes occur within seconds of receptor activation, and target receptor internalization is not responsible for desensitization between these receptors. These results have implications for several essential processes including neuronal and lymphocyte development, inflammatory responses, and pain/sensitivity.

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Section: Discussionmentioning

confidence: 99%

Bi-directional heterologous desensitization between the major HIV-1 co-receptor CXCR4 and the κ-opioid receptor

Finley

Chen

Bardi

et al. 2008

Journal of Neuroimmunology

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“…Indeed, both proENK and proDYN promoter/enhancer regions contain an identical AP-1-like domain, ENKCRE-2 (enkephalin CRE-2) or DYNCRE-3 (dynorphin CRE-3), which may play a critical role in the regulation of their gene expression through interaction with AP-1 and CREB proteins (Comb et al, 1986;Douglass et al, 1989;Sonnenberg et al, 1989a,b,c;Messersmith et al, 1994). However, in the rat hippocampus, the modulatory role of melatonin in the regulation of KA-induced opioid gene expressions has been unveiled.…”

Section: Introductionmentioning

confidence: 99%

Effect of melatonin on the regulation of proenkephalin and prodynorphin mRNA levels induced by kainic acid in the rat hippocampus

et al. 2000

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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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Basal and Inducible Transcriptional Activity of an Upstream AP-1/CRE Element (DYNCRE3)in the Prodynorphin Promoter

Cited by 39 publications

References 0 publications

Bi-directional heterologous desensitization between the major HIV-1 co-receptor CXCR4 and the κ-opioid receptor

Bi-directional heterologous desensitization between the major HIV-1 co-receptor CXCR4 and the κ-opioid receptor

Effect of melatonin on the regulation of proenkephalin and prodynorphin mRNA levels induced by kainic acid in the rat hippocampus

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

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