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A novel function of Goalpha: mediation of extracellular signal-regulated kinase activation by opioid receptors in neural cells

Go is the most abundant G protein expressed in brain but its function is less known. Here we show a novel function of Goalpha as a mediator of opioid receptor-induced extracellular signal-regulated kinase activation in neural cells. The current study found that, in neuroblastoma x glioma NG108-15 hy... Full description

Journal Title: Journal of neurochemistry September 2003, Vol.86(5), pp.1213-22
Main Author: Zhang, Wen-Bo
Other Authors: Zhang, Zhe , Ni, Yan-Xiang , Wu, Ya-Lan , Pei, Gang
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0022-3042 ; PMID: 12911629 Version:1
Link: http://pubmed.gov/12911629
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recordid: medline12911629
title: A novel function of Goalpha: mediation of extracellular signal-regulated kinase activation by opioid receptors in neural cells
format: Article
creator:
  • Zhang, Wen-Bo
  • Zhang, Zhe
  • Ni, Yan-Xiang
  • Wu, Ya-Lan
  • Pei, Gang
subjects:
  • DNA-Binding Proteins
  • Transcription Factors
  • Heterotrimeric Gtp-Binding Proteins -- Physiology
  • Mitogen-Activated Protein Kinases -- Metabolism
  • Neurons -- Metabolism
  • Receptors, Opioid, Delta -- Metabolism
ispartof: Journal of neurochemistry, September 2003, Vol.86(5), pp.1213-22
description: Go is the most abundant G protein expressed in brain but its function is less known. Here we show a novel function of Goalpha as a mediator of opioid receptor-induced extracellular signal-regulated kinase activation in neural cells. The current study found that, in neuroblastoma x glioma NG108-15 hybrid cells, activation of extracellular signal-regulated kinase through delta opioid receptors was mediated by pertussis toxin-sensitive G protein and independent of Gbetagamma subunits, PI3 kinase and receptor internalization. Overexpression of a dominant negative form of Goalpha1, but not Gialpha2, completely blocked delta opioid receptor-induced extracellular signal-regulated kinase activity. Decreasing Goalpha expression by RNA interference greatly reduced delta opioid receptor-induced extracellular signal-regulated kinase activity and extracellular signal-regulated kinase-dependent gene expression, while knocking down Gialpha2 did not. By taking advantage of differences between human and...
language: eng
source:
identifier: ISSN: 0022-3042 ; PMID: 12911629 Version:1
fulltext: fulltext
issn:
  • 00223042
  • 0022-3042
url: Link


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titleA novel function of Goalpha: mediation of extracellular signal-regulated kinase activation by opioid receptors in neural cells
creatorZhang, Wen-Bo ; Zhang, Zhe ; Ni, Yan-Xiang ; Wu, Ya-Lan ; Pei, Gang
ispartofJournal of neurochemistry, September 2003, Vol.86(5), pp.1213-22
identifierISSN: 0022-3042 ; PMID: 12911629 Version:1
subjectDNA-Binding Proteins ; Transcription Factors ; Heterotrimeric Gtp-Binding Proteins -- Physiology ; Mitogen-Activated Protein Kinases -- Metabolism ; Neurons -- Metabolism ; Receptors, Opioid, Delta -- Metabolism
descriptionGo is the most abundant G protein expressed in brain but its function is less known. Here we show a novel function of Goalpha as a mediator of opioid receptor-induced extracellular signal-regulated kinase activation in neural cells. The current study found that, in neuroblastoma x glioma NG108-15 hybrid cells, activation of extracellular signal-regulated kinase through delta opioid receptors was mediated by pertussis toxin-sensitive G protein and independent of Gbetagamma subunits, PI3 kinase and receptor internalization. Overexpression of a dominant negative form of Goalpha1, but not Gialpha2, completely blocked delta opioid receptor-induced extracellular signal-regulated kinase activity. Decreasing Goalpha expression by RNA interference greatly reduced delta opioid receptor-induced extracellular signal-regulated kinase activity and extracellular signal-regulated kinase-dependent gene expression, while knocking down Gialpha2 did not. By taking advantage of differences between human and...
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titleA novel function of Goalpha: mediation of extracellular signal-regulated kinase activation by opioid receptors in neural cells
descriptionGo is the most abundant G protein expressed in brain but its function is less known. Here we show a novel function of Goalpha as a mediator of opioid receptor-induced extracellular signal-regulated kinase activation in neural cells. The current study found that, in neuroblastoma x glioma NG108-15 hybrid cells, activation of extracellular signal-regulated kinase through delta opioid receptors was mediated by pertussis toxin-sensitive G protein and independent of Gbetagamma subunits, PI3 kinase and receptor internalization. Overexpression of a dominant negative form of Goalpha1, but not Gialpha2, completely blocked delta opioid receptor-induced extracellular signal-regulated kinase activity. Decreasing Goalpha expression by RNA interference greatly reduced delta opioid receptor-induced extracellular signal-regulated kinase activity and extracellular signal-regulated kinase-dependent gene expression, while knocking down Gialpha2 did not. By taking advantage of differences between human and...
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abstractGo is the most abundant G protein expressed in brain but its function is less known. Here we show a novel function of Goalpha as a mediator of opioid receptor-induced extracellular signal-regulated kinase activation in neural cells. The current study found that, in neuroblastoma x glioma NG108-15 hybrid cells, activation of extracellular signal-regulated kinase through delta opioid receptors was mediated by pertussis toxin-sensitive G protein and independent of Gbetagamma subunits, PI3 kinase and receptor internalization. Overexpression of a dominant negative form of Goalpha1, but not Gialpha2, completely blocked delta opioid receptor-induced extracellular signal-regulated kinase activity. Decreasing Goalpha expression by RNA interference greatly reduced delta opioid receptor-induced extracellular signal-regulated kinase activity and extracellular signal-regulated kinase-dependent gene expression, while knocking down Gialpha2 did not. By taking advantage of differences between human and...
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