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-Arrestin-Dependent {micro}-Opioid Receptor-Activated Extracellular Signal-Regulated Kinases (ERKs) Translocate to Nucleus in Contrast to G Protein-Dependent ERK Activation.

-Arrestin-Dependent {micro}-Opioid Receptor-Activated Extracellular Signal-Regulated Kinases (ERKs) Translocate to Nucleus in Contrast to G Protein-Dependent ERK Activation. Research Abstract Details 

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  • -Arrestin-Dependent {micro}-Opioid Receptor-Activated Extracellular Signal-Regulated Kinases (ERKs) Translocate to Nucleus in Contrast to G Protein-Dependent ERK Activation. Abstract Text:

    hui zhengHui Zheng,horace h lohHorace H Loh,ping-yee lawPing-Yee Law,hui zhengHui Zheng,horace h lohHorace H Loh,ping-yee lawPing-Yee Law,hui zhengHui Zheng,horace h lohHorace H Loh,ping-yee lawPing-Yee Law,hui zhengHui Zheng,horace h lohHorace H Loh,ping-yee lawPing-Yee Law,

    The cellular location of extracellular signal-regulated kinases (ERKs) activated by a G protein-coupled receptor was shown to be dependent on the pathway that mediated their activation. In general, fast activation of ERKs (2 min) mediated by G proteins resulted in the nuclear translocation of phosphorylated ERKs, whereas a slower activation of ERKs (10 min) mediated by beta-arrestins resulted in the cytosolic retention of the phosphorylated ERKs. However, we observed distinct differences from this established ERKs cellular itinerary with the mu-opioid receptor-activated ERKs. Agonists such as morphine and methadone activated ERKs via the protein kinase C-dependent pathway but not the beta-arrestin-dependent pathway. The activated ERKs did not translocate into the nucleus, but phosphorylated 90-kDa ribosomal S6 kinase and induced the activity of transcription factor cAMP response element-binding protein. In contrast, agonists such as etorphine and fentanyl activated ERKs in a beta-arrestin-dependent manner. The phosphorylated ERKs translocated into the nucleus, resulting in increases in Elk-1 activity and GRK2 and beta-arrestin2 transcriptions. Thus, the cellular location of phosphorylated ERKs and subsequent activities on gene transcriptions are dictated by the agonist used to activate the receptor and the subsequent signaling pathway involved.

    -Arrestin-Dependent {micro}-Opioid Receptor-Activated Extracellular Signal-Regulated Kinases (ERKs) Translocate to Nucleus in Contrast to G Protein-Dependent ERK Activation. Publishing Authors By Initials

    h zhengH Zheng,hh lohHH Loh,py lawPY Law,h zhengH Zheng,hh lohHH Loh,py lawPY Law,h zhengH Zheng,hh lohHH Loh,py lawPY Law,h zhengH Zheng,hh lohHH Loh,py lawPY Law,

    For similar abstracts research abstracts see: abstracts research

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    -Arrestin-Dependent {micro}-Opioid Receptor-Activated Extracellular Signal-Regulated Kinases (ERKs) Translocate to Nucleus in Contrast to G Protein-Dependent ERK Activation. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: Molecular pharmacology

    VOLUME: 73

    Page Numbers: 178-90

    Journal Abbreviation: Mol. Pharmacol.

    ISSN: 1521-0111

    DAY: 18

    MONTH: 10

    YEAR: 2007

    -Arrestin-Dependent {micro}-Opioid Receptor-Activated Extracellular Signal-Regulated Kinases (ERKs) Translocate to Nucleus in Contrast to G Protein-Dependent ERK Activation. Information

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    LANGUAGE: eng

    NlmUniqueID: 35623

    -Arrestin-Dependent {micro}-Opioid Receptor-Activated Extracellular Signal-Regulated Kinases (ERKs) Translocate to Nucleus in Contrast to G Protein-Dependent ERK Activation. Keywords Mesh Terms:

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    Grant and Affiliation Information for -Arrestin-Dependent {micro}-Opioid Receptor-Activated Extracellular Signal-Regulated Kinases (ERKs) Translocate to Nucleus in Contrast to G Protein-Dependent ERK Activation.

    AFFILIATION: Department of Pharmacology, Medical School, University of Minnesota. 6-120 Jackson Hall, 321 Church Street S.E., Minneapolis, MN 55455-0217. zhen0091@umn.edu.

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: Mol Pharmacol

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    -Arrestin-Dependent {micro}-Opioid Receptor-Activated Extracellular Signal-Regulated Kinases ERKs Translocate to Nucleus in Contrast to G Protein-Dependent ERK Activation Related Publications

     

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