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ERK1/2 activation by the C. elegans muscarinic acetylcholine receptor GAR-3 in cultured mammalian cells involves multiple signaling pathways

  • Shin, Young-Mi (Department of Biochemistry, College of Natural Sciences, Chungbuk National University) ;
  • Shin, Young-Ju (Department of Biochemistry, College of Natural Sciences, Chungbuk National University) ;
  • Kim, Seung-Woo (Department of Biochemistry, College of Natural Sciences, Chungbuk National University) ;
  • Park, Yang-Seo (Department of Biochemistry, College of Natural Sciences, Chungbuk National University) ;
  • Cho, Nam-Jeong (Department of Biochemistry, College of Natural Sciences, Chungbuk National University)
  • Received : 2010.03.31
  • Accepted : 2010.06.10
  • Published : 2010.09.30

Abstract

Extracellular signal-regulated kinases 1/2 (ERK1/2) play important roles in a variety of biological processes including cell growth and differentiation. We have previously reported that GAR-3 activates ERK1/2 via phospholipase C and protein kinase C, presumably through pertussis toxin (PTX)-insensitive Gq proteins, in Chinese hamster ovary (CHO) cells. Here we provide evidence that GAR-3 also activates ERK1/2 through PTX-sensitive G proteins, phosphatidylinositol 3-kinase (PI 3-kinase), and Src family kinases in CHO cells. We further show that in human embryonic kidney (HEK293) cells, epidermal growth factor receptor and Ras are required for efficient ERK1/2 activation by GAR-3. Taken together, our data indicate that GAR-3 evokes ERK1/2 activation through multiple signaling pathways in cultured mammalian cells.

Keywords

References

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