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Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C

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Phospholipase C-eta 1 is activated by intracellular Ca2+ mobilization and enhances GPCRs/PLC/Ca2+ signaling

Cited 14 times inthomson ciCited 16 times inthomson ci
Title
Phospholipase C-eta 1 is activated by intracellular Ca2+ mobilization and enhances GPCRs/PLC/Ca2+ signaling
Author
Kim, Jung KukChoi, Jung WoongLim, SeyoungKwon, OhmanSeo, Jeong KonRyu, Sung HoSuh, Pann-Ghill
Keywords
G protein coupled receptor; Intracellular ca 2+ mobilization; Neuro2A cells; Phospholipase c-η1; Signal amplifier
Issue Date
201106
Publisher
ELSEVIER SCIENCE INC
Citation
CELLULAR SIGNALLING, v.23, no.6, pp.1022 - 1029
Abstract
Phospholipase C-eta 1 (PLC-eta 1) is the most recently identified PLC isotype and is primarily expressed in nerve tissue. However, its functional role is unclear. In the present study, we report for the first time that PLC-eta 1 acts as a signal amplifier in G protein-coupled receptor (GPCR)-mediated PLC and Ca2+ signaling. Short-hairpin RNA (shRNA)-mediated knockdown of endogenous PLC-eta 1 reduced lysophosphatidic acid (LPA)-, bradykinin (BK)-, and PACAP-induced PLC activity in mouse neuroblastoma Neuro2A (N2A) cells, indicating that PLC-eta 1 participates in GPCR-mediated PLC activation. Interestingly, ionomycin-induced PLC activity was significantly decreased by PLC-eta 1, but not PLC-eta 2, knockdown. In addition, we found that intracellular Ca2+ source is enough for PLC-eta 1 activation. Furthermore, the IP3 receptor inhibitor, 2-APB, inhibited LPA-induced PLC activity in control N2A cells, whereas this effect was not observed in PLC-eta 1 knockdown N2A cells, suggesting a pivotal role of intracellular Ca-2+ mobilization in PLC-eta 1 activation. Finally, we found that LPA-induced ERK1/2 phosphorylation and expression of the downstream target gene, krox-24, were significantly decreased by PLC-eta 1 knockdown, and these knockdown effects were abolished by 2-APB. Taken together, our results strongly suggest that PLC-eta 1 is activated via intracellular Ca2+ mobilization from the ER, and therefore amplifies GPCR-mediated signaling.
URI
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DOI
http://dx.doi.org/10.1016/j.cellsig.2011.01.017
ISSN
0898-6568
Appears in Collections:
UCRF_Journal Papers
SLS_Journal Papers

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