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Sci. Signal., 23 August 2011
[DOI: 10.1126/scisignal.2002006]

Supplementary Materials for:

Tumor Progression Locus 2 Mediates Signal-Induced Increases in Cytoplasmic Calcium and Cell Migration

Maria Hatziapostolou, Georgios Koukos, Christos Polytarchou, Filippos Kottakis, Oksana Serebrennikova, Athan Kuliopulos, Philip N. Tsichlis*

*To whom correspondence should be addressed. E-mail: ptsichlis{at}tuftsmedicalcenter.org

This PDF file includes:

  • Table S1. Statistical differences between samples 25 s after treatment with thrombin.
  • Table S2. Statistical differences between samples 25 s after treatment with PAR1 agonist.
  • Fig. S1. Gαi2 promotes phosphorylation of ERK1/2 through Tpl2.
  • Fig. S2. Phosphorylation and activation of classical and novel PKCs by thrombin depends on Tpl2.
  • Fig. S3. The phosphorylation of classical PKCs after thrombin stimulation depends on Gαi2.
  • Fig. S4. PKC inhibition attenuates thrombin-induced ERK1/2 phosphorylation but not Ca2+ signals.
  • Fig. S5. Expression profile of PLCβ isoforms in Rec-WT and Rec-EV cells.
  • Fig. S6. Thrombin-induced PLCβ3 phosphorylation at Ser537 depends on Tpl2.
  • Fig. S7. Specificity of the antibody that recognizes PLCβ3 phosphorylated at Ser537.
  • Fig. S8. The knockdown of Gβ1, Gβ2, or Gβ3, singly or in combination, interferes only partially with thrombin-induced ERK phosphorylation and Ca2+ signals.
  • Fig. S9. Number of cells before and after thrombin stimulation.
  • Fig. S10. ERK and JNK phosphorylation by S1P in immortalized MEFs and BMDMs is Tpl2-dependent.
  • Fig. S11. The increase in cytoplasmic Ca2+, induced by Wnt5a and IL-1β, but not TNF-α, depends on Tpl2.

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Citation: M. Hatziapostolou, G. Koukos, C. Polytarchou, F. Kottakis, O. Serebrennikova, A. Kuliopulos, P. N. Tsichlis, Tumor Progression Locus 2 Mediates Signal-Induced Increases in Cytoplasmic Calcium and Cell Migration. Sci. Signal. 4, ra55 (2011).

© 2011 American Association for the Advancement of Science


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