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To observe the induction of PLD isozymes in response to Wnt signaling, we chose cancer cells in which the status of the Wnt pathway is normal.
We did not observe the induction or NO and ROI, which strongly suggests that it was TNFR2 but not TNFR1 that was involved in TNF-α signalling in infected hepatocytes.
In addition, we could observe the induction of PAK1 in Smad4-expressed cancer tissues.
As expected, during RA-dependent granulocytic differentiation, we did not observe the induction of the above-mentioned genes.
In these cell lines, we did not observe the induction of Smad4 including K562 (Supplementary Figures 1e and f).
We could observe the induction of Smad4 in response to serum starvation in normal cell, indicating that SF condition-induced Smad4 is a general event.
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The expected damage can be assessed by observing the induction of plasticity.
In addition, we observed the induction of the Bowman Birk family of proteinase inhibitors (BBPI) in both PLA and PLW libraries.
We observed the induction of the OsIAA7-Auxin-responsive Aux/IAA gene family (os.7355.1.s1_at), the indole-3-acetic acid-amido synthetase GH3.2 (os.12501.1.s1_and and the OsSAUR39 - Auxin-responsive SAUR gene family (os.39652.1.s1_at) in Kavya.
We also have observed the induction of NOX by ceramide treatment (Rizvi et al unpublished).
We also observed the induction of genes associated with cytokine activity, immune effector functions, and IKB kinase activity (figure S1C).
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