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The empty MSCV retroviral vector in our studies exhibited measurable transforming activity in 3T3 fibroblasts, and this was abrogated by E2F4 and E2F5.
This was abrogated by WXC-340.
This was abrogated by cMET inhibition with INC280 (* P <0.05).
XRT enriched G2/M-phase-fraction, and this was abrogated by co-treatment with VE-822.
This was abrogated by mutation of both asparagines in combination, but not by mutation of either asparagine alone.
Knockdown of S100A2 in MDA468-BR cells led to the expected increase in mutant p53, but this was abrogated by treatment with 17-AAG.
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This is abrogated in the absence of Lck or Zap70.
This increase was abrogated by β-adrenergic receptor and gap junction (GJ) blockade.
Importantly, this reduction was abrogated by mutation of both proximal and distal Tia1 binding sites (Fig. 5d).
A similar effect was recorded in A549 cells (Supplementary Fig. S4a) and this enhancement was abrogated in the presence of CXCR4 antagonist, AMD3100 (Fig. 4b).
FIT stimulation of H9C2 cells also caused a time-dependent phosphorylation of STAT3, Akt, and GSK-3beta, and this effect was abrogated by AG-490.
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