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To test this hypothesis, we analysed the induction of Mixl1 in response to combinations of growth factors added to cells at d3.
We therefore used MEF.BakxBax−/− and MEF.Casp3x7−/− (mock-treated, peptide-pulsed or Mo-ECTV-infected) target cells with ex vivo ECTV-immune gzmB+ Tc cells and analysed the induction of pro-apoptotic features (Fig. 4).
We then analysed the induction of the p53 endogenous target genes, p21waf1/CIP1 and Bax.
We analysed the induction of these BMP target genes in primary TAK1-deficient chondrocytes by using a quantitative RT PCR assay.
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The effects of MD were assessed by analysing the induction of the immediate-early gene c-Fos in response to visual stimulation of the deprived eye.
Foxp3-IRES-mRFP mice were transferred with EPIT-induced Tregs to analyse the induction of host Tregs.
We characterised the Nrf2 activation in AML cells by analysing the induction of known Nrf2 targets in response to different drugs used currently in APL therapy, that is, Ara-C, daunorubicin and ATO.
Quantitative PCR analyses verified the induction of genes in the phenylpropanoid and flavonoid pathway.
In addition, in vivo analyses demonstrated the induction of CTL, with significant cell lysis observed for Core- and Polymerase-specific peptides.
Consequently, molecular analyses of the induction of pluripotency and of (re- differention tre- differentionl chemical compounds is of high intriggered the human as well as in the mouse system.
We also performed Western blot analyses of the induction of P-ERK after treatment of the cells with two known activating agents, fetal bovine serum (20%) and TPA (100 ng ml−1) (data not shown).
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