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We monitored activation of five protein kinases that are perturbed during viral infection and reactivation, including phospho-ERK (p-ERK), p-AKT, p-p38, p-JNK, and p-IκBα (Supplementary Table S1).
To determine whether the sensitivity of set2Δ was due to defective DNA-damage signalling, we exposed asynchronous cultures of WT and set2Δ strains to either MMS (M) or phleomycin (P) and monitored activation of γ-H2A.X (or H2AS129ph) and Rad53 (yeast homologue of mammalian Chk2).
To test whether this might also be through the ATM/APMK pathway, we monitored activation of ATM and AMPK.
We prepared alternative inputs for the eight signaling molecules and monitored activation of the integrated transcriptional reporter PFUS1-GFP (Figure 5, details in Materials and Methods).
Since activation of these stress responses could be due to a general increase in stress associated with cell death, we also monitored activation of the cytoplasmic stress response mediated by σ32 using the σ32-regulated htpG-lacZ reporter fusion.
We monitored activation of the DNA damage checkpoint in the experiment described in Figure 2B.
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Novel luciferase-based reporter system to monitor activation of ErbB2/Her2/neu pathway noninvasively during radiotherapy.
In order to monitor activation of the UPR pathway, we investigated the expression level of GRP78, phospho-eIF2α and unconventional splicing of Xbp1 mRNA.
The induction of AMP genes depends upon signaling through the Toll and/or Imd pathway and therefore AMP expression has been used to monitor activation of these pathways during infection.
We used primers in FlyPrimerBank to monitor activation of the JNK signaling pathway.
To monitor activation of the canonical NF- κB pathway, we analyzed I κB α phosphorylation.
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