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Both morphotypes elicited poor IL-6 responses in the early stages of infection, with slightly increased induction at 24 hpi in MAB-R-infected cells (Fig.  4).

Given that the increased induction of inducible Hsp70 is observed at both the RNA and protein levels, this indicates the upregulation is due to increased HSF1-mediated gene transcription, and not due to an altered half-life of Hsp70.

However, we also observed significantly increased induction of Ifng in CD103−/− mice at day 14, suggesting that the absence of CD103 may result in a global dysregulation of T cell responses.

These combinations may increase induction of apoptosis.

A substantial increase in the number of PFUs coincides with the peak of biofilm development (Fig. 1A and 1B), indicating increased phage induction at the later stages of biofilm formation.

Contrary to what we observed for the self-contained vector, analysis of the autoregulated MOV-scT6cA vector showed that M2-mRNA levels in the off-state were approximately doubled (0.5 vs. 1.2) in the enriched population and strongly increased upon induction at low Dox concentration.

The extracellular GadB activity quickly increased after IPTG induction at 14 h and reached 13.12 U/mL at 28 h.

3-MA markedly increased apoptosis induction by METH at 72 h, as measured by Annexin V labeling.

Later experiments with the pnit-6_1.5 strain showed that levels of GFP mRNA were elevated at 1 hr of induction, increased slightly at 3 hr, and then greatly diminished at 6 hr.

As shown in Supplementary Fig S5B, the expression of AChRα started to increase (2-fold induction) at 1 DPC, reached a plateau between 3 DPC and 1 WPC with a 40- to 60-fold induction, and then returned to control level by weeks 4 and 8. Pdk4 mRNA levels were increased by 50% during the early phase of synaptic destabilization with no significant changes on Pdk2 mRNA levels (Supplementary Fig S5B).

These data confirm that hypersensitivity toward IFNα, i.e. increased IFN target gene induction at low IFN concentrations, is a general feature detectable for all target genes in primary cells with endogenous Wnt5a upregulation.