Interestingly, A431 cells were the only cells to express EGFR significantly more than HaCaT cells (Figure 8F), Ki67 and CCHCR1 expression remaining at a lower level (Figure 8D,E).
Wild-type macrophages could also produce TNF-α and IL-6 while MyD88-deficient macrophages produced these cytokines at a significantly lower level (Figure S6A).
The R667A mutant was functional and exhibited virus entry activity similar to that induced by wild-type SARS-CoVpp, albeit at a slightly lower level (Figure 4D).
It should be noted that we could detect Ndi1 as early as 1or 2 weeks after the rAAV5-NDI1 injection albeit at a much lower level (Figure S2).
Notably, the peak activity of Ras-GTP in E1/4 cells was placed at the upper level of ERK activity over the steep slope in comparison with that of E1 cells, which was placed at the lower level (Figure 5B).
The same pattern observed at stage 6 persists to stage 8, although at lower levels (Figure 7D).
Maximal repression (approximately 7 fold) was observed with full length CRTR-1 and CRTR-1(48-479) (Figure 2B), although CRTR-1(48–479) is expressed at lower levels (Figure 2C).
Comparing the cytokine profile of mDCs and pDCs, we found that both subsets make a similar pattern of cytokines, although pDCs expressed them at lower levels (Figure S3).
In untreated cells, actin was readily detected in the avidin pull downs while lovastatin treated cells had significantly lower levels (Figure 1B).
To determine whether the glucose intolerance was due to islet-intrinsic or extrinsic factors, we measured fasting insulin levels and found mTR+/− mice with short telomeres had lower levels (Figure 1C).
Using RT-PCR on individual WT and Hnf6 Tg pancreatic RNA extracts, we were also able to detect an increase in Hnf6 transcript, albeit at slightly lower levels (Figure 3).
