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Importantly, similar structures could not be detected when we replaced R23E with the assembly-incompetent variant P83R.

However, no statistically significant difference could be detected when we examined possible correlations between hepaCAM expression levels and various clinicopathological parameters [Fig. 1A, B. Table 1].

We next examined if lacZ expression in the periodontal ligament could be detected when we stained maxillary bone and teeth as whole maxillary tissues.

This could be because there were no subtype-specific clusters present, but it is also possible that our samples became too small for clusters to be detected when we subdivided the study population.

For Mmp13, again, a significantly higher basal expression level in AP-2ε-deficient articular chondrocytes could be detected when we compared the sham joints of Tfap2e−/− mice with the sham joints of WT mice at both time points (Fig.  7b).

In contrast, SLX1 foci could not be detected when we overexpressed a mutant form of SLX4 (C1805R) that is incapable of interacting with SLX1 (D.C., N. Nair, A.C. Declais, C. Lachaud, R.T., T.J. Macartney, D.M.J. Lilley, J.S.C. Arthur, and J.R., unpublished data).

In addition, no significant differences were detected when we used the different model to pooling the data (Supplementary Fig. S1 and Fig. S2 online).

No signal was detected when we blocked the antibody with the specific epitope (data not shown).

Similarly, no significant differences between the AtCRT3 and CRT3m were detected when we assessed the BK-induced Ca2+ releases (Figures 5H, I, and S3).

In presence of 2,5 µM genistein, Luc activity is well induced (215 fold), but no induction is detected when we co-treated with 1 µM of ICI (Table 2) clearly suggesting that this effect is ER-dependent.

Since spongy bone is lower in density and strength than compact bone, this result may explain why no significant difference was detected when we compared the strength of WT and Mmp13−/−calluses at late stages of healing.