Importantly, 14 out of these 169 predicted piRNA target genes have been shown to be essential for spermatogenesis in mouse models (Supplementary information, Table S3).
Hematoxylin and eosin staining of tumour sections clearly showed PanINs as well as areas with well-developed tumours compared with the control pancreas from contemporary littermates of both KC: K-rasG12D; Pdx1-Cre (40th and 50th weeks) and KPC: K-rasG12D; Trp53R172H/+; Pdx1-Cre (5th, 10th, 15th, 20th and 25th weeks) mouse models (Supplementary Figures 1a and b).
We first checked the effect of pazopanib in vivo tumor bearing mouse model (Supplementary Fig. 7).
These results suggest that HMGB1 does not trigger brain inflammation in our mouse model (Supplementary Fig S1).
This motoneuronal expression pattern was also preserved in an ALS patient (Fig. 2D F) and the SOD1(G93A) mouse model (Supplementary Fig. S1).
These findings stimulated many studies in Lambert Eaton myasthenic syndrome; Peter Molenaar showed that acetylcholine contents of Lambert Eaton myasthenic syndrome muscle were normal, but confirmed that the release was deficient (Supplementary material B42), as also found in the mouse model (Supplementary material B60).
To study the role of Ankrd2, we took advantage of the Ankrd2 knockout (KO) mouse model (Supplementary Figure S1) and performed global transcriptome analysis on proliferating, fusing, and differentiated primary myoblasts derived from wild-type (WT and KOO mice infected with adenovirus expressing HA-tagged Ankrd2 (AdAnkrd2) or control GFP (AdGFP).
It was interesting to note a similar increase in hepatic p-CREB in P2 Smn +/−;SMN2 and P21 Smn 2B/− mice, an intermediate SMA mouse model (see Supplementary Material, Fig. S1).
Thus, although cognitive deficits have been identified in RTT mouse models (Table 2; supplementary material Table S5), the face validity of these findings has been difficult to establish.
The expression of the embryonic and neonatal MHC transcripts was mis-regulated in a similar fashion as the myogenic regulatory factors in both mouse models of SMA (Supplementary Material, Fig. S6).
This finding is consistent with our previously published targeted mouse models of chondrodysplasia (supplementary material Table S1) and is a well-documented clinical feature in individuals with PSACH, MED and MCDS (Briggs and Chapman, 2002; Lachman et al., 1988; Leighton et al., 2007; Piróg-Garcia et al., 2007; Rajpar et al., 2009; Suleman et al., 2012).
