br Experimental design materials and methods br Acknowledgem

Experimental design, materials and methods
Acknowledgements
This work was supported by European Commission Sixth Framework Research and Technological Development Program ‘SPINE2-COMPLEXES’ Project, under contract No. 031220.
Data DNA replication is the major source of mutations in proliferating cells. However, mutations also arise in resting cells. The mechanisms responsible for the latter are less well understood than replication-dependent mutagenesis. The most interesting subset of mutations in resting cells are such that appear to be adaptive, i.e. that provide a selective advantage to the mutants by enabling a resumption of proliferation. For the study of such adaptive mutations, a combination of a useful test allele and appropriate cell cycle-arresting but non-lethal conditions is necessary [2]. In this article, we present data on the implementation of a novel adaptive mutation assay (Fig. 1 and Table 1) as a tool to generate adaptive revertants for further analysis. We monitored the quality of the induced nucleoside transporters arrest (Fig. 2) and provide a sequence analysis of representative sets of revertants (Fig. 3 and Table 2).
Experimental design, materials and methods
Acknowledgements We kindly thank M. Hubmann for technical assistance. This work was supported by a Grant from the Herzfeldersche Familienstiftung (AP00601OFF) to E.H.
Data Diets rich in saturated fatty acids (SFA) can exacerbate obesity [2] and increase the risk of insulin resistance. This condition is characterized by an inadequate response of the insulin-sensitive tissues to insulin, leading to type 2 diabetes and metabolic syndrome [3]. Obesity modulates aberrantly the expression of certain miRNAs targeting the mRNAs of the insulin signaling molecules, and participates actively in the pathogenesis of insulin resistance [4,5]. A previous study reported that a high fat diet (HFD) induces miR-15b in the liver of mice, which suppresses the expression of hepatic INSR, but not IRS-1, by targeting INSR 3’UTR directly [1]. Therefore, certain types of miRNA induced by obesity can be linked causally to the development of hepatic insulin resistance, which may in turn lead to type 2 diabetes. This study provides accompanying data collected using Affymetrix GeneChip microarrays to identify the changes in miRNA expression in the liver of mice fed with a HFD for 14 weeks. Differentially expressed miRNA analyses in the liver of HFD-fed mice showed that a range of miRNAs were upregulated more than 1.5-fold (Supplement File. 1) or downregulated less than 0.5-fold (Supplement File. 2). Among those differentially expressed miRNAs, the upregulated miRNAs may be involved in the reduction of INSR and IRS-1 levels observed in the liver of HFD-fed mice. Therefore, this study next examined whether the 3’UTRs of INSR and IRS-1 possess direct binding sites for the upregulated miRNAs. In silico target analysis using TargetScan, PicTar, and miRWalk showed that a range of certain miRNAs have putative binding sites for the 3’UTRs of INSR (Table 1) and/or IRS-1 (Table 2). An interpretation of the data and further extensive insights into the implication of miRNAs, particularly miR-15b, in hepatic insulin resistance can be found elsewhere [1].
Experimental design, materials and methods
Acknowledgments This research was supported by National Research Foundation of Korea (NRF) grants funded by Ministry of Education (2013R1A1A2057932) and Ministry of Science, ICT and Future Planning, South Korea (2016M2B2A4912473).
Data The immunohistochemistry data show expression of NC-B27 forms (HC10 and HD6 staining) in synovial tissues from B27+ve SpA patients (Fig. 1), and in joint and gastrointestinal tissues from B27 TG1 rats with M.tb-induced SpA and in healthy WT and B7 TG controls (Figs. 2–7). The flow cytometry data describe and quantify the expression of HC10- and HD6-reactive NC-B27 molecules in spleens and lymph nodes from B27 TG1 rats in a spontaneous and M.tb-induced SpA before and after disease onset (Figs. 8–10).