br Acknowledgments Francesco Palmas gratefully acknowledges

Acknowledgments Francesco Palmas gratefully acknowledges Sardinia Regional Government (F.S.E. 2007-2013 UniCa) for the financial support of his PhD scholarship (P.O.R. Sardegna F.S.E. Operational Programme of the Autonomous Region of Sardinia, European Social Fund 2007–2013—Axis IV Human Resources, Objective l.3, Line of Activity l.3.1.).
Data Recombinases GdDMC1A and GdDMC1B amino online sequences were compared with recombinases from other organisms (Structure-based sequence alignments) and phylogenetic reconstructions and 3D modeling were made to identify similarity (Figs. 1–3). Also, GdDMC1A and GdDMC1B protein sequences from other assemblages within Giardia duodenalis were identified (Table 1) and compared among them (Figs. 4 and 5). Finally, GdDMC1A and GdDMC1B were expressed in a rad51 defective yeast strain (Fig. 6) and LD50 using ionizing radiation was calculated in G. duodenalis trophozoites (Fig. 7).
Experimental design, materials and methods Bioinformatic tools (Structure-based sequence alignments and phylogenetic reconstructions) were used to create Figs. 1–5. Fig. 6 shows transforming a rad51 defective Saccharomyces cerevisiae strain with either GdDMC1A or GdDMC1B containing plasmids looking for a rescue phenotype under DNA damaging conditions and Fig. 7 is generated by determining LD50 at 12, 32 y 48h after ionizing radiation exposure in G. duodenalis. This experimental design was used only for this work.
Acknowledgments This research was supported by CONACyT, Mexico (Grant no. 82622). Ana Laura Torres Huerta was supported by a doctoral Grant from the National Council of Science and Technology, CONACyT (207433).
Specifications Table
Data DDIAS is highly expressed in lung cancers and is involved in cisplatin resistance [2,3]. In HeLa cells, genetic and pharmacological inhibition of MEK/ERK5 suppressed EGF-induced DDIAS transcription, whereas ERK5 overexpression increased DDIAS mRNA level (Fig. 1). DDIAS knockdown dramatically decreased β-catenin protein level in HeLa cells (Fig. 2). Consistent with data in HeLa cells, inhibition of ERK5 suppressed DDIAS transcription on EGF exposure in lung cancer cell lines (Fig. 3). In addition, MEF2B knockdown reduced EGF-induced DDIAS expression in lung cancer cells (Fig. 4). Furthermore, DDIAS knockdown inhibited β-catenin accumulation and lung cancer cell invasion (Fig. 5).
Experimental design, materials and methods
Acknowledgments This work was supported by National Research Foundation of Korea, South Korea (NRF) grants (2013R1A2A2A01069026, and 2015M3A9A8032460), Health Technology R&D grant (HI13C2162) and the KRIBB Initiative program of the Korea Research Council of Fundamental Science and Technology (KGM4751612), South Korea.
Data The RNA-Seq and gene expression datasets were deposited in NCBI׳s Gene expression Omnibus [2], accessible through GEO series accession number GEO: GSE76176. Fig. 1 shows the distribution of deregulated genes in E. coli upon exposure to 50µM Ni. 2545 genes were deregulated considering a Fold-Change (FC) of 1.5, representing 57 % of the 4440 annotated transcripts of E. coli K-12 strain W3110. Gene Ontology was applied to classify differentially expressed genes according to their biological function (see Fig. 1 in [1]). GO Terms that were enriched in the list of differentially expressed genes were identified using the DAVID tools (Database for Annotation, Visualization and Integrated Discovery) [3,4]. Pathways that were significantly affected were mapped using KEGG and are listed in Table 1.
Experimental design, materials and methods
Acknowledgments This work was supported by a BQR (BIOVIME) INSA Lyon. MG is the recipient of a doctoral fellowship from the French Ministry of Higher Education and Research.
Data Dorsal keratinocytes were isolated from female C57Bl/6 mice in the age of 7–9 weeks and sorted using flow cytometry. Cells were stained with conjugated antibodies and visualized by fluorescence microscopy. Global microarray data was used to generate Venn diagrams, which show the number of shared differently expressed genes (DEGs) between the different populations and a reference. See Figs. 1–6.