br Experimental design materials and methods br Acknowledgme

Experimental design, materials and methods
Acknowledgments This work was supported by Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq 44371/2014-0), Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ E26/110.271/2014) and Programa Estratégico De Apoio à Pesquisa Em Saúde (PAPES-FIOCRUZ 407764/2012-7).
Data Here we present data illustrating the effects of the dietary flavonol rutin on the blood-glucose (see Fig. 1A) and fluid-intake profiles (Fig. 1B) of h-amylin transgenic male mice and their non-transgenic littermates versus mice treated with water (vehicle) only. We employ a novel parametric change-point regression analysis to extract, for each animal, baseline levels of blood nicotinic acetylcholine receptor and fluid intake, the change-point time at which blood glucose (diabetes-onset) and fluid intake (onset of polydipsia) accelerated away from baseline, and the rate of this acceleration (Table 1). This enabled more exact measurement of the impact of rutin on the survival of diabetic mice.
Experimental design and methods
Funding This research was supported by grants from Endocore Research Trust (60147); Maurice and Phyllis Paykel Trust, New Zealand (various equipment grants; 3601069; co-funding of CD-Spectrometer); Health Research Council of New Zealand, New Zealand (HRC 03/190); Ministry of Business, Innovation & Employment, New Zealand (MBIE; UOAX0815); Maurice Wilkins Centre for Molecular Biodiscovery (Tertiary Education Commission 9431–48507); Lottery Health New Zealand (3354520; co-funding of CD-Spectrometer); Medical Research Council, United Kingdom (UK, MR/L010445/1 and MR/L011093/1); Guangdong High-end Foreign Expert Fund; a Key International Collaborative Fund from Chinese Academy of Sciences (154144KYSB20150019,DW); University of Manchester, the Central Manchester NHS Foundation Trust, and the Northwest Regional Development Agency through a combined programme grant to CADET; and was facilitated by the Manchester Biomedical Research Centre and the Greater Manchester Comprehensive Local Research Network.
Acknowledgements
Data The data reveal the content of LC3-II, an autophagosome marker protein in primary rHSC treated with or without TGF-β for 48h in the presence and absence of bafilomycin A1 (treated during the final 4h before harvest). Bafilomycin A1 inhibits the lysosome proton pump to prevent lysosome acidification, thereby blocking degradation of cargo, including LC3-II. This experiment is also known as LC3-II or autophagy flux experiment [2].
Experimental design, materials and methods
Data Data reported here are related to the article entitled “Structural Pliability Adjacent to the Kinase Domain Highlights Contribution of FAK1 IDRs to Cytoskeletal Remodeling” [1]. Six figures and nine tables are presented in this article. The figures illustrate the function of IDRs in FAK1 and its effects on cytoskeletal remodeling. The tables provide raw data utilized to build PPI networks. Evolutionary scores of IDRs, kinase domains, and whole kinases are also reported in tables. One single Microsoft Excel file is provided with one table on each of the nine sheets (Fig. 6).
Experimental design, materials and methods
Data The antibody microarray identified 110 regulated proteins in human umbilical vein endothelial cells (HUVEC) cells after 1-h stimulation with Ang-(1–7), 119 after 3h, 31 after 6h, and 86 after 9h. The first 25 regulated proteins have been published in Meinert et al.[1] in Tables 1–4. Here the name and ranking of the next regulated proteins are shown (Tables 1–4). Additionally, further intracellular pathways affected by Ang-(1–7) are shown in Table 5A–D.
Experimental design, materials and methods
Acknowledgements The study was supported by the NIH (R01HL091191-01A2) and the Deutsche Forschungsgemeinschaft (WA1441/22-2). We thank Victoria Hodgkinson for introducing us into the analysis of the antibody microarray data.