br Experimental design material and methods br Acknowledgmen

Experimental design, material and methods
Acknowledgments The authors would like to thank Carlos Mazorra from Tinamenor S.L. and the personnel from the facilities at the School of Biology for the maintenance of the fish. E.J.V. is supported by a predoctoral fellowship from the “Ministerio de Ciencia e Innovación” (MICINN). This data article was supported by the projects from the MICINNAGL2009-12427 and AGL2012-39768 to J.G., and the “Xarxa de Refèrencia d’R+D+I en Aqüicultura (FBG 308146) and the 2009SGR-00402 and 2014SGR-01371 from the “Generalitat de Catalunya”.
Value of the data
Data Quantitative Western blotting reveals that podocyte injury markers active beta-catenin, desmin and fibronectin show a trend of upregulation in the glomeruli of 40 weeks old obese Zucker rats compared to lean controls (Fig. 1A and B). Nephrin, the key protein of the interpodocyte slit diaphragm, shows a trend of downregulation in the glomeruli of obese rats (Fig. 1C and D), with the most albuminuric rats expressing least nephrin (Fig. 1E). Exposure of differentiated human podocytes to factors associated with obesity, insulin resistance and type 2 diabetes did not increase the expression of FOXC2 as observed by quantitative RT-PCR for tumor necrosis factor-α (TNF-α) and transforming growth factor β (TGF-β) (Fig. 2A and B), and by quantitative Western blotting for angiotensin II and a combination of glucose and palmitate (Fig. 2C-F). The data also show that overexpression of FOXC2 in differentiated human podocytes by lentiviral transduction does not change the ratio of filamentous (F) GM6001 and globular (G) actin (Fig. 3A and B) or the expression level of the tight junction protein ZO-1 (Fig. 4A and B).
Experimental design, materials and methods
Acknowledgments This study was supported by the European Research Council (242820; SLe), the Academy of Finland (131255, 218021, 255551; SLe), the Sigrid Jusélius Foundation (SLe), the Päivikki and Sakari Sohlberg Foundation (SL and SLe), the Diabetes Research Foundation (SLe) and the Faculty of Medicine, University of Helsinki (SLe). We thank Prof. Enerbäck (University of Gothenburg, Gothenburg, Sweden) for the FOXC2 construct in pCDNA3.1Hyg. Niina Ruoho (University of Helsinki, Helsinki, Finland) is acknowledged for technical support.
Experimental design, materials and methods
Acknowledgments This research was funded by the NSF (1149387) (CP). The authors would like to thank Dr. S. Maria Packiam, S.J. for his assistance in preparing samples and Ms. Gina Kuffel at Loyola’s Center for Biomedical Informatics for sequencing preparation.
Data, experimental design, materials and methods
Materials and methods
Acknowledgment We thank the Shanghai Synchrotron Radiation Facility for the X-ray beam time and the scientists at beamline BL17U for assistance with X-ray data collection. This work was supported by Grants from the National Natural Science Foundation of China (31170707, 31370737) and CAS/SFEA International Partnership Program for Creative Research Teams.
Specifications Table
Direct link to deposited data: http://www.ncbi.nlm.nih.gov.eleen.top/geo/query/acc.cgi?acc=GSE58495
Value of the data
Data mRNA profiles of murine populations of lineage negative cKit+ SCA1+ (LSK) hematopoietic progenitors, and naïve or activated B cell populations from 8 weeks-old wild-type (WT) and Usp3-deleted (Usp3Δ/Δ) mice were generated by deep sequencing using Illumina Hiseq2000. Here we present validation of the datasets by comparative analysis and qRT-PCR (Fig. 1). qRT-PCR validation of the RNA-seq on LSK cells was performed using SYBR Green assays.
Experimental design and materials and methods
Conflict of interest
Data We prepared the XPC fragment (residues 109–156) and the p62 PH domain (residues 1–108) from Escherichia coli expression systems [1,2]. The XPC fragment contains an intrinsically disordered acidic region (residues 124–141), which forms an elongated string-like structure upon binding to the p62 PH domain [1]. We used four samples for the structure determination by NMR, namely: