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  • EAI045 cost Further we sort the lipids into

    2018-10-23

    Further, we sort the EAI045 cost into annular and non-annual regions (Fig. 12). Finally, we plot the lipid-number mismatch and surface area per lipid mismatch of several asymmetric lipid membrane systems (Fig. 13). The design of the initial structures (Fig. 8) of the dimer protein and lipid bilayer systems is provided in Materials and Methods of the research article [1]. The data was created using in-house scripts (surround for annular and non-annular region identification, and a python script for sorting of DSSP output) [6,7], g-tools (a suite of analysis programs available through the GROMACs MD engine [8]) for secondary structure analysis, binding kinetics, and residue contact maps, and VMD [9] for visualization of structures.
    Acknowledgments This work was supported by the Robert A. Welch Research Foundation grant (D-1158), NIH grant (GM090897-02), National Science Foundation (ACI 1531594), Williams Endowment Fund of Trinity University, Texas Advanced Computing Center (TACC) for the use of Lonestar Cluster under the project (G-803132) “Protein Unfolding in Lipid Membranes”, and Texas Tech University High Performance Computing Center (TTU-HPCC). The authors acknowledge the valuable help of Dr. Andrey A. Gurtovenko of the Institute of Macromolecular Compounds, Russian Academy of Sciences for allowing us to use the published asymmetric PC/PS bilayer system and valuable advices on the simulation details of the PC/PS bilayer system.
    Experimental design, materials and methods All experimental design, materials and methods were based on reported paper [1]
    Acknowledgment This work was supported by a grant from the National Research Foundation of Korea (NRF) funded by the Korean government (MSIP; Grant nos. NRF-2014K1A4A7A01074642), Gyeonggi-do, KISTI, and the Korean Health Technology R&D Project, Ministry of Health & Welfare, Republic of Korea (Grant no. HI12C1804)
    Value of the data
    Data This data provides supporting information of the role of Notch signaling on osteoclast differentiation and function [1]. Notch signaling has been shown to regulate osteoclastogenesis negatively by Notch1 or positively by Notch2 [2]. To investigate whether Notch signaling affects osteoclast differentiation and spreading, we assessed the inhibitory potential of four GSIs from BMM to mature osteoclast forming period.
    Experimental design, materials and methods
    Acknowledgments This study was supported by the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning (NRF-2014R1A2A2A01002531).
    Value of the data
    Data C2C12 mouse myoblasts are used to perform in vitro analyses related to skeletal muscle as they express proteins involved with membrane depolarization, calcium (Ca2+) storage and release, and contraction [1,2]. Previously, it was shown that Ca2+ depletion prevented starvation-induced autophagy in cardiomyocytes [3]. In this report we present data on the degree of autophagic flux in differentiated C2C12 myotubes in response to acetylcholine and caffeine (two stimuli that can influence Ca2+ signaling and contraction).
    Experimental design, materials and methods
    Acknowledgments This research was supported by funds (341256) provided by the Natural Sciences and Engineering Research Council of Canada (NSERC) to Joe Quadrilatero. Darin Bloemberg is the recipient of a NSERC postgraduate scholarship. NSERC did not participate in study design, the collection, analysis and interpretation of data, the writing of the report, or the decision to submit the article for publication.
    Specifications table
    Value of the data
    Data Among 175 A. niger/A. welwitschiae strains analyzed, we found four mPCR profiles (Fig. 1). Profile 1 (17%) highlights strains harboring the pks (shown in blue, 554bp), radH (blue, 328bp) and fum8 (blue, 128bp) genes. Profile 2 (3.5%) highlights strains harboring only genes involved in OTA biosynthesis (radH and pks). Profile 3 (51.5%) highlights strains harboring only the gene fum8. Profile 4 (28%) highlights strains not carrying the mycotoxigenic genes studied herein.