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7,673 results for “inhibitor”
Dataset - Decrypting lysine deacetylase inhibitor action and protein modifications by dose-resolved proteomics
<h4><strong>Dataset Summary</strong></h4> <p>Lysine deacetylase inhibitors (KDACis) are approved for cutaneous T-cell lymphoma (CTCL), peripheral T-cell lymphoma (PTCL), and multiple myeloma. Despite the mechanism of action(s) (MoA) remains elusive, these inhibitors lead to increasing acetylation levels of histones and other proteins, altered gene expression and cell death. To characterize the MoA of these drugs in more detail, we systematically measured dose-dependent changes in protein expression, acetylation, and phosphorylation in response to 21 clinical and pre-clinical KDACis. MV4-11 cells were treated for 6 h with 1 vehicle control and 10 increasing doses of the respective drug (from 100 pM to 30 mM). Proteins were digested with trypsin, and the resulting 11 peptide preparations corresponding to one drug dose each were encoded by stable isotopes (tandem mass tags, TMT-11plex) and combined. Acetylated peptides were subsequently enriched by immunoprecipitation and phosphopeptides by immobilized metal affinity chromatography (IMAC). PTM-carrying and unmodified peptides were analyzed separately by liquid chromatography tandem mass spectrometry (LC-MS/MS) for peptide and protein identification and quantification. Additionally, Vorinostat and Panobinostat were also recorded as time-dependent experiments at their pEC50 concentration, respectively. </p> <h4><strong>Dataset structure</strong></h4> <p>Here, we provide all curve data processed with CurveCurator v0.4.0 (<a href="https://github.com/kusterlab/curve_curator">https://github.com/kusterlab/curve_curator</a>). Each drug is a zip folder containing acetylome, phosphoproteome, and fullproteome data. Next to each data set is the toml parameter file used to generate the curves.txt and dashboard.html files. Time-dependent data is indicated by "td" and dose-dependent data is indicated by "dd".</p> <p> </p>
Diffraction images used to solve the structures published in the article "Exploration of Strategies for Mechanism-Based Inhibitor Design for Family GH99 endo-alpha-1,2-Mannanases."
<p>Raw diffraction images used for generating the structures published in the article "Exploration of Strategies for Mechanism-Based Inhibitor Design for Family GH99 endo-a-1,2-Mannanases" (available <a href="https://doi.org/10.1002/chem.201800435">here</a>). Full single-crystal datasets are published. The software used for the processing of each dataset is listed in their respective PDB entries.</p> <p> </p> <p>If you find this useful, please contact me at <a href="mailto:lukasz.sobala@hirszfeld.pl">lukasz.sobala@hirszfeld.pl</a>, I am just interested in how these data are used!</p>
Diffraction images used to solve the structures published in the article "From 1,4-Disaccharide to 1,3-Glycosyl Carbasugar: Synthesis of a Bespoke Inhibitor of Family GH99 Endo-α-mannosidase"
<p>Raw diffraction images used for generating the structures published in the article "From 1,4-Disaccharide to 1,3-Glycosyl Carbasugar: Synthesis of a Bespoke Inhibitor of Family GH99 Endo-α-mannosidase" (available <a href="https://doi.org/10.1021/acs.orglett.8b03260">here</a>). Full single-crystal datasets, including images that were not used in the final analyses, are published. The software used for the processing of each dataset is listed in their respective PDB entries. An additional 720 degree dataset is provided, which has been collected from the same crystal as PDB 6HMH. This dataset has not been used to solve the structure presented in the paper. It works very well as an example of sulfur SAD phasing.</p> <p> </p> <p>If you find this useful, please contact me at <a href="mailto:lukasz.sobala@hirszfeld.pl">lukasz.sobala@hirszfeld.pl</a>, I am just interested in how these data are used!</p>
RNA datasets to derive predictors for immune checkpoint inhibitor therapy of non-small cell lung cancer
<p>Nanostring nCounter datasets and corresponding clinical data of tumor samples of patients with advanced NSCLC who received anti-PD-1 immuntherapy. Prospectively divided into a discovery and a validation cohort.</p> <p>Please cite the corresponding publication in Annals of Oncology (10.1093/annonc/mdz049)</p>
Hydrogen sulfide release via the ACE inhibitor Zofenopril prevents intimal hyperplasia in human vein segments and in a mouse model of carotid artery stenosis
<p>The current strategies to reduce intimal hyperplasia (IH) principally rely on local drug delivery, in endovascular approach. The oral angiotensin converting enzyme inhibitor (ACEi) Zofenopril has additional effects compared to other non-sulfyhydrated ACEi to prevent intimal hyperplasia and restenosis. Given the number of patients treated with ACEi worldwide, these findings call for further prospective clinical trials to test the benefits of sulfhydrated ACEi over classic ACEi for the prevention of restenosis in hypertensive patients.</p> <p>Abstract</p> <p>Objectives</p> <p>Hypertension is a major risk factor for intimal hyperplasia (IH) and restenosis following vascular and endovascular interventions. Pre-clinical studies suggest that hydrogen sulfide (H2S), an endogenous gasotransmitter, limits restenosis. While there is no clinically available pure H2S releasing compound, the sulfhydryl-containing angiotensin-converting enzyme inhibitor Zofenopril is a source of H2S. Here, we hypothesized that Zofenopril, due to H2S release, would be superior to other non-sulfhydryl containing angiotensin converting enzyme inhibitor (ACEi), in reducing intimal hyperplasia in the context of hypertension.</p> <p>Materials</p> <p>Spontaneously hypertensive male Cx40 deleted mice (Cx40-/-) or WT littermates were randomly treated with Enalapril 20 mg (Mepha Pharma) or Zofenopril 30 mg (Mylan SA). Discarded human vein segments and primary human smooth muscle cells (SMC) were treated with the active compound Enalaprilat or Zofenoprilat.</p> <p>Methods</p> <p>IH was evaluated in mice 28 days after focal carotid artery stenosis surgery and in human vein segments cultured for 7 days ex vivo. Human primary smooth muscle cell (SMC) proliferation and migration were studied in vitro.</p> <p>Results</p> <p>Compared to control animals (intima/media thickness=2.3±0.33), Enalapril reduced IH in Cx40-/- hypertensive mice by 30% (1.7±0.35; p=0.037), while Zofenopril abrogated IH (0.4±0.16; p<.0015 vs. Ctrl and p>0.99 vs. sham-operated Cx40-/-mice). In WT normotensive mice, enalapril had no effect (0.9665±0.2 in control vs 1.140±0.27; p>.99), while Zofenopril also abrogated IH (0.1623±0.07, p<.008 vs. Ctrl and p>0.99 vs. sham-operated WT mice). Zofenoprilat, but not Enalaprilat, also prevented intimal hyperplasia in human veins segments ex vivo. The effect of Zofenopril on carotid and SMC correlated with reduced SMC proliferation and migration. Zofenoprilat inhibited the MAPK and mTOR pathways in SMC and human vein segments.</p> <p>Conclusion</p> <p>Zofenopril provides extra beneficial effects compared to non-sulfhydryl ACEi to reduce SMC proliferation and restenosis, even in normotensive animals. These findings may hold broad clinical implications for patients suffering from vascular occlusive diseases and hypertension.</p>
KSR inhibitor APS-2-79 sensitivity test in JURKAT and ALL-SIL T-cell acute lymphoblastic leukemia cell lines measured by Cell Counting Kit 8
<p>APS-2-79 compound was purchased from MedChemExpress (Monmoutyh Junction, NJ, USA). The 20 mg/ml stock solution was prepared in DMSO. To calculate the IC50, JURKAT and ALL-SIL cells were cultured for 72h with a range of APS-2-79 concentrations (5-15 µM) added as equal volumes. Cells treated with 0.5% DMSO (vehicle) were used as negative control. Cells treated with 10% DMSO were used as positive control. The viability of cells was measured using Cell Counting Kit 8 (Sigma Aldrich) and GloMax Microplate Reader system (Promega) with 450 nm wavelength and 600 nm as reference wavelength. The relevant reads are made from following wells: 2A-2D (15 µM APS-2-79), 3A-3D (12.5 µM APS-2-79), 4A-4D (10 µM APS-2-79), 5A-5D (7.5 µM APS-2-79), 6A-6D (5 µM APS-2-79), 7A-7D (vehicle), 8A-8D (positive control).</p>
Supporting data for "The methylome of Biomphalaria glabrata and other mollusks: enduring modification of epigenetic landscape and phenotypic traits by a new DNA methylation inhibitor"
<p>Methylome of the fresh water snail <em>Biomphalaria glabrata</em>. DNA was extracted from the feet of 10 individuals of <em>B. glabrata</em> originally isolated from Brazil. These snails have been cultivated in the laboratory since 1960. Tissue were grinded at 4°C and incubated in 1 ml volume of lysis buffer (20 mM TRIS pH 8; 1 mM EDTA; 100 mM NaCl; 0.5% SDS), with 0.3 mg of proteinase K at 55°C for 1 night. Afterwards, lysate was purified with phenol-chloroform and DNA was isopropanol precipitated. The extracted DNA (around 138ng/µL) was poled in equivalent amounts and Whole Genome Bisulfite Sequencing was done by GATC-biotech (www.gatc-biotech.com). The principle of this treatment is to convert non-methylated cytosines of gDNA into deoxy-uracil, whereas methylated cytosines remain intact. WGBS was done according to the Lister protocol (sequence 2 forward strands only). The reference genome (Biomphalaria-glabrata-BB02_SCAFFOLDS_BglaB1.fa) and annotation (Biomphalaria-glabrata-BB02_BASEFEATURES_BglaB1.3.gff3) used in this project are available on VectorBase (https://www.vectorbase.org/). To align our short reads, we chose to use two specific bisulfite mapping tools, BSMAP 1.0.0 (https://code.google.com/p/bsmap/) and Bismark 0.10.2 (www.bioinformatics.babraham.ac.uk /projects/bismark/), to compare their efficiency and convenience to finally work with the more suitable one on our datasets. IGV (Interactive Genomics Viewer, https://www.broadinstitute.org/igv/) was used to visualized final alignments.<br> BSMAP performed better than Bismark and was used for downstream analyses. Without default parameters alignement efficiency for BSMAP is 47.1%, allowing for 2 mismatches increases it to 55.6%. Methylation occurs predominantly in CpGs. (C methylated in CpG context: 12.4%, C methylated in CHG context: 0.5%, C methylated in CHH context: 0.5%) The major part of CpG sites, 95.7% were unmethylated, of the remaining 4.3% of CpG sites around 3.8% had low methylation, and 0.5% were completely methylated. Methylation is of the mosaic type. Methylation is relatively low with 1.2% of total cytosines. Our analyses suggested that conserved genes and genes with stable expression are localized in high methylated regions of the genome. Finally, we see that repetitive sequences were predominantly situated in low methylated regions of <em>B. glabrata</em>. </p> <p>Wiggle files were generated for CpG pairs only.</p> <p>Produced at IHPE (http://ihpe.univ-perp.fr/)</p>
Stabilizing or Destabilizing: Simulations of Chymotrypsin Inhibitor 2 under Crowding Reveal Existence of a Crossover Temperature
<p>This data accompanies the paper entitled <em>Stabilizing or Destabilizing: Simulations of Chymotrypsin Inhibitor 2 under Crowding Reveal Existence of a Crossover Temperature</em> (https://dx.doi.org/10.1021/acs.jpclett.0c03626).</p> <p>CI2_REST2.zip: The zip archive includes REST2 trajectories for the three systems investigated in the paper: dilute conditions, crowding by BSA, and crowding by lysozyme. The trajectories are saved in the GROMACS XTC file format, separately for each temperature (i=0,...,23). Given the large trajectory sizes, only protein coordinates (CI2 + crowder(s)) are reported, and the output frequency is reduced to 100 ps. A starting geometry (in the Gromos87 GRO format) after a short relaxation is provided for each REST2 simulation (conf_prot.gro). Moreover, for each REST2 simulation, an xarray (http://xarray.pydata.org) dataset, saved in the netCDF file format, is included with the following observables computed for CI2: fraction of native contacts relative to crystal structure, radius of gyration, secondary-structure content, fraction of native contacts evaluated separately for the alpha helix and the two beta strands.</p>
MelanoDB: Dataset files of clinical and molecular features of advanced melanoma patients treated with MAPK inhibitors
<p>MAPK inhibitors have significantly improved overall survival in patients with metastatic melanoma disease but their efficacy is still limited by primary or acquired resistance. Several studies have attempted to predict response to MAPK inhibitor therapy, however the lack of a consistent cohort prevents better definition of associations between treatment efficacy and clinical and/or molecular features. Here, we present MelanoDB, a collection of patients with metastatic melanoma treated with MAPK inhibitors. We formatted data from 8 different studies for a total of 417 cases to gather common clinical and molecular features. Whole or partial exome sequencing is available for 191 cases and gene expression for 132 cases. We provide a web application to explore the integrated data and its distribution among the collected studies, and we share this dataset to the scientific community according to FAIR principles</p> <p>These data are available under the licence CC-BY-SA.</p> <p>Here we provide a web application viewer of the database content: http://melanodb-ircm.montp.inserm.fr/</p> <p>You are requested to cite this repository in the case of using these data in a publication.</p>
The coupling mechanism of ligands with SERT distinguishes substrates from inhibitors (raw data)
<p>Raw data of the manuscript: Ligand coupling mechanism of the human serotonin transporter differentiates substrates from inhibitors</p> <p><strong>Abstract:</strong></p> <p>The presynaptic serotonin transporter (SERT) reuptakes the serotonin (5HT) released into the synaptic cleft, thus ensuring temporal and spatial regulation of serotonergic signalling. Clinically approved drugs used for the treatment of neurological disorders, including depression and anxiety modulate SERT by trapping the transporter in the outward-open conformation. Illicit drugs of abuse as amphetamines act as substrates but reverse the transport direction, thereby releasing intracellular accumulated 5HT. Both mechanisms increase extracellular 5HT levels. Stoichiometry of the transport cycle has been described by kinetic schemes, the structures of the main conformations within the transport cycle revealed static coordinates. By combining <em>in-silico</em> approaches with <em>in-vitro</em> experiments and making use of a homologous series of 5HT analogues, we decoded the essential coupling mechanism between the substrate and the transporter which triggers uptake. The free energy calculations showed that only scaffold-bound substrates can correctly close the extracellular gate by pulling on the bundle domain through long-range electrostatic interactions. The associated spatial and physico-chemical requirements define substrate and inhibitor properties, opening new possibilities for rational drug design approaches.</p>
Raw gel images accompanying the publication: Koralewska et al, NAR 2024, Short 2'-O-methyl/LNA oligomers as highly-selective inhibitors of miRNA production in vitro and in vivo, DOI 10.1093/nar/gkae284
<p>A set of raw gel images used in the article: Koralewska <em>et al</em>. Short 2’-O-methyl/LNA oligomers as highly-selective inhibitors of miRNA production <em>in vitro</em> and <em>in vivo, </em>NAR 2024, DOI 10.1093/nar/gkae284.</p>
Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor therapy reduces the level of DNA damage in patients with heterozygous familial hypercholesterolemia
<p><span><span>Heterozygous Familial Hypercholesterolaemia (HeFH) is a common autosomal dominant genetic disease (1:300) characterized by elevated LDL-C leading to premature atherosclerosis. Treatment with a PCSK9 inhibitor (iPCSK9) is recommended in high cardiovascular risk FH patients if the treatment goal is not achieved on maximal tolerated statin plus ezetimibe. </span></span><span>The aim of this study was to </span><span><span>examine the changes in DNA damage in HeFH patients associated with iPCSK9 use. </span></span><span>Fifty-seven patients were included: a normolipidemic group (control; n=20) and patients with HeFH (study group; n=36). DNA damage was determined by alkaline comet assay. PCSK9 protein level was assessed by ELISA. </span><span>The levels of Lp(a) in human serum were quantitatively turbidimetrically assay.</span><span> </span><span>PCSK9i treatment was associated with lower DNA damage, Lp(a), PCSK9 and lipid profile than before treatment. However, 20 of 36 patients still had Lp(a) values above 125 nmol/L, and reduced Lp(a) did not correlate with reduced DNA damage. Reduced PCSK9 moderately (r=0.48) correlates with reduced DNA damage</span><span><span>. PCSK9i therapy reduces the level of DNA damage in HeFH patients, regardless of the type of inhibitor. The reduction in DNA damage is not related to the changes in lipid profile or Lp(a) induced by PCSK9i, but it is dependent on PCSK9 level.</span></span></p>
Inhibition of striatal dopamine release by the L-type calcium channel inhibitor isradipine co-varies with risk factors for Parkinson's
<h3><strong>ABSTRACT</strong></h3> <p>Ca<sup>2+</sup> entry into nigrostriatal dopamine (DA) neurons and axons via L-type voltage-gated Ca<sup>2+</sup> channels (LTCCs) contributes respectively to pacemaker activity and DA release, and has long been thought to contribute to vulnerability to degeneration in Parkinson’s disease. LTCC function is greater in DA axons and neurons from substantia nigra pars compacta than from ventral tegmental area, but this is not explained by channel expression level. We tested the hypothesis that LTCC-control of DA release is governed rather by local mechanisms, focussing on candidate biological factors known to operate differently between types of DA neurons and/or be associated with their differing vulnerability to parkinsonism, including biological sex, α-synuclein, DA transporters (DATs), and calbindin-D28k (Calb1). We detected evoked DA release <em>ex vivo </em>in mouse striatal slices using fast-scan cyclic voltammetry, and assessed LTCC support of DA release by detecting the inhibition of DA release by the LTCC inhibitors isradipine or CP8. Using genetic knockouts or pharmacological manipulations we identified that striatal LTCC support of DA release depended on multiple intersecting factors, in a regionally and sexually divergent manner. LTCC function was promoted by factors associated with Parkinsonian risk, including male sex, α-synuclein, DAT, and a dorsolateral co-ordinate, but limited by factors associated with protection i.e. female sex, glucocerebrosidase activity, Calb1, and ventromedial co-ordinate. Together, these data show that LTCC function in DA axons, and isradipine effect, are locally governed and suggest they vary in a manner that in turn might impact on, or reflect, the cellular stress that leads to parkinsonian degeneration.</p> <p> </p> <h3><strong>FILE DESCRIPTIONS</strong></h3> <p>This repository contains the following files:</p> <ul> <li>Key Resources Table (.xlsx) - Table containing details on key lab materials (antibodies, mouse lines, and software), and the persistent identifiers for protocols and code used and generated in this study. </li> <li>Source Data (.xlsx) - Excel spreadsheet containing all tabular datasets plotted in Main Figures 1 to 5 (.xlsx).</li> <li>R_Scritps (.R) - Custom written R scripts to perform a classification tree analysis.</li> </ul>
Schistosoma mansoni ATAC-seq results for IGV (female and male worms with and without LSD1 inhibitor)
<p>In this study, the anti-schistosomal activity of 39 <em>Homo sapiens</em> Lysine Specific Demethylase 1 (HsLSD1) inhibitors was investigated on parasitic life cycle stages associated with both definitive and intermediate host infection. Amongst this collection of small molecules, compound <strong>33</strong> was the most potent and reduced <em>ex vivo</em> viabilities of schistosomula, juveniles, miracidia and adults. At its sub-lethal concentration to adults (3.13 µM), compound <strong>33 </strong>also significantly impacted oviposition, ovarian as well as vitellarian architecture and gonadal/neoblast stem cell proliferation. ATAC-seq analysis of adults demonstrated that compound <strong>33</strong> significantly affected chromatin structure (intragenic regions > intergenic regions), especially in genes differentially expressed in cell populations (e.g., germinal stem cells, hes2<em><sup>+</sup></em>stem cell progeny, S1 cells and late female germinal cells) linked to these <em>ex vivo</em> phenotypes.</p> <p>The data presented here allow for visualisation in IGV https://igv.org/app/</p> <p>Produced in collaboration with IHPE. </p>
Dataset for article: Pro-cognitive effects of dual tacrine derivatives acting as cholinesterase inhibitors and NMDA receptor antagonists
<p>Figure 1. Chemical structures of tacrine (<strong>a</strong>) and its derivatives created by introducing substituents on the aromatic core and/or altering the size of the cycloalkyl moiety attached to the aromatic region: 7-MEOTA (<strong>b</strong>), K1578 (7-chloro-1<em>H</em>,2<em>H</em>,3<em>H</em>-cyclopenta[<em>b</em>]quinolin-9-amine; <strong>c</strong>), K1592 (1-chloro-6<em>H</em>,7<em>H</em>,8<em>H</em>,9<em>H</em>,10<em>H</em>-cyclohepta[<em>b</em>]quinolin-11-amine; <strong>d</strong>), K1594 (6-methyl-1,2,3,4-tetrahydroacridin-9-amine; <strong>e</strong>), and K1599 (7-methoxy-1<em>H</em>,2<em>H</em>,3<em>H</em>-cyclopenta[<em>b</em>]quinolin-9-amine; <strong>f</strong>). Compounds in this study were used in the form of hydrochloride salts.</p> <p>Figure_2_values. Test results. Morris water maze: scopolamine-induced model of cognitive deficit in the acquisition and reversal phases. The graphs show the effects of K1578 (<strong>a</strong>), K1592 (<strong>b</strong>), K1594 (<strong>c</strong>), and K1599 (<strong>d</strong>) on escape latency during the acquisition phase, where none of the compounds ameliorated the deficit of spatial learning. The remaining graphs display the effects of K1578 (<strong>e</strong>), K1592 (<strong>f</strong>), K1594 (<strong>g</strong>), and K1599 (<strong>h</strong>) in the reversal phase, where K1578 (1 mg/kg) and K1599 (at both doses), and marginally K1592 (1 mg/kg; see in the text), mitigated the scopolamine-induced deficit of reversal learning. VEH – vehicle, the numbers in brackets denote the dose applied (mg/kg). Data are presented as the mean + SEM, * vs. VEH, * p < 0.05, ** p < 0.01, *** p < 0.001. <em>n</em> = 6–9 animals per group. Statistical significance was determined using two-way repeated measures ANOVA (a–d) or ANOVA (e, f, h) followed by Dunnett’s multiple comparisons tests.</p> <p>Figure-3_values. Test results. Morris water maze: MK-801-induced model of cognitive deficit in the acquisition phase. The graphs illustrate the effects of the compounds K1578 (<strong>a</strong>), K1592 (<strong>b</strong>), K1594 (<strong>c</strong>), and K1599 (<strong>d</strong>) on escape latency. Only K1599 (1 mg/kg) ameliorated the MK-801-induced deficit of spatial learning. VEH – vehicle, the numbers in brackets denote the dose (mg/kg). Data are presented as the mean + SEM, * vs. VEH, * p < 0.05, ** p < 0.01. <em>n</em> = 5–7 animals per group. Statistical significance was determined using two-way repeated measures ANOVA followed by Dunnett’s multiple comparisons tests.</p> <p>Figure_4_values. Open field test. The results demonstrate the effects of K1578 (<strong>a</strong>), K1592 (<strong>b</strong>), K1594 (<strong>c</strong>), and K1599 (<strong>d</strong>) on the distance moved by intact and MK-801-treated animals. VEH – vehicle, the numbers in brackets denote the dose (mg/kg). Data are presented as the mean + SEM, * vs. VEH group of the corresponding phenotype, * p < 0.05, ** p < 0.01, **** p < 0.0001. <em>n</em> = 6–14 animals per group. A significant effect of both factors (treatment and phenotype) was determined using two-way ANOVA, followed by Dunnett’s multiple comparisons tests.</p> <p>Figure-5_values. Acetylcholinesterase activity. The results document the effect of the compounds (1 mg/kg ip) on AChE activity in the hippocampus (<strong>a</strong>), prefrontal cortex (<strong>b</strong>), striatum (<strong>c</strong>), and whole brain sample (<strong>d</strong>). K1578 and K1599 decreased AChE activity in the striatum. VEH – vehicle. Data are presented as the median with minimum to maximum range, * vs. VEH, *** p < 0.001, **** p < 0.0001. VEH samples AChE enzyme activities reached the following absolute values (a) 15.19 ± 3.09 U/mg protein, (b) 9.810 ± 1.54 U/mg protein, (c) 26.05 ± 3.27 U/mg protein, and (d) 27.38 ± 3.36 U/mg protein. Significance was determined by ANOVA (graphs c, d), followed by Dunnett’s multiple comparisons tests.</p> <p>Figure_6_values. Electrophysiology: Inhibition of GluN1/GluN2A receptors by K1599. Representative whole-cell patch-clamp recordings measured from HEK293 cells expressing the GluN1/GluN2A receptors held at a membrane voltage of −80 mV and +60 mV; 30 μM K1599 was applied as indicated. Results summarizing the relative inhibition induced by 30 µM K1599, measured at the indicated membrane potentials. <em>n</em> ≥ 5 cells per each condition.</p> <p>Table_1. The rats were pseudo-randomly assigned to one of the 18 treatment groups listed in. Each group received two injections: one containing the study compound and another containing either MK-801 or scopolamine, as indicated by the group name. The vehicle group (VEH) received the DMSO vehicle (2.5 mL/kg) and saline. The “scopolamine” and “MK-801” groups received scopolamine or MK-801, respectively, along with the DMSO vehicle (2.5 mL/kg).</p> <p>Table 2. Treatment groups and <em>n</em> in biochemical experiments - AChE activity assay.</p>
Promiscuity cliffs (PCs), promiscuity cliff pathways (PCPs), and promiscuity hubs (PHs) formed by inhibitors of human kinases
<p>The PC, PCP, and PH data structures have been introduced for the analysis of compound promiscuity [1-3]. A comprehensive collection of PCs, PCPs, and PHs formed by kinase inhibitors covering more than 80% of the human kinome is made available. See readme.txt for more information regarding the provided files.</p> <p>References:</p> <ol> <li>Dimova, D.; Gilberg, E.; Bajorath, J. Identification and Analysis of Promiscuity Cliffs Formed by Bioactive Compounds and Experimental Implications. RSC Adv. 2017, 7, 58–66.</li> <li>Miljković, F.; Bajorath, J. Computational Analysis of Kinase Inhibitors Identifies Promiscuity Cliffs across the Human Kinome. ACS Omega 2018, 3, 17295–17308.</li> <li>Miljković, F; Vogt, M; Bajorath, J. Systematic Computational Identification of Promiscuity Cliff Pathways Formed by Inhibitors of the Human Kinome. J. Comput. Aided Mol. Des. 2019, in press, doi: doi.org/10.1007/s10822-019-00198-9</li> </ol>
Supplementary material: Efficient in vivo screening method for the identification of C4 photosynthesis inhibitors based on cell suspensions of the single-cell C4 plant Bienertia sinuspersici
<p>Data described in Minges et al. (2019) Efficient <em>in vivo</em> screening method for the identification of C<sub>4</sub> photosynthesis inhibitors based on cell suspensions of the single-cell C<sub>4</sub> plant <em>Bienertia sinuspersici</em>. doi: <a href="https://doi.org/10.3389/fpls.2019.01350">10.3389/fpls.2019.01350</a></p> <p> </p>
Data From: Harnessing Deep Belief Networks for Selective HDAC6 Inhibitors Identification
<p>This dataset contains the results from virtual screening of SPECS library after predicting the selectivity of molecules against HDAC6 over using a Deep Belief Network model that was trained and tested by the authors.</p> <p>The docking poses of 10 molecules with best docking scores were given along with their MMGBSA scores. </p> <p>The MD trajectory files along with the analysis were also provided for the selected three molecules as well as the reference molecule (co-crystalized ligand).</p>
Molecular dynamics trajectories for SARS-CoV-2 Mpro with 7 HIV inhibitors
<p>Raw trajectory data (GROMACS format) of all atom molecular dynamics simulation of COVID-19 related SARS-CoV-2 dimeric main protease (based on PDB 6LU7) with 7 kinds of HIV inhibitors (darunavir, indinavir, lopinavir, nelfinavir, ritonavir, saquinavir, and tipranavir) were calculated on massively parallel supercomputer HOKUSAI Big Waterfall at RIKEN ISC, and a special-purpose computer, MDGRAPE-4A, at RIKEN BDR, JAPAN. For each ligand, 200ns length 28 trajectories were calculated. Some of these trajectories were calculated further longer. We can observe formation of encounter complex and investigate potential binding sites on the surface of the dimeric protease. We hope that these raw data are valuable for further drug repurposing/development research targeting the SARS-CoV-2 main protease. We will submit analysis of these data to refereed journal.</p> <p>Molecular dynamics simulations were performed under NVT at 310K, with the time step 2.5fs. The starting structure was prepared based on PDB 6LU7, with amber14sb force field in about 10nm cubic box with periodic boundary conditions. The ligands were initially placed apart from the active sites of the dimeric main protease.</p> <p>We have also already deposited 10 microseconds trajectories of the dimeric protease without ligand (with amber99sb-ildn force field) in the repository https://data.mendeley.com/datasets/vpps4vhryg/1 (DOI:10.17632/vpps4vhryg.1).</p> <p>Files:</p> <ul> <li><strong><em>LIG</em></strong>_28traj200ns_every200ps.zip (28trajectories for each ligand) <ul> <li>traj200ns_every200ps/<strong><em>LIG</em></strong>/<strong><em>a</em></strong>/traj200ns_every200ps_<em><strong>LIG</strong>-<strong>a</strong>-<strong>n</strong></em>.xtc <ul> <li>(trajectory in GROMACS XTC)</li> </ul> </li> <li>traj200ns_every200ps/<strong><em>LIG</em></strong>/<strong><em>a</em></strong>/conf.gro <ul> <li>(initial condition in GROMACS GRO)</li> </ul> </li> <li>traj200ns_every200ps/<em><strong>LIG</strong></em>/topology/ <ul> <li>(contains topology files)</li> </ul> </li> <li>traj200ns_every200ps/<strong><em>LIG</em></strong>/mdp/ <ul> <li>(contains run paramter files)</li> </ul> </li> </ul> </li> <li>ZZZ_20traj1us_every200ps.zip (20trajectories extended to 1microsecond) <ul> <li>traj1us_every200ps/traj1us_every200ps_<em><strong>LIG</strong>-<strong>a</strong>-<strong>n</strong></em>.xtc <ul> <li>DAR-C-06, DAR-D-07</li> <li>IND-C-05, IND-C-06, IND-D-06</li> <li>LOP-A-02, LOP-D-03</li> <li>NEL-B-01, NEL-C-07, NEL-D-02</li> <li>RIT-B-07, RIT-C-07</li> <li>SAQ-B-01, SAQ-C-04, SAQ-D-03</li> <li>TPR-A-07, TPR-B-04, TPR-B-06, TPR-C-05, TPR-D-02</li> </ul> </li> </ul> </li> <li>ZZZ_3traj6us_every1ns.zip (3trajectories extended to 6microseconds or more) <ul> <li>traj6us_every1ns/traj6us_every1ns_<em><strong>LIG</strong>-<strong>a</strong>-<strong>n</strong></em>.xtc <ul> <li>IND-D-06, NEL-B-01, TPR-B-04</li> </ul> </li> </ul> </li> </ul> <p> </p> <ul> <li>ZZZ_LigandBindingPosePDBs.zip (pickup 3 snapshots for each ligand) <ul> <li>LigandBindingPosePDBs/<em><strong>LIG</strong>-<strong>a</strong>-<strong>n</strong></em>_frame.pdb</li> </ul> </li> </ul> <p> </p> <ul> <li>movies_overlooking_28traj200ns.zip (7x2movies) <ul> <li>movies_28traj200ns/movie_overlooking_<strong><em>LIG</em></strong>_28traj200ns-viewA.mp4 <ul> <li>inspecting 28traj at once</li> </ul> </li> <li>movies_28traj200ns/movie_overlooking_<strong><em>LIG</em></strong>_28traj200ns-viewB.mp4 <ul> <li>from the opposite angle</li> </ul> </li> </ul> </li> <li>movies_1us.zip (17movies) <ul> <li>movies_1us/movie_<em><strong>LIG</strong>-<strong>a</strong>-<strong>n</strong></em>_1us.mp4</li> </ul> </li> <li>movies_6us.zip (3movies) <ul> <li>movies_6us/movie_<em><strong>LIG</strong>-<strong>a</strong>-<strong>n</strong></em>_6us.mp4</li> </ul> </li> </ul> <p> where</p> <p> <em><strong>LIG</strong></em>={DAR,IND,LOP,NEL,RIT,SAQ,TPR}<br> DAR:darunavir<br> IND:indinavir<br> NEL:nelfinavir<br> RIT:ritonavir<br> SAQ:saquinavir<br> TPR:tipranavir<br> <em><strong>a</strong></em>={A,B,C,D}<br> <em><strong>n</strong></em>={01,02,03,04,05,06,07}</p> <p> </p> <ul> <li>ZZZz_3traj1us_every200ps_unbinding.zip (3trajectories extended to 1microsecond exhibiting unbinding)</li> <li>ZZZz_56traj200ns_every200ps_negative_control.zip (56trajectories as a negative control)</li> <li>ZZZz_LigandBindingPosePDBsRevised.zip (pickuped 3 snapshots for each ligand)</li> </ul> <p> </p>
Atomic resolution X-ray diffraction images for endothiapepsin complexed with the inhibitor H261.
<p>X-ray diffraction images for a complex of endothiapepsin with the hydroxyethylene renin inhibitor H261 which were collected at DESY (Hamburg) in June 1998 using the beamline BW7B with a Mar image plate detector in two passes. The data extend to a resolution of almost 1.1 Angstroms. More details are given in the accompanying notes. </p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.