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6,818 results for “inhibition”
Structure and Function of Axo-axonic Inhibition — Calcium Traces
<p>These files contain the calcium traces and behavioral data for the functional imaging in the paper:</p> <p><strong>Chandelier cell anatomy and function suggest a variably distributed but common signal.</strong><br> Schneider-Mizell, C. Bodor, A.L., Collman, F. Brittain,D. Bleckert, AA, Dorkenwald, S., Turner N.L. Macrina, T. Lee, K. Lu, R. Wu, J. et al. (2020) bioRxiv 2020.03.31.018952v1; doi: <a href="https://doi.org/10.1101/2020.03.31.018952">https://doi.org/10.1101/2020.03.31.018952</a></p> <p>Descriptions of the files can be found in the metadata of the nwb files.</p>
tRNA-derived fragment tRF-Glu49 inhibits cell proliferation, migration and invasion in cervical cancer by targeting FGL1
<p>A transfer RNA (tRNA)-derived fragment was found to be a new possible biological marker and target in carcinoma therapy. However, the effect exerted by tRFs on cervical carcinoma is still unclear. We identify the potential tumor suppressor gene tRF-Glu49 in cervical carcinoma through tRF and ti-RNA microarray investigation. We then demonstrated that tRF-Glu49 showed downregulation within the cervical carcinoma tissue and was associated with less aggressive clinical features and a better prognosis. Phenotypic studies revealed that tRF-Glu49 inhibited cervical cell proliferation, migration, and invasion processes. Mechanistic investigation revealed that tRF-Glu49 directly regulated the oncogene, fibrinogen-like protein-1 (FGL1). In general, according to the result achieved in this study, tRF-Glu49 can modulate cervical cell proliferation, migration, and invasion processes through the target process for FGL1, and tRF-Glu49 is likely to be a possible prognostic biological marker in patients with cervical carcinoma.</p>
Inhibition of Lung Microbiota-derived Proapoptotic Peptides Ameliorate Acute Exacerbation of Pulmonary Fibrosis
<p>The files show the microarray data obtained during epitope mapping of the newly developed monoclonal antibodies against corisin, the complete protein sequences of newly isolated <em>Staphylococcus haemolyticus</em> strains (1b, 7b and 12b), and the raw data of all figures and tables.</p>
Severe hypoxia exposure inhibits larval brain development but does not affect the capacity to mount a cortisol stress response in zebrafish
<p>Fish nursery habitats are increasingly hypoxic and the brain is recognized as highly hypoxia-sensitive, yet there is a lack of information on the effects of hypoxia on the development and function of the larval fish brain. Here, we tested the hypothesis that by inhibiting brain development, larval exposure to severe hypoxia has persistent functional effects on the cortisol stress response in zebrafish (<i>Danio rerio</i>). Exposing 5 days post-fertilization (dpf) larvae to 10% dissolved O<sub>2</sub> (DO) for 16 h only marginally reduced survival, but it decreased forebrain neural proliferation by 55%, and reduced the expression of <i>neurod1</i>, <i>gfap,</i> and <i>mbpa, </i>markers of determined neurons, glia, and oligodendrocytes, respectively. The 5 dpf hypoxic exposure also elicited transient increases in whole body cortisol and in <i>crf</i>, <i>uts1</i>, and <i>hsd20b2</i> expression, key regulators of the endocrine stress response. Hypoxia exposure at 5 dpf also inhibited the cortisol stress response to hypoxia in 10 dpf larvae and increased hypoxia tolerance. However, 10% DO exposure at 5 dpf for 16h did not affect the cortisol stress response to a novel stressor in 10 dpf larvae or the cortisol stress response to hypoxia in adult fish. Therefore, while larval exposure to severe hypoxia can inhibit brain development, it also increases hypoxia tolerance. These effects may transiently reduce the impact of hypoxia on the cortisol stress response but not its functional capacity to respond to novel stressors. We conclude that the larval cortisol stress response in zebrafish has a high capacity to cope with severe hypoxia-induced neurogenic impairment.</p>
Decreased ultraviolet radiation and decomposer biodiversity inhibit litter decomposition under continuous nitrogen inputs
<p>Atmospheric nitrogen (N) deposition has altered biogeochemical cycles and ecosystem functioning. As a key process involved in carbon and nutrient cycles in terrestrial ecosystems, litter decomposition is sensitive to external N inputs. However, it remains unclear how the interactions of ultraviolet (UV) radiation, soil biodiversity (bacteria, fungi and invertebrates) and conventional drivers (e.g., litter chemistry and microbial activities) regulate the responses of litter decomposition to continuous N inputs.</p> <p>Based on an N-addition experimental platform, we conducted a two-year litter decomposition experiment to examine the relative importance of N-induced changes in biotic and abiotic factors in mediating changes in the decomposition rates of four litter types (three representative species and their mixture) along an experimental N gradient in a Tibetan alpine steppe.</p> <p>Our results showed that litter decomposition rates exhibited a consistent decrease in response to N enrichment among all species and their mixture. The slowed decomposition rates with increasing N addition were associated with N-induced reductions in UV radiation and soil bacterial diversity. An additional UV radiation manipulative experiment further confirmed that photodegradation had strong effects on plant litter decomposition at our study site.</p> <p>These results demonstrated that N-induced declines in UV radiation and soil bacterial diversity inhibited litter decomposition, challenging the traditional view that changes in litter chemistry and microbial activities determine the responses of litter decomposition to external N inputs.</p>
Structural Basis for the Inhibition of IAPP Fibril Formation by the Co-Chaperonin Prefoldin - Experimental Data
<p>Experimental data (EM, AFM, BLI, ThT and Cell viability assays, as well as docking models) used for the study :</p> <p><strong>Structural Basis for the Inhibition of IAPP Fibril Formation by the </strong><strong>Co-Chaperonin Prefoldin</strong></p> <p>by Ricarda Törner, Tatsiana Kupreichyk, Lothar Gremer, Elisa Colas Debled, Daphna Fenel, Sarah Schemmert, Pierre Gans<sub>, </sub>Dieter Willbold, Guy Schoehn, Wolfgang Hoyer, Jerome Boisbouvier</p>
NMR-Guided Rational Engineering of Endocellulase from Acidothermus Cellulolyticus for Reducing Product Inhibition
<p>These are the plumed input files needed to reproduce the funnel metadynamics results for cellobiose binding to WT 1ECE, Y245G mutant, and W212A mutant. </p>
Structural insights into the inhibition site in the phosphorylcholine phosphatase enzyme of Pseudomonas aeruginosa
<p>Inputs for the simulations (MDs and FEP), plus scripts used to obtain results of the manuscript entitled "Structural insights into the inhibition site in the phosphorylcholine phosphatase enzyme of Pseudomonas aeruginosa"</p>
MicroRNA-574-5p targeting HOXC6 expression inhibits the hepatocyte lipid uptake to alleviate NAFLD
<p>In recent times, the non-alcoholic fatty liver disease (NAFLD) is increasing worldwide. Increasing evidence supports the role of miRNAs in the pathogenesis of NAFLD. The miR-574-5p has been shown to be involved in lipid metabolism. However, studies on the correlation between miR-574-5p and NAFLD are lacking. Hence, in this study, we wanted to investigate <strong>whether miR-574-5p is associated with the pathogenesis of NAFLD</strong>. Through various <em>in vivo</em> and <em>in vitro</em> experiments, we found that miR-574-5p can inhibit lipid accumulation and lipid formation by targeting the HOXC6 3' UTR. We believe that our study makes a significant contribution to the literature because <strong>this study is the first to show that miR-574-5p is downregulated in liver tissue in </strong><strong>a</strong><strong> mouse NAFLD model</strong>. Further, understanding the miRNAs and their targets that regulate NAFLD may help us better understand the disease and lead to the design of a potential therapeutic against NAFLD in the future.In recent times, the non-alcoholic fatty liver disease (NAFLD) is increasing worldwide. Increasing evidence supports the role of miRNAs in the pathogenesis of NAFLD. The miR-574-5p has been shown to be involved in lipid metabolism. However, studies on the correlation between miR-574-5p and NAFLD are lacking. Hence, in this study, we wanted to investigate <strong>whether miR-574-5p is associated with the pathogenesis of NAFLD</strong>. Through various <em>in vivo</em> and <em>in vitro</em> experiments, we found that miR-574-5p can inhibit lipid accumulation and lipid formation by targeting the HOXC6 3' UTR. We believe that our study makes a significant contribution to the literature because <strong>this study is the first to show that miR-574-5p is downregulated in liver tissue in </strong><strong>a</strong><strong> mouse NAFLD model</strong>. Further, understanding the miRNAs and their targets that regulate NAFLD may help us better understand the disease and lead to the design of a potential therapeutic against NAFLD in the future.</p>
Structure-guided discovery of potent antifungals that prevent Ras signaling by inhibiting protein farnesyltransferase
<p>Infections by fungal pathogens are difficult to treat due to a paucity of antifungals and emerging resistances. Next-generation antifungals therefore are needed urgently. We have developed compounds that prevent farnesylation of <em>Cryptoccoccus</em> <em>neoformans</em> Ras protein by inhibiting protein farnesyltransferase with 3–4 nanomolar affinities. Farnesylation directs Ras to the cell membrane and is required for infectivity of this lethal pathogenic fungus. Our high-affinity compounds inhibit fungal growth with 3–6 micromolar minimum inhibitory concentrations, 4- to 8-fold better than Fluconazole, an antifungal commonly used in the clinic. Compounds bound with distinct inhibition mechanisms at two alternative, partially overlapping binding sites, accessed via different inhibitor conformations. We showed that antifungal potency depends critically on the selected inhibition mechanism, because this determines the efficacy of an inhibitor at low <em>in</em> <em>vivo</em> levels of enzyme and farnesyl substrate. We elucidated how chemical modifications of the antifungals encode the desired inhibitor conformation and concomitant inhibitory mechanism.</p>
Zbtb14 regulates monocyte and macrophage development through inhibiting pu.1 expression in zebrafish
<p>To elucidate the mechanism underlying the aberrant monocyte/macrophage development of <em>zbtb14<sup>-/- </sup></em>mutant, GFP-positive cells were isolated from either wild-type <em>Tg(mpeg1.1:eGFP)</em> or <em>zbtb14 <sup>-/-</sup> //Tg(mpeg1.1:eGFP) </em>larvae at 2dpf by FACS. mRNA was extracted from sorted cells using RNeasy Micro (Qiagen, Manchester, UK) and mRNA libraries were constructed using NEBNext Ultra RNA Library Prep Kit for52 Illumina and sequenced under Illumina HiSeq X Ten with pair end 150bp (PE150). </p>
Library of Two Million Unique Small Molecules with Precalculated Fingerprints, Descriptors, and Cardiotoxicity Inhibition Data
<p>This repository comprises a dataset of ~2 million unique compounds saved in an hdf5 small molecule library store, which includes the following fields for each molecule:</p> <ul> <li>InChI key</li> <li>Standardized SMILES string</li> <li>Compound source</li> <li>ChEMBL identifier if the compound exists in this open access database</li> <li>1024-bit Morgan fingerprint</li> <li>2048-bit Morgan fingerprint</li> <li>881-bit PubChem fingerprints</li> <li>854 vector-length of preprocessed and standardized Mordred descriptors</li> <li>and cardiotoxicity inhibition predictions for each of the three cardiac ion channels (hERG, Nav1.5, and Cav1.2) using <a href="https://github.com/issararab/CToxPred2">CtoxPred2</a> along with the model confidence scores.</li> </ul> <p>The repository also includes a Jupyter notebook that serves as an initial guide for querying the small molecule library store. Export both files to the same folder, allocate approximately 40 GB of available memory disk space, unzip the library store, and then launch the notebook to begin querying.</p> <p><strong>Upon usage, please cite this publication:</strong></p> <ul> <li>Issar Arab, Kris Laukens, Wout Bittremieux, <strong>Semisupervised Learning to Boost hERG, Nav1.5, and Cav1.2 Cardiac Ion Channel Toxicity Prediction by Mining a Large Unlabeled Small Molecule Data Set</strong>, <em>Journal of Chemical Information and Modeling</em>, (2024). doi:<a title="DOI URL" href="https://doi.org/10.1021/acs.jcim.4c01102">10.1021/acs.jcim.4c01102</a></li> </ul>
Data from: Puerarin alleviates atherosclerosis via the inhibition of Prevotella copri and its trimethylamine production
<p><strong>Objective </strong>Puerarin (PU) is a natural compound that exhibits limited oral bioavailability but has shown promise in the treatment of atherosclerosis (AS). However, the precise mechanisms underlying its therapeutic effects remain incompletely understood. This study aimed to investigate the effects of PU and its mechanisms in mitigating AS in both mice and humans.</p> <p><strong>Design </strong>The impact of PU on AS was examined in <em>ApoE</em><sup>-/-</sup> mice fed a high-fat diet (HFD) and in human patients with carotid artery plaque. To explore the causal link between PU-associated gut microbiota and AS, faecal microbiota transplantation (FMT) and mono-colonization of mice with <em>Prevotella copri</em> (<em>P. copri</em>) were employed.</p> <p><strong>Results </strong>PU alleviated AS by modulating the gut microbiota, as evidenced by alterations in gut microbiota composition and the amelioration of AS following FMT from PU-treated mice into <em>ApoE</em><sup>-/-</sup> mice fed HFD. Specifically, PU reduced the abundance of <em>P. copri</em>, which exacerbated AS by producing trimethylamine (TMA). Prolonged mono-colonization of <em>P. copri</em> undermines the beneficial effects of PU on AS. In clinical, the plaque scores of AS patients were positively correlated with the abundance of <em>P. copri</em> and plasma trimethylamine-N-oxide (TMAO) levels. A 1-week oral intervention with PU effectively decreased <em>P. copri</em> levels and reduced TMAO concentrations in patients with carotid artery plaque.</p> <p><strong>Conclusion </strong>PU may provide therapeutic benefits in combating AS by targeting <em>P. copri</em> and its production of TMA.</p>
Raw data for: Structure of the human dopamine transporter and mechanisms of allosteric inhibition
<p>This repository contains raw data related to "Structure of the human dopamine transporter and mechanisms of allosteric inhibition" by Srivastava et al.</p> <p>Included are molecular dynamics input parameter files, amber prmtop, production trajectories and analysis scripts. Trajectories are subsampled with one frame every 10 ns. </p> <p> </p> <p>Contact information:</p> <p>Name: Md Fulbabu Sk</p> <p>Institution: Theoretical and Computational Biophysics Group (TCBG), Beckman Institute, University of Illinois Urbana Champaign</p> <p>Address: 405 N. Mathews Avenue, Urbana, Illinois 61801</p> <p>Email: mfsk@illinois.edu</p>
The dataset for the manuscript entitled "Seawater intrusion inhibits nitrate removal in tidal marsh aquifers"
<p>This is the dataset for the manuscript entitled "Seawater intrusion inhibits nitrate removal in tidal marsh aquifers".</p>
Molecular insights into human phosphatidylserine synthase 1 reveal its inhibition promotes LDL uptake
<p>Supporting molecular dynamics (MD) files for the manuscript with the same title. It includes three parts: MD initial files, trajectory files with the membrane and solvent water stripped, and an example binding free energy calculation setting file using Molecular Mechanics Poisson-Boltzmann Surface Area (MM-PBSA) method with an implicit membrane model.</p> <p>The MD initial files include MD parameters (folder 0_mdin) and specific topology (.parm7), initial structure (.rst7), and structural restraint files (.rest) in the corresponding folder for each simulation.</p> <p>The trajectory files include the topology files with membrane and solvent water stripped (.rst7) and 50-snapshot (4 ns interval) coordinate files (.nc) for each MD run.</p> <p>The MM-PBSA setting file (.in) is supposed to be used as the input of the MMPBSA.py utility of the AMBER simulation suite.</p>
Inhibition of toxic Pseudo-nitzschia spp. by the kelp, Saccharina latissima, and other seaweeds
<p><span>This package contains the datasets and R code used to produce the article “Inhibition of toxic <em>Pseudo-nitzschia </em>spp. by the kelp, <em>Saccharina latissima</em>, and other seaweeds,” which is to appear in Limnology and Oceanography.</span></p>
Inhibition of Distractors: The Interaction between Stimuli Characteristics and Habituation
<p><span><span>Data and analysis of the manuscript </span></span></p>
ISOLATION AND IDENTIFICATION OF A NOVEL COMPOUND FROM WITHANIASOMNIFERA: IN VITRO STUDIES ON HIV-1 REVERSE TRANSCRIPTASE INHIBITION
<p><strong><span>ABSTRACT</span></strong></p> <p><span>The emergence of drug-resistant strains of HIV-1 underscores the need for novel therapeutic agents with improved efficacy and safety profiles. Therefore, this study aims to assess the in vitro HIV-1 RT inhibition of active molecule isolated form W. somnifera. Crude extract was prepared from W. sominfera stem bark my using methanol solvent. Isolation and Purification was done using TLC, column chromatography techniques. Characterization of isolated compound was done with using spectral studies. HIV-1 RT inhibition of isolated compound was done. Cell viability against PBMC cells of isolated compound was performed with MTT assay. The compound exhibited a dosedependent inhibition of HIV-1 RT activity, with increasing percentages of inhibition observed at higher concentrations. At 50 µg/mL, Compound displayed a 31.5% inhibition, which progressively increased to 76.4% at 800 µg/mL. The IC50 value for Compound was determined to be 152 µg/mL, indicating the concentration at which 50% inhibition of HIV-1 RT activity is achieved. The isolated compound exhibited decreasing cell viability as the concentration increased, with values of 91%, 85.1%, 75.5%, 68.0%, and 65.4% at 50 µg/mL, 100 µg/mL, 200 µg/mL, 400 µg/mL, and 800 µg/mL, respectively. These findings underscore the importance of comprehensive assessment of compound activity, considering both antiviral potency against HIV-1 RT and cytotoxic effects on healthy cells.<br></span></p> <p><strong><span>Keywords</span><span>: </span></strong><span>HIV-1 RT, W. somnifera, TLC, Column, Cell viability, MTT assay</span> </p>
FIGURE 3. Mitodiplosis graminis. a–d in Redescription of Mitodiplosis graminis (Diptera: Cecidomyiidae), a gall midge inhibiting the flowering of pyp grass Ehrharta villosa (Poaceae) in South Africa
FIGURE 3. Mitodiplosis graminis. a–d: pupa, e–h: larva, i: egg. (a) anterior part ventrally, arrow indicates facial horn, second prothoracic spiracle not drawn (b) contour of anterior part laterally, arrow indicates facial horn, (c) prothoracic spiracle, (d) facial horn ventrally, (e) last two segments in dorsal view, (f) head in ventral view, (g) head in anterior view, (h) sternal spatula, (i) eggs from inside of female abdomen.
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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.
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