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6,818 results for “inhibition”
Benzalkonium Chloride Disinfectants Induce Apoptosis, Inhibit Proliferation, and Activate the Integrated Stress Response in a 3-D in Vitro Model of Neurodevelopment
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Data from: Spatial structure maintains diversity of pyocin inhibition in household Pseudomonas aeruginosa
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Data from: The enemy within: how does a bacterium inhibit the foraging aptitude and risk management behavior of Allenby’s gerbils?
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Data for: Screening of stapled peptides for inhibition of calcium-triggered exocytosis
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The ribosome-inactivating proteins MAP30 and Momordin inhibit SARS-CoV-2
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Data from: Foliar fungal pathogen inhibition increases ecosystem carbon sequestration independently of nitrogen enrichment in a Tibetan alpine meadow
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Assessing the impact of product inhibition in a chromogenic assay
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Early noninvasive metabolic biomarkers of mutant IDH inhibition in glioma
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Peptidomimetics-based identification of FDA approved compounds inhibiting IRE1 activity: Simulation Data
<p>Protocols and data sets for docking and MD simulations of Methotrexate, Cefoperazone, Folinic acd and Folic acid interaction with IRE1. All docking data based on Glide (Schrödinger), and all MD simulations are based on the Gromacs software. 2D interaction maps from the initial docking of the four molecules to the four Lysine sites, and from snapshots every 100 ns of the 500 ns MD simulations of the molecules interacting with Lys599 (kinase site) and Lys907 (RNase site). 2D interaction maps produced using Schrödinger. </p>
LTP of inhibition at PV interneuron output synapses requires developmental BMP signaling
<p>This dataset represents the raw data that gave rise to the study by Vickers et al., 2020 in Scientific Reports (<a href="https://doi.org/10.1038/s41598-020-66862-5">DOI: 10.1038/s41598-020-66862-5</a>). Please refer to the original publication regarding experimental design and methodological details of data acquisition and analysis. Below we supply information on the provided metadata files (which, in turn, refer to individual raw data files), and essential details on the specific data formats:</p> <ol> <li>raw data is organized in the datasets related to Figs. 1, 2, 3, 4-E, 4F-H of the paper (Vickers et al., 2020);</li> <li>the metadata for each individual dataset, listing individual data filenames from the respective dataset, are stored in separate “.csv” files, one per each dataset. Field separator: comma;</li> <li>individual metadata files for each dataset are described in the master metadata file “metadata_master.csv”;</li> <li>patch clamp recordings (Figs. 1-3, 4F-H) are provided as “.dat” files, unmodified from the original version created by the acquisition software PatchMaster (HEKA Elektronik, Germany). Besides original PatchMaster software, these files can be imported using one of the following methods: I) via Igor Pro extension bpc_ReadHeka.xop (for 32-bit Igor Pro versions 5.xx - 6.37) by Holger Taschenberger (<a href="https://www.wavemetrics.com/project/bpc_ReadHeka">https://www.wavemetrics.com/project/bpc_ReadHeka</a>); II) via Python script by Luke Campagnola (<a href="https://github.com/campagnola/heka_reader">https://github.com/campagnola/heka_reader</a>); III) via Matlab script HEKA PatchMaster Importer by Christian Keine (<a href="https://github.com/ChristianKeine/HEKA_Patchmaster_Importer">https://github.com/ChristianKeine/HEKA_Patchmaster_Importer</a>);</li> <li>exact names of patch-clamp traces used for each Figure are provided in the corresponding “.csv” metadata files. Traces names are given in the format: ExperimentName_1_SeriesNumber_SweepNumber_ChannelNumber. When “*” is used, it means that every sweep of corresponding series was used for analysis (e.g. Nov0317_1_13_*_2 all sweeps from series number 13 were used). Description in the metadata files also specifies which series correspond to which experimental epoch (baseline or plasticity testing), and to pharmacological manipulations, if applicable;</li> <li>widefield fluorescent images of coronal brain slices, cropped images of subregions in the primary auditory cortex used for quantification, and confocal Z-stacks zooming onto single nuclei of neurons stained for FISH experiments (Fig. 4A-E) were converted into composite TIFF format from the proprietary formats of Axioscan Z1 slide scanning microscope and LSM700 confocal microscope (Carl Zeiss). TIFF format is readable by FIJI/ImageJ (<a href="https://fiji.sc/">https://fiji.sc/</a> or <a href="https://imagej.net/Fiji/Downloads">https://imagej.net/Fiji/Downloads</a>). Pixel resolution and voxel sizes are embedded in these TIFF files. Assignment of the color channels for each image is described in the metadata file.</li> </ol>
Evaluating the inhibition of ALK2 phosphorylation of SMAD1/5 by M4K lead compounds in DIPG patient-derived cells (SU-DIPG-IV, HSJD-DIPG-007, HSJD-DIPG-018 and SU-DIPG-XXI)
<p>The binding potency of M4K compounds to ALK2 has been assayed in biochemical assay and cellular assays in HEK293 or C2C12 myoblast cell lines. However, the potency of ALK2 inhibition by M4K compounds has not determined directly in DIPG patient-derived cell lines. While no major deviation from existing assay data is expected, direct experimental evidence is essential.</p> <p>DIPG cells will be trypsinized and resuspended in TSM-base medium without any growth factor for one-hour starvation. Subsequently, equal volume of TSM-base with 2X Activin A (200ng/mL) and M4K compounds or DMSO vehicle control will be added. After one-hour treatment, the cells will be pelleted and lysed in buffer with protease and phosphatase inhibitors for Western Blot analysis.</p> <p>For other related studies, please refer to my opennotebook blog.</p> <p><a href="https://openlabnotebooks.org/evaluating-the-inhibition-of-alk2-phosphorylation-of-smad1-5-by-m4k-lead-compounds-in-dipg-patient-derived-cells-su-dipg-iv-hsjd-dipg-007-hsjd-dipg-018-and-su-dipg-xxi/">https://openlabnotebooks.org/evaluating-the-inhibition-of-alk2-phosphorylation-of-smad1-5-by-m4k-lead-compounds-in-dipg-patient-derived-cells-su-dipg-iv-hsjd-dipg-007-hsjd-dipg-018-and-su-dipg-xxi/</a></p>
Identification of seminal proteins related to the inhibition of mate searching in female crickets
<p>In response to the reduction in fitness associated with sperm competition, males are expected to evolve tactics that hinder female remating. For example, females often display a post-mating reduction in their sexual receptivity that has been shown to be mediated by proteins contained in a male's seminal fluid (sfps). However, although there has been comprehensive research on sfps in genetically well characterized species, few non-model species have been studied in such detail. We initially confirm that female Australian field crickets, <i>Teleogryllus oceanicus</i>, do display a significant reduction in their mate searching behavior 24 hours after mating. This effect was still apparent three days after mating but was entirely absent after one week. We then attempted to identify the sfps that might play a role in inducing this behavioral response. We identified two proteins, ToSfp022 and ToSfp011, that were associated with the alteration in female post-mating behavior. The knockdown of both proteins resulted in mated females that displayed a significant increase in their mate searching behaviors compared with females mated to males having the full compliment of seminal fluid proteins in their ejaculate. Our results indicate that the female refractory period in <i>T. oceanicus</i> likely reflects a sperm competition avoidance tactic by males, achieved through the action of male seminal fluid proteins.</p>
Data from: Down-regulation of CXCL12/CXCR4 expression alleviates ischemia-reperfusion-induced inflammatory pain via inhibiting glial TLR4 activation in the spinal cord
Toll-like receptor 4 (TLR4) is important for the pathogenesis of inflammatory reactions and the promotion of pain processing after ischemia/reperfusion (IR) in spinal cord. Recently, C-X-C chemokine ligand 12 (CXCL12) and its receptor, C-X-C chemokine receptor 4 (CXCR4), were demonstrated to be simultaneously critical for inflammatory reactions, thereby facilitating glial activation. However, whether CXCL12/CXCR4 expression can contribute to IR-induced inflammatory pain via spinal TLR4 remained unclear. A rat model was established by 8 min of aortic arch occlusion. The effects of CXCL12/CXCR4 expression and TLR4 activation on inflammatory hyperalgesia were investigated by pretreatments with CXCL12-neutralizing antibody, CXCR4 antagonist (AMD3100) and TLR4 antagonist (TAK-242) for 5 consecutive days before surgery. The results indicated that IR induced significant and sustained inflammatory pain, observed as decreases in paw withdrawal threshold (PWT) and paw withdrawal latency (PWL), throughout the post-injury period. The increased levels of TLR4 and proinflammatory chemokine CXCL12, as well as its receptor, CXCR4, were closely correlated with the PWT and PWL trends. Double immunostaining further suggested that TLR4, which is mainly expressed on astrocytes and microglia, was closely co-localized with CXCL12 and CXCR4 in spinal dorsal horn. As expected, intrathecal pretreatment with the TLR4 antagonist, TAK-242 markedly ameliorated pain by inhibiting astrocytic and microglial activation, as shown by decreases in TLR4 immunoreactivity and the percentage of double-labeled cells. These protective effects were likely due in part to the reduced production of the downstream cytokines IL-1β and TNF-α, as well as for the recruitment of CXCL12 and CXCR4. Additionally, intrathecal pretreatment with CXCL12-neutralizing antibody and AMD3100 resulted in similar analgesic and anti-inflammatory effects as those receiving TAK-242 pretreatment. These results suggest that intrathecal blockade of CXCL12/CXCR4 expression may attenuate IR-induced pain sensation and the release of inflammatory cytokines by limiting glial TLR4 activation in spinal cord.
Data from: PCB126 inhibits the activation of AMPK-CREB signal transduction required for energy sensing in liver
3,3',4,4',5-pentachlorobiphenyl (PCB126), a dioxin-like PCB, elicits toxicity through a wide array of non-carcinogenic effects, including metabolic syndrome, wasting, and non-alcoholic fatty-liver disease (NAFLD). Previously, we reported decreases in the transcription of several enzymes involved in gluconeogenesis, before the early onset of lipid accumulation. Hence, this study was aimed at understanding the impact of resultant decreases gluconeogenic enzymes on growth, weight and metabolism in the liver, upon extended exposure. Male Sprague-Dawley rats (75-100 g), fed a defined AIN-93G diet, were injected (ip) with single dose of soy oil (5 ml/kg body weight; n=14) or PCB126 (5 µmol/kg; n=15), 28 d, prior euthanasia. A subset of rats from each group were fasted for 12h (vehicle (n=6) and PCB126 (n=4)). Rats only showed significant weight loss between days 14 and 28 (P<0.05) and some mortality (P=0.0413). As in our previous studies, the expression levels of enzymes involved in gluconeogenesis (Pepck-c, G6Pase, Sds, Pc and Ldh-A) and glycogenolysis (Pygl) were strongly downregulated. The decreased expression of these enzymes in PCB126 treated rats after a 12 h fast decreased hepatic glucose production from glycogen and gluconeogenic substrates, exacerbating the hypoglycemia. Additionally, PCB126 caused hepatic steatosis and decreased the expression of the transcription factor Pparα and its targets, necessary for fatty-acid oxidation. The observed metabolic disruption across multiple branches of fasting metabolism resulted from inhibition in the activation of enzyme AMPK and transcription factor CREB signaling, necessary for "sensing" energy-deprivation and the induction of enzymes that respond to the PCB126 triggered fuel crisis in liver.
Data from: Chemogenetic inhibition of the medial prefrontal cortex reverses the effects of REM sleep loss on sucrose consumption
Rapid eye movement (REM) sleep loss is associated with increased consumption of weight-promoting foods. The prefrontal cortex (PFC) is thought to mediate reward anticipation. However, the precise role of the PFC in mediating reward responses to highly palatable foods (HPF) after REM sleep deprivation is unclear. We selectively reduced REM sleep in mice over a 25–48 hr period and chemogenetically inhibited the medial PFC (mPFC) by using an altered glutamate-gated and ivermectin-gated chloride channel that facilitated neuronal inhibition through hyperpolarizing infected neurons. HPF consumption was measured while the mPFC was inactivated and REM sleep loss was induced. We found that REM sleep loss increased HPF consumption compared to control animals. However, mPFC inactivation reversed the effect of REM sleep loss on sucrose consumption without affecting fat consumption. Our findings provide, for the first time, a causal link between REM sleep, mPFC function and HPF consumption.
Data from: Inhibition of Smurf2 translation by miR-322/503 protects from ischemia reperfusion injury by modulating EZH2/Akt/GSK3β signaling
BACKGROUND: myocardial ischemia/reperfusion (I/R) is a common and lethal disease that threatens people's life worldwide. The underlying mechanisms are under intensive study and yet remain unclear. Here, we explored the function of miR-322/503 in myocardial I/R injury. METHODS: We used isolated rat perfused heart as an in vivo model and H9c2 cells subjected with the oxygen and glucose deprivation followed by reperfusion (OGD/R) as in vitro model to study myocardial I/R injury. TTC staining was used to measure the infarct size and TUNEL staining was used to examine apoptosis. qRT-PCR and western blot were used to determine expression levels of miR-322/503, Smurf2, EZH2, p-Akt, p-GSK3β. RESULTS: Overexpression of miR-322/503 decreased infarct size, inhibited cell apoptosis and promoted cell proliferation through up-regulation of p-Akt and p-GSK3β. Thus, the expression of miR-322/503 was reduced during I/R process. On the molecular level, miR-322/503 directly bound Smurf2 mRNA and suppressed its translation. Smurf2 ubiquitinated EZH2 and degraded EZH2 which could activate Akt/GSK3β signaling. CONCLUSIONS: Our study demonstrates that miR-322/503 plays a beneficial role in myocardial I/R injury. By inhibition of Smurf2 translation, miR-322/503 induces EZH2 expression and activates Akt/GSK3β pathway, thereby protecting cells from ischemia reperfusion injury.
Data from: Inhibition of BTK and ITK with ibrutinib is effective in the prevention of chronic graft-versus-host disease in mice
Bruton's Tyrosine Kinase (BTK) and IL-2 Inducible T-cell Kinase (ITK) are enzymes responsible for the phosphorylation and activation of downstream effectors in the B-cell receptor (BCR) signaling and T cell receptor (TCR) signaling pathways, respectively. Ibrutinib is an FDA-approved potent inhibitor of both BTK and ITK that impairs B-cell and T-cell function. CD4 T cells and B cells are essential for the induction of chronic graft-versus-host disease (cGVHD). We evaluated these targets by testing the ability of Ibrutinib to prevent or ameliorate cGVHD, which is one of the major complications for patients undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT). We found that Ibrutinib significantly alleviated cGVHD across four different mouse models, accompanied by increased long-term survival and reduced clinical score. The clinical improvements in Ibrutinib-treated recipients were associated with decreased serum-autoantibodies, costimulatory molecule activation, B-cell proliferation, and glomerulonephritis compared to vehicle controls. Ibrutinib was also able to alleviate the clinical manifestations in acute GVHD (aGVHD), where the recipients were given grafts with or without B cells, suggesting that an inhibitory effect of Ibrutinib on T cells contributes to a reduction in both aGVHD and cGVHD pathogenesis. An effective prophylactic regimen is still lacking to both reduce the incidence and severity of human cGVHD following allo-HSCT. Our study shows that Ibrutinib is an effective prophylaxis against several mouse models of cGVHD with minimal toxicity and could be a promising strategy to combat human cGVHD clinically.
Data from: Life in interstitial space: biocrusts inhibit exotic but not native plant establishment in semi-arid grasslands
1. Exotic plant species commonly exploit disturbances more successfully than native plants. This outcome is widely attributed to the fact that disturbance reduces biotic resistance from native plant competitors. However, biocrusts, communities of mosses, lichens and microorganisms, are a prominent component of semi-arid grasslands occurring in the interstitial spaces between vascular plants. Biocrusts may provide an important source of biotic resistance to invaders, different from native plant competition, but poorly understood. 2. We established a large-scale field experiment to examine how intact versus disturbed biocrusts influenced the emergence and establishment of four native and four exotic plant species in intermountain bunchgrass systems over two years - one wet and one dry. We also conducted a complementary greenhouse experiment to explore how differences in moisture might influence biocrust effects on germination. 3. In the greenhouse, biocrusts inhibited the germination of both native and exotic plants in the high moisture treatment only. In field experiments, biocrusts inhibited the overall emergence of exotic seedlings in the wetter of the two years and inhibited the establishment of exotic seedlings in both years, but they had no overall effect on the emergence or establishment of native seedlings. Our results demonstrate that intact biocrusts in intermountain grasslands can suppress the establishment of some exotic plants, but have much weaker effects on natives. They also suggest that water availability may influence biocrust effects on seed germination. 4. Synthesis. Our results indicate that intact biocrusts may provide an important source of biotic resistance to exotic plant invasions in intermountain grasslands. Furthermore, precipitation inputs may mediate biocrust effects on plant establishment.
Data from: Th2 cytokines inhibit lymphangiogenesis
Lymphangiogenesis is the process by which new lymphatic vessels grow in response to pathologic stimuli such as wound healing, inflammation, and tumor metastasis. It is well-recognized that growth factors and cytokines regulate lymphangiogenesis by promoting or inhibiting lymphatic endothelial cell (LEC) proliferation, migration and differentiation. Our group has shown that the expression of T-helper 2 (Th2) cytokines is markedly increased in lymphedema, and that these cytokines inhibit lymphatic function by increasing fibrosis and promoting changes in the extracellular matrix. However, while the evidence supporting a role for T cells and Th2 cytokines as negative regulators of lymphatic function is clear, the direct effects of Th2 cytokines on isolated LECs remains poorly understood. Using in vitro and in vivo studies, we show that physiologic doses of interleukin-4 (IL-4) and interleukin-13 (IL-13) have profound anti-lymphangiogenic effects and potently impair LEC survival, proliferation, migration, and tubule formation. Inhibition of these cytokines with targeted monoclonal antibodies in the cornea suture model specifically increases inflammatory lymphangiogenesis without concomitant changes in angiogenesis. These findings suggest that manipulation of anti-lymphangiogenic pathways may represent a novel and potent means of improving lymphangiogenesis.
Data from: Genetic loci inherited from hens lacking maternal behaviour both inhibit and paradoxically promote this behaviour
Background: A major step towards the success of chickens as a domesticated species was the separation between maternal care and reproduction. Artificial incubation replaced the natural maternal behaviour of incubation and, thus, in certain breeds, it became possible to breed chickens with persistent egg production and no incubation behaviour; a typical example is the White Leghorn strain. Conversely, some strains, such as the Silkie breed, are prized for their maternal behaviour and their willingness to incubate eggs. This is often colloquially known as broodiness. Results: Using an F2 linkage mapping approach and a cross between White Leghorn and Silkie chicken breeds, we have mapped, for the first time, genetic loci that affect maternal behaviour on chromosomes 1, 5, 8, 13, 18 and 19 and linkage group E22C19W28. Paradoxically, heterozygous and White Leghorn homozygous genotypes were associated with an increased incidence of incubation behaviour, which exceeded that of the Silkie homozygotes for most loci. In such cases, it is likely that the loci involved are associated with increased egg production. Increased egg production increases the probability of incubation behaviour occurring because egg laying must precede incubation. For the loci on chromosomes 8 and 1, alleles from the Silkie breed promote incubation behaviour and influence maternal behaviour (these explain 12 and 26 % of the phenotypic difference between the two founder breeds, respectively). Conclusions: The over-dominant locus on chromosome 5 coincides with the strongest selective sweep reported in chickens and together with the loci on chromosomes 1 and 8, they include genes of the thyrotrophic axis. This suggests that thyroid hormones may play a critical role in the loss of incubation behaviour and the improved egg laying behaviour of the White Leghorn breed. Our findings support the view that loss of maternal incubation behaviour in the White Leghorn breed is the result of selection for fertility and egg laying persistency and against maternal incubation behaviour.
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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.