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6,818 results for “inhibition”
Silencing of TRAF5 enhances necroptosis in hepatocellular carcinoma by inhibiting LTBR-mediated NF-κB signaling
<p>Raw data of the article titled Silencing of TRAF5 enhances necroptosis in hepatocellular carcinoma by inhibiting LTBR-mediated NF-κB signaling</p>
Microbial reductive dechlorination by a commercially-available dechlorinating consortium is not inhibited by perfluoroalkyl acids (PFAAs) at field relevant concentrations
<p>Chlorinated ethene and microbial abundance data for batch reactor and microcosm experiments completed as described in the associated paper: Microbial reductive dechlorination by a commercially-available dechlorinating consortium is not inhibited by perfluoroalkyl acids (PFAAs) at field relevant concentrations</p>
Thiazides attenuate insulin secretion through inhibition of mitochondrial carbonic anhydrase 5b in β-islet cells in mice
<p><span><em><strong>Background</strong></em>:</span><span> Thiazides </span><span>are associated with glucose intolerance and new onset diabetes mellitus. Previous studies demonstrated that thiazides attenuate insulin secretion, but the molecular mechanisms remain elusive. We hypothesized that thiazides attenuate insulin secretion via one of the known molecular thiazide targets</span> <span>in β-cells.</span></p> <p><span><em><strong>Methods</strong></em>:</span><span> We performed static insulin secretion experiments with islets of wild-type, NCC (SLC12A3) and NDCBE (SLC4A8) knock-out (KO) mice and with murine Min6 cells with individual knock-down of carbonic anhydrase (CA) isoforms to identify the molecular target of thiazides in </span><span>β-cells</span><span>. CA5b KO mice were then used to assess the role of the putative thiazide target CA5b in </span><span>β-cell </span><span>function and in mediating thiazide sensitivity<em> in vitro</em> and<em> in vivo</em>.</span></p> <p><span><em><strong>Results</strong></em>:</span><span> Thiazides inhibited glucose- and sulfonylurea-stimulated insulin secretion in islets and Min6 cells at pharmacologically relevant concentrations.</span> <span>Inhibition of insulin secretion by thiazides was CO2/HCO3--dependent, not additive to unselective CA inhibition with acetazolamide and independent of extracellular potassium. In contrast, insulin secretion was unaltered in islets of mice lacking the known molecular thiazide targets NCC or NDCBE. CA expression profiling with subsequent knock-down of individual CA isoforms suggested mitochondrial CA5b as molecular target.</span><span> In support of these findings, thiazides significantly attenuated Krebs cycle anaplerosis through reduction of mitochondrial oxaloacetate synthesis</span><span>. </span><span>CA5b KO mice were resistant to thiazide-induced glucose intolerance, and thiazides did not alter insulin secretion in CA5b KO islets. </span></p> <p><span><em><strong>Conclusions</strong></em>:</span><span> In summary, our study reveals that thiazides attenuate insulin secretion via inhibition of the mitochondrial CA5b isoform in </span><span>β</span><span>-cells.</span></p>
Germline Immunomodulatory Expression Quantitative Trait Loci (ieQTLs) Associated with Immune-Related Toxicity from Checkpoint Inhibition
<p>Robert Ferguson<sup>1,2,3*</sup>, Vylyny Chat<sup>1,2,3*</sup>, Leah Morales<sup>1,2,3</sup>, Danny Simpson<sup>1,2,3</sup>, Kelsey Monson<sup>1,2,3</sup>, Elisheva Cohen<sup>1,2,3</sup>,Sarah Zusin<sup>1,2,3</sup>, Gabriele Madonna<sup>4</sup>, Mariaelena Capone<sup>4</sup>, Ester Simeone<sup>4</sup>, Anna Pavlick<sup>5</sup>, Jason Luke<sup>6,7</sup>, Thomas F Gajewski<sup>8,9,10</sup>, Iman Osman<sup>1,3,11,12</sup>, Paolo Antonio Ascierto<sup>4</sup>, Jeffrey Weber<sup>1,3,11</sup>, Tomas Kirchhoff<sup>1,2,3</sup></p> <p>1Laura and Isaac Perlmutter Cancer Center, New York University Langone Health, New York, NY, USA<br> 2Departments of Population Health and Environmental Medicine, New York University- Grossman School of Medicine, New York, NY, USA<br> 3The Interdisciplinary Melanoma Cooperative Group, New York University-Grossman School of Medicine, New York, NY, USA<br> 4Melanoma Cancer Immunotherapy and Innovative Therapy Unit, Istituto Nazionale Tumori IRCCS Fondazione G. Pascale, Napoli, Italy<br> 5Division of Hematology & Medical Oncology, the Cutaneous Oncology Program, Weill Cornell Medicine and New York-Presbyterian, New York, USA<br> 6Department of Immunology, University of Pittsburgh, Pittsburgh, PA 15213, USA.<br> 7UPMC Hillman Cancer Center, Pittsburgh, PA 15232, USA.<br> 8Department of Pathology, University of Chicago, Chicago, IL, USA.</p> <p>9Section of Hematology/Oncology, Department of Medicine, University of Chicago, Chicago, IL, USA.<br> 10Ben May Department for Cancer Research, University of Chicago, Chicago, IL, USA.<br> 11Department of Medicine, New York University-Grossman School of Medicine, New York, NY, USA<br> 12Ronald O. Perelman Department of Dermatology, New York University-Grossman School of Medicine, New York, NY, USA</p> <p>*These authors contributed equally to the work</p> <p>Corresponding author: Tomas Kirchhoff, PhD</p> <p><strong>ABSTRACT</strong><br> <strong>Background:</strong> Immune-checkpoint inhibition (ICI) has improved clinical outcomes for metastatic melanoma patients, however, 65-80% of patients treated with ICI experience immune-related adverse events (irAEs). Given the plausible link of irAEs with underlying host immunity, we explored if germline genetic variants controlling the expression of 42 immunomodulatory genes<br> were associated with the risk of irAEs in melanoma patients treated with the single-agent anti- CTLA-4 antibody ipilimumab (IPI).<br> <strong>Methods:</strong> We identified 42 immunomodulatory expression quantitative trait loci (ieQTLs) most significantly associated with the expression of 382 immune-related genes. These germline variants were genotyped in IPI-treated melanoma patients, collected as part of a multiinstitutional collaboration. We tested the association of ieQTLs with irAEs in a discovery cohort of 95 patients followed by validation in an additional 97 patients.<br> Results: We found that the alternate allele of rs7036417, a variant linked to increased expression of SYK, was strongly associated with an increased risk of grade 3-4 toxicity (OR= 7.46; 95% CI=2.65-21.03; p=1.43E-04). This variant was not associated with response (OR= 0.90; 95% CI=0.37-2.21; p=0.82).<br> Conclusion: We report that rs7036417 associates with increased risk of severe irAEs, independent of IPI efficacy. SYK plays an important role in B-cell/T-cell expansion and increased pSYK has been reported in patients with autoimmune disease. The association between rs7036417 and IPI irAEs in our data suggests a role of SYK over-expression in irAE development. These findings support the hypothesis that inherited variation in immune-related pathways modulate ICI toxicity and suggest SYK as a possible future target for therapies to reduce irAEs.</p> <p> </p> <p><strong>Keywords:</strong> irAEs; germline variants; immune checkpoint inhibition; melanoma</p> <p><strong>Funding:</strong> This research was funded by the Italian Ministry of Health (IT-MOH) through “Ricerca Corrente”, grants number M2/2 and L2-1.</p> <p> </p> <p> </p> <p> </p> <p> </p> <p> </p>
MD trajectories for "Kinetic barrier to enzyme inhibition is manipulated by dynamical local interactions in E. coli DHFR"
<p>Dihydrofolate reductase (DHFR) is an important drug target and a highly studied model<br> protein for understanding enzyme dynamics. DHFR’s crucial role in folate synthesis renders it<br> an ideal candidate to understand protein function and protein evolution mechanisms. In this<br> study, to understand how a newly proposed DHFR inhibitor, 4’-deoxy methyl trimethoprim<br> (4’-DTMP), alters evolutionary trajectories, we studied interactions that lead to its superior<br> performance over trimethoprim (TMP). To elucidate the inhibition mechanism of 4’-DTMP,<br> we first confirmed, both computationally and experimentally, that the relative binding free<br> energy cost for the mutation of TMP and 4’-DTMP are the same, pointing to the origin of the<br> characteristic differences to be kinetic rather than thermodynamic. We then employed an<br> interaction-based analysis by focusing first on the active site, then on the whole enzyme. We<br> confirmed that the polar modification in 4’-DTMP induces additional local interactions with<br> the enzyme, particularly the M20 loop. These changes are propagated to the whole enzyme as<br> shifts in the hydrogen bond networks. To shed light on the allosteric interactions, we support<br> our analysis with network-based community analysis and show that segmentation of the loop<br> domain of the inhibitor-bound DHFR must be avoided by a successful inhibitor.</p>
Adsorbed polymer conjugates to adaptively inhibit blood coagulation activation by medical membranes
<p>Dataset to the manuscript</p> <p><strong>'Adsorbed polymer conjugates to adaptively inhibit blood coagulation activation by medical membranes'</strong></p> <p>Tina Helmecke, Dominik Hahn, André Ruland, Mikhail V. Tsurkan, Manfred F. Maitz, Carsten Werner</p>
The ribosome-inactivating proteins MAP30 and Momordin inhibit SARS-CoV-2
<p>These data are related to a manuscript submitted to PLOS ONE. The recombinant proteins MAP30 and Momordin, prepared at the National Institute of Arthritis and Musculoskeletal and Skin Diseases, were analyzed for SARS-CoV-2 inhibition using A549-NLRV human lung cell assays performed at Southern Research during the Covid-19 pandemic. All viral inhibition and cell viability values reported can be derived from the raw data provided here. Some data are replicates. File dates correspond to those originally provided by and preserved at Southern Research, Birmingham AL.</p>
Dataset for study of inhibition or activation of yeast and human IRE1 dimers, by Quercetin and Quercitrine.
<p>Docked structures, MD trajectories, BPMD simulation files and video of RNase motion cycles in apo scIre1p dimer. </p>
Fig. 2. Selected 1H–1H in Coumaronochromones, flavanones, and isoflavones from the twigs and leaves of Erythrina subumbrans inhibit PTP1B and nitric oxide production
Fig. 2. Selected 1H–1H COSY (green bold lines) and HMBC (blue arrows) correlations of compounds 1, 2, 4–7, 15, 25, and 26. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
Fig. 5 in Coumaronochromones, flavanones, and isoflavones from the twigs and leaves of Erythrina subumbrans inhibit PTP1B and nitric oxide production
Fig. 5. Experimental ECD spectra of 15a and 15b and calculated ECD spectra for (1′′R,2′′R)-15 and (1′′S,2′′S)-15.
Fig. 8. Ochrathinols A in Ochrathinols A and B, two pairs of sulfur-containing racemates from an Antarctic fungus Aspergillus ochraceopetaliformis SCSIO 05702 inhibit LPS-induced pro-inflammatory cytokines and NO production
Fig. 8. Ochrathinols A (±)-1 compensated the NAD+/NADH ratio induced by LPS. Cells were exposed to 0.1 μg/mL LPS and co-treated with compounds of (±)-1 (10 μM) for 24 h. Intracellular NAD+/NADH ratios were determined by NAD+/NADH assay kit. Data are shown as mean ± SD (n = 3). *P <0.05, ****P <0.001 vs. LPS group, n = 3. P value was assessed by two-tailed Student's t-test.
Fig. 7 in Ochrathinols A and B, two pairs of sulfur-containing racemates from an Antarctic fungus Aspergillus ochraceopetaliformis SCSIO 05702 inhibit LPS-induced pro-inflammatory cytokines and NO production
Fig. 7. Anti-inflammation activity of ochrathinols A and B ((±)-1, (±)-2). Cells were exposed to 0.1 μg/mL LPS and co-treated with compounds of (+)-1, ()-1, (±)-1, (+)-2, ()-2, (±)-2 (10 μM) for 24 h, respectively. (A) (±)-1 reduced the release of LPS-induced IL-6, TNF-α, and MCP-1 in culture medium, n = 3. (B) qPCR analysis of pro-inflammatory cytokines genes (IL-1β, IL-6, TNF-α, and MCP-1) normalized by β-actin, n = 3. All data are presented as the mean ± SD of three independent experiments. ns, P> 0.05, *P <0.05, **P <0.01, ***P <0.005, ****P <0.001 vs. LPS group; #P <0.05, ##P <0.01, ###P <0.005, ####P <0.001 vs. control group, n = 3. P value was assessed by two-tailed Student's t-test.
Fig. 6 in Germacranolide- and guaianolide-type sesquiterpenoids from Achillea alpina L. reduce insulin resistance in palmitic acid-treated HepG2 cells via inhibition of the NLRP3 inflammasome pathway
Fig. 6. The inhibitory effects of 4 on the production of IL-1β and ROS in HepG2-IR cells. The expression levels of IL-1β were measured by ELISA analysis (A), Fluorescence intensity of ROS was recorded by a multimode microplate reader (B). ##P <0.01 vs CON group, *P <0.05, **P <0.01 vs PA treatment group.
Fig. 5 in Germacranolide- and guaianolide-type sesquiterpenoids from Achillea alpina L. reduce insulin resistance in palmitic acid-treated HepG2 cells via inhibition of the NLRP3 inflammasome pathway
Fig. 5. The glucose consumption assay of compounds 4–6, 10 and 11 in different concentrations. The concentrations of these compounds were from 1.56 to 50 μM, ROSI was the positive control. *p <0.05, **p <0.01, compared to the PA treatment group. ##p <0.01, compared to the control (CON) group.
Fig. 7 in Germacranolide- and guaianolide-type sesquiterpenoids from Achillea alpina L. reduce insulin resistance in palmitic acid-treated HepG2 cells via inhibition of the NLRP3 inflammasome pathway
Fig. 7. Inhibitory effects of 4 on the expression of proteins related to NLRP3 inflammasome in PA-induced HepG2-IR cells. Representative protein bands of Western blot (A and B). Densitometric analysis of the Western blot analysis results (C). Glibenclamide (1 μM, Gliben) was a positive control. ##P <0.01 vs CON group, *P <0.05, **P <0.01 vs PA treatment group.
Fig. 7 in Sesquiterpenes from Kadsura coccinea attenuate rheumatoid arthritis-related inflammation by inhibiting the NF-κB and JAK2/STAT3 signal pathways
Fig. 7. Experimental validation of the representative signaling pathways in vitro. Compound 19 inhibited the NF-kB (A) and JAK2/STAT3 (B) signaling pathways in RAW 264.7 cells induced by LPS. #p <0.05 compared with control group. *p <0.05, **p <0.01 compared with model group.
Fig. 6 in Sesquiterpenes from Kadsura coccinea attenuate rheumatoid arthritis-related inflammation by inhibiting the NF-κB and JAK2/STAT3 signal pathways
Fig. 6. (A) The gene ontology (GO) enrichment analysis for potential targets. (B) The KEGG pathway enrichment analysis of potential targets. (C) The drugcompound-target-pathway (D-C-T-P) network established by Cytoscape V 3.6.0. The red node represents K. coccinea, the yellow represents active compounds, the blue nodes represent targets, and the green nodes represent the pathways. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 5 in Sesquiterpenes from Kadsura coccinea attenuate rheumatoid arthritis-related inflammation by inhibiting the NF-κB and JAK2/STAT3 signal pathways
Fig. 5. The networks of sesquiterpenoid compounds of K. coccinea in treating rheumatoid arthritis. (A) The drug-compound-target (D-C-T) network of K. coccinea. The red node represents K. coccinea, the yellow represents active compounds, and the blue nodes represent targets. (B) The protein-protein interaction (PPI) network of protein targets obtained from the STRING database and visualized by Cytoscape V 3.6.0. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 8. Compound 4 inhibited IL-1 in Guaianolides from Artemisia codonocephala suppress interleukine-1β secretion in macrophages
Fig. 8. Compound 4 inhibited IL-1β production in THP-1 macrophages. (A) Immunofluorescence staining of IL-1β was performed. Scale bar = 10 μm. (B) The protein level of IL-1β in the culture medium from THP-1 cells was determined by ELISA. (C) Cleaved IL- 1β, NLRP3 and Caspase 1 in the supernatant or lysates of THP-1 cells were detected by western blotting. GAPDH was used as an internal loading control. (D) Expression of autophagy related proteins were detected by Western blotting. GAPDH was used as an internal loading control. (E) Expression of autophagy related proteins in THP-1 cells treated with or without 10 μM compound 4 and 5 mM 3-MA. GAPDH was used as an internal loading control. (F) mRFP- GFP-LC3 puncta were measured using a confocal microscope. Scale bar = 5 μm. (G) The levels of IL-1β in the culture medium from THP-1 cells treated with or without 10 μM compound 4 and 5 mM 3-MA. Data are expressed as means ± SD (n = 6). ###P <0.001, LPS + ATP vs. control, **P <0.01 and ***P <0.001, 4 vs. LPS + ATP.
Fig. 5 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway
Fig. 5. Nerolidol suppressed the protein and mRNA expression of ATM in rat leiomyoma cells. (A, B) ELT3 cells were treated with nerolidol for 48 h and were then harvested for the western blot analysis of phosphorylated ATM and total ATM (A) and for determining ATM mRNA expression using quantitative RT-PCR (B). GAPDH was used as the loading control. The inserted numbers in (A) represent the relative expression level compared to that of the vehicle control (indicated as 0 μM). (C, D, E, F) ELT3 cells were treated with the indicated concentrations of KU-55933, an ATM inhibitor, for 48 h, following which the cells were harvested for further analysis. (C) The expression levels of p-ATMser1981, total ATM, p-Aktser473, total Akt, CDK4, and CDK6 were determined using western blot analysis. β-Actin was used as the loading control. The inserted numbers in (C) represent the relative expression level compared to that of the vehicle control (indicated as 0 μM). (D, E) Cell cycle analysis was performed after propidium iodide staining and FACS, and the results were analyzed using the FlowJo software (D). The percentages of cells in each cell cycle phase are plotted in (E). (F) Cell proliferation was determined using the MTT assay. DMSO (0.1 %) was used as the vehicle control. The data are presented as relative percentage compared to that of the vehicle control. The p-value was calculated using one-way ANOVA with Tukey's multiple post hoc test for each group. *, p <0.05; **, p <0.01, and ***, p <0.001 compared to the control group.
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Annotated Behaviour and Observability Dataset (ABODe)
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