Methyl 3 indoleglyoxylate
. Reactant for preparation of sotrastaurin analogs as protein kinase inhibitors. Reactant for synthesis of GSK-3 inhibitors. Reactant for Diels-Alder cycloaddition. Reactant for preparation of a Janus kinase 3 inhibitor. Reactant for synthesis of cephalandole alkaloids. Reactant for stereoselective preparation of COX-2 inhibitor as anticancer agent. Reactant for synthesis of cycloalkene indole carbazole alkaloids via ring-closing metathesis
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1) Product Images from "IL‐7 induces sCD127 release and mCD127 downregulation in human CD8+ T cells by distinct yet overlapping mechanisms, both of which are impaired in HIV infection"
Article Title: IL‐7 induces sCD127 release and mCD127 downregulation in human CD8+ T cells by distinct yet overlapping mechanisms, both of which are impaired in HIV infection
Journal: European Journal of Immunology
Figure Legend Snippet: IL‐7‐induced downregulation of mCD127 is dependent on JAK and PI3K but not STAT5. CD8 + T cells were magnetically isolated from PBMCs derived from healthy individuals and cultured with or without IL‐7. For some experiments, inhibitors were used as described. Flow cytometry was performed to evaluate expression of CD127. (A) Representative flow cytometry histogram showing the CD127 median fluorescence intensity (MFI) and the percentage of CD127 + cells among unstained cells (light gray), medium control (dark gray), and the IL‐7‐ (10 ng/mL) treated cells (black unfilled). The gating strategy is shown in Supporting Information Fig. S6. (B) Time course of CD127 expression on CD8 + cells with media control (dotted line), 1 ng/mL IL‐7 (gray line), and 10 ng/mL IL‐7 (black line). Significance was calculated between each IL‐7 concentration in relation to the medium control (* p
Techniques Used: Isolation, Derivative Assay, Cell Culture, Flow Cytometry, Expressing, Fluorescence, Concentration Assay
Figure Legend Snippet: IL‐7‐induced sCD127 release from CD8 + T cells involves JAK, STAT5, and PI3K. CD8 + T cells were magnetically isolated from PBMCs derived from healthy individuals and cultured with or without IL‐7. For some experiments, inhibitors were used as described. ELISA assays were performed to evaluate secretion of sCD127. (A) sCD127 release with media alone (dotted line), 1 ng/mL IL‐7 (gray line), and 10 ng/mL IL‐7 (black line) over time. sCD127 release was compared in the different time points between media alone and 1 ng/mL IL‐7 or media alone and 10 ng/mL IL‐7 (two‐way ANOVA with Bonferroni posttest); between 1 ng/mL IL‐7 and 10 ng/mL IL‐7 on each time point (two‐way ANOVA with Bonferroni posttest); and between the time points in the media alone (one‐way ANOVA with Bonferroni post‐test), n = 4. Data are shown as mean ± SEM of four samples from two independent experiments. (B) sCD127 release was normalized to the control values (values obtained in the media alone cell cultures were subtracted) and compared between cells treated with 1 ng/mL IL‐7 (grey line) or 10 ng/mL IL‐7 (black line) over time (two‐way ANOVA with Bonferroni posttest), n = 4. Data are shown as mean ± SEM of four samples from two independent experiments. (C) The impact of JAK inhibitor (10 μM), (D) STAT5 inhibitor (250 μM), and (E) PI3K (25 μM) inhibitor in the IL‐7‐induced sCD127 secretion in 48 h (paired t test), n = 7. Graphs show the distribution of seven samples from four independent experiments. The dotted line represents the limit of detection for this assay (125 pg/mL) (* p
Techniques Used: Isolation, Derivative Assay, Cell Culture, Enzyme-linked Immunosorbent Assay
2) Product Images from "Autocrine Regulation of Pulmonary Inflammation by Effector T-Cell Derived IL-10 during Infection with Respiratory Syncytial Virus"
Article Title: Autocrine Regulation of Pulmonary Inflammation by Effector T-Cell Derived IL-10 during Infection with Respiratory Syncytial Virus
Journal: PLoS Pathogens
Figure Legend Snippet: Autocrine regulation of pulmonary inflammation by effector T cell-derived IL-10 during RSV infection. (A, B). BALB/c mice were infected with RSV. At d7 p.i., Lung CD8 + cells were purified and stimulated as indicated in vitro . (A) CD8 + T cells were stimulated with rIL-10 in the absence or presence of JAK inhibitor. STAT3 phophorylation was determined by ICS. (B) CD8 + T cells were left un-stimulated or stimulated with plate-bound a-CD3 overnight in the absence or presence of rIL-10 or rIL-10 plus α-IL-10R. IFN-γ release to the medium was determined by ELISA. (C – F) IL-10Rα fl/fl mice or CD4-Cre + IL-10Rα fl/fl mice were infected with RSV. (C) The expression of IL-10Rα in lung monocytes, NK cells, CD4 + and CD8 + T cells at d6 post infection was determined by flow cytometry. (D) IFN-γ levels in the BALF were determined by ELISA. P value was determined by unpaired two-tailed Student t test. * indicates P
Techniques Used: Derivative Assay, Infection, Mouse Assay, Purification, In Vitro, Enzyme-linked Immunosorbent Assay, Expressing, Flow Cytometry, Cytometry, Two Tailed Test
3) Product Images from "Oncostatin M decreases interleukin-1 β secretion by human synovial fibroblasts and attenuates an acute inflammatory reaction in vivo"
Article Title: Oncostatin M decreases interleukin-1 β secretion by human synovial fibroblasts and attenuates an acute inflammatory reaction in vivo
Journal: Journal of Cellular and Molecular Medicine
Figure Legend Snippet: Signalling pathways mediating the OSM-effects on the IL-1β, CXCL8, IL-6 and CCL2 expression in stimulated HSFs. (A) HSFs were stimulated or not with a combination of LPS and GM-CSF for 10 min. in the absence or presence of OSM (10 ng/ml) and its neutralizing antibody (10 μg/ml), as indicated, prior to lysis and subsequent immunoblot analysis using primary antibodies raised against phospho-ERK1/2, phospho-STAT-1 (Tyr 701) and total STAT-1 (as a loading control). Immunoblots shown are representative of three independent experiments; bands were quantified by densitometric analysis and results presented as mean ± S.E.M. When indicated, cells were pre-incubated for 15 min. with the MEK inhibitor U0126 (10 μM) or the Jak inhibitor (0.5 μM) before stimulation in the presence of OSM. * P
Techniques Used: Expressing, Lysis, Western Blot, Incubation
4) Product Images from "Glucocorticoids potentiate IL-6-induced SP-B expression in H441 cells by enhancing the JAK-STAT signaling pathway"
Article Title: Glucocorticoids potentiate IL-6-induced SP-B expression in H441 cells by enhancing the JAK-STAT signaling pathway
Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology
Figure Legend Snippet: Effect of a JAK inhibitor on the synergistic effect of glucocorticoids and IL-6 on SP-B mRNA expression. H441 cells were incubated with IL-6 or DXM alone for 48 h or a combination of IL-6 with DXM for 48 h. Subsequent incubation with a JAK inhibitor significantly
Techniques Used: Expressing, Incubation
Figure Legend Snippet: Effect of JAK inhibition on the glucocorticoid effect on IL-6-induced STAT3 phosphorylation. H441 cells were incubated with IL-6 and DXM alone or a combination of IL-6 and DXM. Subsequent incubation with a JAK inhibitor significantly reduced the effect
Techniques Used: Inhibition, Incubation
Article Title: Human foreskin fibroblast produces interleukin-6 to support derivation and self-renewal of mouse embryonic stem cells
Article Snippet: The derivation and culture medium was DMEM (Gibco) with 10% fetal bovine serum, 100 U/ml penicillin, 100 μg/ml streptomycin, 0.1 mM β-mercaptoethanol (Sigma, St. Louis, MO, USA) and 2 mM L -glutamine. .. To determine the effect of the JAK pathway, 10 or 20 μM
Article Title: Apoptosis induced by JAK2 inhibition is mediated by Bim and enhanced by the BH3 mimetic ABT-737 in JAK2 mutant human erythroid cells