Staurosporine, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Cdk5 and GSK3β inhibit Fast Endophilin-Mediated Endocytosis"
Article Title: Cdk5 and GSK3β inhibit Fast Endophilin-Mediated Endocytosis
Figure Legend Snippet: Acute inhibition of Cdk5 and GSK3 activates FEME. a , Scoring criteria used in the kinase screen. Representative images of ‘decreased’, ‘normal’ and ‘increased’ FEME in resting human RPE1 cells treated with 10μM dobutamine, 10μM DMSO and 10 nM GDC-0941 (PI3Ki), respectively. Arrowheads point at FEME carriers. ‘Decreased’ FEME was assigned for samples with > 80% reduction in the number of EPAs, in at least 50% of the cells. ‘Increased’ FEME was attributed to samples with > 200% elevation in the number of EPAs, in at least 50% of the cells. The corresponding scoring marks were 0, 1 and 2, respectively. b , Kinase screen using small compound inhibitors. RPE1 cells grown in complete medium were incubated for 10min at 37°C with the following inhibitors: DMSO, (vehicle); dobutamine, 10μM (positive control); Dinaciclib (Cdk1/2/5/9i), 1μM; CHIR-99041 (GSK3i1), 1μM; BIO (GSK3i2), 1μM; Roscovitine (Cdk1/2/5i), 1 m M; PHA-793887 (Cdk2/5/7i), 100nM; VX-745 (p38i), 10μM; JNK-IN-8 (JNKi), 1μM; staurosporine (broad kinases), 1μM; GNE-7915 (LRRK2i), 1μM; GSK2334470 (PDKi), 10μM; PF-4708671 (p70S6Ki), 10μM; AZ191 (DYRKi), 10μM; AZD0530 (SRCi), 1μM; TAK-632 (panRAFi), 10μM; GW 5074 (CRAFi), 1μM; PD0332991 (Cdk4/6i), 1μM; MK2206 (AKTi), 1μM; GDC-0879 (BRAFi), 1μM; CX-4945 (CK2i), 1μM; ZM 447439 (AurA/AurBi), 1μM; RO-3306 (Cdk1i), 100nM; BI 2536 (PLKi), 1μM; PD0325901 (MEKi), 100nM; Genistein (Y-kinases), 1μM; Purvalanol A (Cdk1/2/4i), 100nM; MLR 1023 (LYNi), 1μM; CDK1/2 inhibitor III (Cdk1/2i), 100nM; KT 5720 (PKAi), 100nM; BI-D1870 (p90RSKi), 100nM; PF-4800567 (CK1Ei), 1μM; SCH772984 (ERKi), 100nM; STO609 (CaMKK1/2ii), 100nM; P505-15 (SYKi), 1μM; PND-1186 (FAKi), 100nM; Torin 1 (mTORC1/2i), 10μM and GDC-0941 (PI3Ki), 100nM (negative control). c , Number of FEME carriers (cytoplasmic Endophilin-positive assemblies, EPAs) upon titration of CHIR-99021, BIO, Roscovitine and Dinaciclib. Dobutamine and GDC-0941 were used as positive and negative controls, respectively. d , β1-adrenergic receptor (β1AR) uptake into FEME carriers in RPE1 cells pre-treated with 5μM CHIR-99021 (GSK3i) for 5 min, followed by 10μM dobutamine for 4 min or not (resting). Histograms show the mean ± SEM of the number of FEME carriers (left axis) and the number of FEME carriers positive for β1AR per 100 μm 2 (right axis) ( n =30 cells per condition, from biological triplicates). Arrowheads point at FEME carriers. All experiments were repeated at least three times with similar results. Statistical analysis was performed by one-way ANOVA (b, and c) or two-way ANOVA (d); NS , non significant; *, P
Techniques Used: Inhibition, Incubation, Positive Control, Negative Control, Titration
2) Product Images from "Protein kinase C enhances the rapidly activating delayed rectifier potassium current, IKr, through a reduction in C-type inactivation in guinea-pig ventricular myocytes"
Article Title: Protein kinase C enhances the rapidly activating delayed rectifier potassium current, IKr, through a reduction in C-type inactivation in guinea-pig ventricular myocytes
Journal: The Journal of Physiology
Figure Legend Snippet: The role of protein kinases in the forskolin- and isoprenaline-induced increase in I Kr Aa , effect of 3 μM staurosporine on I Kr tail current amplitude and the effect of forskolin (5 μM) in the continued presence of staurosporine ( n = 4). The protein kinase C inhibitor bisindolylmaleimide I (100 nM) completely inhibited the increase in I Kr induced by forskolin ( Ab ) and isoprenaline ( Ac) . Ad , phorbol dibutyrate (100 nM) increased I Kr tail current amplitude. B , the effect of isoprenaline on I Kr (upper traces) and I Ca (lower traces) in the presence of bisindolylmaleimide I (100 nM). I Kr and I Ca in B were recorded from the same cells and the arrows indicate 100 pA above zero current in the upper figures and zero current in the lower figures. * P
3) Product Images from "Sulfated Glycosphingolipid as Mediator of Phagocytosis: SM4s Enhances Apoptotic Cell Clearance and Modulates Macrophage Activity"
Article Title: Sulfated Glycosphingolipid as Mediator of Phagocytosis: SM4s Enhances Apoptotic Cell Clearance and Modulates Macrophage Activity
Journal: Journal of immunology (Baltimore, Md. : 1950)
Figure Legend Snippet: Comparative analysis of uptake of apoptotic cells from different cell lines, distinct apoptotic inducers, and different apoptotic stages. Late apoptotic C26 cells induced by cycloheximide ( left ), late apoptotic Renca cells induced by staurosporine ( middle ), and early apoptotic C26 cells ( right ) were subjected to flow cytometric analysis for PS exposure on the cell surface and membrane permeability ( upper lane ) and cell size and granularity ( middle lane ). The cells were used in FACS phagocytosis assay as described ( bottom lane ). Data in the graphs are presented as mean ± SEM of three experiments in duplicates. Statistical differences were evaluated by paired t test. *, p
Techniques Used: Flow Cytometry, Permeability, FACS, Phagocytosis Assay
Figure Legend Snippet: C26 and Renca cells demonstrate late apoptotic phenotype after induction with staurosporine and successful SM4s painting after exposure to SM4s. A , C26 cells were incubated with staurosporine (1 µ M) for 24 h. PS exposure and membrane permeability were detected by flow cytometry using FITC-conjugated annexin V and PI, respectively. Annexin V/PI double-positive cells were considered as late apoptotic. B , Electron photomicrograph of apoptotic C26 cell with evident nuclear condensation and fragmentation (Zeiss, ×30000). B and C , Electron photomicrographs of apoptotic C26 cells preincubated with 10 µ M SM4s. Gold particle-conjugated goat anti-mouse Ab (particle size of 6 nm) was used for visualization of the sulfatide (arrows). D–F , Apoptotic C26 cells were prepared as described above, spun down, stained with DRAQ5 (nucleus), and immunostained with anti-O4 and AlexaFluor 488 donkey anti-mouse IgG (H+L) mAbs (SM4s). F , Confocal image of a single cell shows predominant membrane localization of the sulfatide (×5000). Data are presented as merge of green and blue channels. G–L , Apoptotic cells subjected to immunocytochemistry analysis with anti-O4 mAb. Photomicrographs of apoptotic cells treated with sulfatide or vehicle (DMSO). G and J , C26 and Renca control cells (Leica, ×400). H and I , C26 cells treated with 10 µ M SM4s (Leica, ×400 and ×1000, respectively). K , Late apoptotic Renca cells painted with sulfatide (Leica, ×400). L , Binding of SM4s to plasma membrane of late apoptotic (arrows) and early apoptotic (star) Renca cells (Leica, ×400).
Techniques Used: Incubation, Permeability, Flow Cytometry, Cytometry, Staining, Immunocytochemistry, Binding Assay
4) Product Images from "Phosphorylation of a chronic pain mutation in the voltage-gated sodium channel Nav1.7 increases voltage sensitivity"
Article Title: Phosphorylation of a chronic pain mutation in the voltage-gated sodium channel Nav1.7 increases voltage sensitivity
Journal: The Journal of Biological Chemistry
Figure Legend Snippet: The nonspecific kinase inhibitor staurosporine reduces the hyperpolarized shift of the I848T mutation . A , voltage dependence of activation using 500 nM staurosporine, incubated for 20 min. Staurosporine reduces the hyperpolarized shift of the I848T mutation from −9.77 ± 1.45 to −6.67 ± 1.54 mV. B , V 1/2 of channel activation (ANOVA F = 25.67; WT versus I848T p
Techniques Used: Mutagenesis, Activation Assay, Incubation