staurosporine (Alomone Labs)

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Alomone Labs staurosporine

Application of protein kinase inhibitor <t>staurosporine</t> only inhibits the endocytosis induced by SQP25ms and SQP50ms: (A), Representative examples of Cm recordings obtained in response to the application of APls (i) and SQP50ms (ii) in two independent cells bathed in standard external solution (with addition of DMSO) (Control, black) or in presence of 100 nM staurosporine (red). (B), (C) and (D), The plots represent average values, standard errors and individual measurements (one measurement/cell) of ΔCm endo , endo/exo ratio and τ endo obtained by application of APls, SQP5ms, SQP10ms, SQP25ms and SQP50ms in Control (black) and staurosporine (red). The data were analyzed by Student’s ‘t’ test. *p

Staurosporine, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 21 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 21 article reviews
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staurosporine - by Bioz Stars, 2022-12

93/100 stars

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1) Product Images from "Membrane Retrieval after Immediately Releasable Pool (IRP) Exocytosis is produced by Dynamin-Dependent and Dynamin-Independent Mechanisms"

Article Title: Membrane Retrieval after Immediately Releasable Pool (IRP) Exocytosis is produced by Dynamin-Dependent and Dynamin-Independent Mechanisms

Journal: bioRxiv

doi: 10.1101/2022.08.31.506099

Application of protein kinase inhibitor staurosporine only inhibits the endocytosis induced by SQP25ms and SQP50ms: (A), Representative examples of Cm recordings obtained in response to the application of APls (i) and SQP50ms (ii) in two independent cells bathed in standard external solution (with addition of DMSO) (Control, black) or in presence of 100 nM staurosporine (red). (B), (C) and (D), The plots represent average values, standard errors and individual measurements (one measurement/cell) of ΔCm endo , endo/exo ratio and τ endo obtained by application of APls, SQP5ms, SQP10ms, SQP25ms and SQP50ms in Control (black) and staurosporine (red). The data were analyzed by Student’s ‘t’ test. *p

Figure Legend Snippet: Application of protein kinase inhibitor staurosporine only inhibits the endocytosis induced by SQP25ms and SQP50ms: (A), Representative examples of Cm recordings obtained in response to the application of APls (i) and SQP50ms (ii) in two independent cells bathed in standard external solution (with addition of DMSO) (Control, black) or in presence of 100 nM staurosporine (red). (B), (C) and (D), The plots represent average values, standard errors and individual measurements (one measurement/cell) of ΔCm endo , endo/exo ratio and τ endo obtained by application of APls, SQP5ms, SQP10ms, SQP25ms and SQP50ms in Control (black) and staurosporine (red). The data were analyzed by Student’s ‘t’ test. *p

Techniques Used:

Protein kinase inhibitor staurosporine abolishes the slow component of IRP replenishment. In order to determine the kinetics of IRP replenishment, a pair of 50 ms depolarizations (SQP50ms 1 and SQP50ms 2 , from −80 to +10 mV), with a variable time interval (Δt) between them, was applied in control conditions (A) and in presence of 100 nM staurosporine (B). The scheme of the stimulation protocol is represented at the top left of panel A. (i), I Ca2+ (above) and Cm (below) recordings obtained during a typical experiment when Δt = 5 s was applied. (ii), Relative replenishment of IRP (expressed as averages of ΔCm 2 /ΔCm 1 for every Δt applied) was plotted against the Δt between paired SQP50ms pulses and fitted to a biexponential growing function of the form (A) or (B). The fitting parameters for the control condition (A) were Y 0 =0.32±0.01, A 1 =0.35±0.03, τ 1 =1.14±0.13 s, A 2 =0.33±0.03, and τ 2 =8.57±1.14 s, R 2 > 0.9993; and for staurosporine (B) were Y 0 =0.25±0.03, A=0.73±0.03, and τ=0.72±0.06 s, R 2 > 0.9827. The points represented in the plots are averages of all the measurements obtained in individual cells (one measurement per cell). The number of individual cells measured (between parentheses) were: for (A), 0.2 s (7), 0.4 s (7), 1 s (6), 2 s (6), 3 s (6), 5 s (7), 7 s (8), 10 s (7), 20 s (7) and 40 s (7); and for (B), 0.2 s (11), 0.4 s (11), 1 s (12), 2 s (12), 3 s (11), 5 s (11), 7 s (12), 10 s (10), 20 s (12) and 40 s (9), obtained in 9 independent cell culture preparations. The fittings were performed on average values.

Figure Legend Snippet: Protein kinase inhibitor staurosporine abolishes the slow component of IRP replenishment. In order to determine the kinetics of IRP replenishment, a pair of 50 ms depolarizations (SQP50ms 1 and SQP50ms 2 , from −80 to +10 mV), with a variable time interval (Δt) between them, was applied in control conditions (A) and in presence of 100 nM staurosporine (B). The scheme of the stimulation protocol is represented at the top left of panel A. (i), I Ca2+ (above) and Cm (below) recordings obtained during a typical experiment when Δt = 5 s was applied. (ii), Relative replenishment of IRP (expressed as averages of ΔCm 2 /ΔCm 1 for every Δt applied) was plotted against the Δt between paired SQP50ms pulses and fitted to a biexponential growing function of the form (A) or (B). The fitting parameters for the control condition (A) were Y 0 =0.32±0.01, A 1 =0.35±0.03, τ 1 =1.14±0.13 s, A 2 =0.33±0.03, and τ 2 =8.57±1.14 s, R 2 > 0.9993; and for staurosporine (B) were Y 0 =0.25±0.03, A=0.73±0.03, and τ=0.72±0.06 s, R 2 > 0.9827. The points represented in the plots are averages of all the measurements obtained in individual cells (one measurement per cell). The number of individual cells measured (between parentheses) were: for (A), 0.2 s (7), 0.4 s (7), 1 s (6), 2 s (6), 3 s (6), 5 s (7), 7 s (8), 10 s (7), 20 s (7) and 40 s (7); and for (B), 0.2 s (11), 0.4 s (11), 1 s (12), 2 s (12), 3 s (11), 5 s (11), 7 s (12), 10 s (10), 20 s (12) and 40 s (9), obtained in 9 independent cell culture preparations. The fittings were performed on average values.

Techniques Used: Cell Culture

2) 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

doi: 10.1074/jbc.RA120.014288

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

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

3) Product Images from "Cdk5 and GSK3β inhibit Fast Endophilin-Mediated Endocytosis"

Article Title: Cdk5 and GSK3β inhibit Fast Endophilin-Mediated Endocytosis

Journal: bioRxiv

doi: 10.1101/2020.04.11.036863

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

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

4) 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)

doi:

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

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

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).

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

5) 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

doi: 10.1111/j.1469-7793.2000.t01-2-00391.x

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

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