staurosporine (Alomone Labs)

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Name:

Staurosporine

Description:

Catalog Number:

S-350

Price:

238.0

Category:

Small Molecule

Source:

Streptomyces staurosporeus.

Applications:

Purity:

>98%

Size:

1 Vials containing 50 mcg each

Format:

Lyophilized/solid.

Formula:

C28H26N4O3

Molecular Weight:

466

Molecule Name:

[9S-(9a,10b,11b,13a)]-2,3,10,11,12,13-Hexahydro-10- meth oxy-9-methyl-11-(methylamino)-9,13-epoxy-1H,9H-diindolo [1,2,3- gh:3',2',1'-lm]pyrrolo[3,4-j][1,7]benzodiazonin-1-one.

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Structured Review

Alomone Labs staurosporine

Staurosporine potently inhibits a variety of kinases including PKC IC50 0 7 nM PKA IC50 7 nM and PKG IC50 8 5 nM It also inhibits CaMK IC50 20 nM and MLCK IC50 1 3 nM In addition Staurosporine can act as an agonist promoting neurite outgrowth4 At higher concentrations Staurosporine induces apoptosis
https://www.bioz.com/result/staurosporine/product/Alomone Labs
Average 93 stars, based on 1 article reviews
Price from $9.99 to $1999.99

staurosporine - by Bioz Stars, 2021-09

93/100 stars

Images

1) 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

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

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

Techniques Used:

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)

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

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

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

other:

Article Title: Interferon-γ induces the cell surface exposure of phosphatidylserine by activating the protein MLKL in the absence of caspase-8 activity
Article Snippet: z-VAD-fmk (Peptide Institute), mouse and human IFN-γ (Pepro Tech), mouse TNFα (ProSpec), Staurosporine (Alomone Labs), Necrostatin-1 (Santa Cruz Biotechnology), anti-mouse TNFα antibody (506310, Biolegend), Smac mimetics (A11928, AdooQ Bioscience), and NSA (Toronto Research Chemicals) were used as a pan-caspase inhibitor, necroptosis inducer, necroptosis inducer, apoptosis inducer, RIPK1 inhibitor, TNFα inhibitor, IAP inhibitor, and human MLKL inhibitor, respectively.

Article Title: Cdk5 and GSK3β inhibit Fast Endophilin-Mediated Endocytosis
Article Snippet: Small compound inhibitors and ligands The following small compound inhibitors (amongst the best-reported inhibitors for each kinase , ) were used: AZ191 (called ‘DYRKi’ in this study Cayman 17693), AZD0530 aka Sacratinib (called ‘SRCi’ in this study, Cayman 11497), BI-D1870 (called ‘p90RSKi’ in this study, Cayman 15264), BIO-6-bromoindirubin-3′-oxime, aka BIO (called ‘GSK3i2’ in this study, (Sigma B1686), BI 2536 (called ‘PLKi’ in this study, Selleckchem S1109), CDK1/2 inhibitor III (called ‘Cdk1/2i’ in this study, Merck 217714), CHIR-99041 (called ‘GSK3i1’ in this study, Cayman 13122), Ciliobrevin D (called ‘Ciliobrevin’ in this study, Calbiochem 250401), CX-4945 (called ‘CK2i’ in this study, Cayman 16779), Dinaciclib (called ‘Cdk1/2/5/9i’ in this study, MedChemExpress Hy-10492), Dobutamine (Sigma D0676), GDC-0879 (called ‘BRAFi’ in this study, Tocris 4453), GDC-0941 (called ‘PI3Ki’ in this study, Symansis SYG0941), Genistein (called ‘Y-kinases’ in this study, Calbiochem 245834), GNE-7915 (called ‘LRRK2i’ in this study, MedChemExpress Hy-10328), GSK2334470 (called ‘PDKi’ in this study, Cayman 18095), GW 5074 (called ‘CRAFi’ in this study, Santa Crux sc-200639), JNK-IN-8 (called ‘JNKi’ in this study MedChemExpress Hy-13319), KT 5720 (called ‘PKAi’ in this study Cayman 10011011), MK2206 (called ‘AKTi’ in this study, LKT Laboratories M4000), MLR 1023 (called ‘LYNa’ in this study, Tocris 4582), PD0325901 (called ‘MEKi’ in this study, Tocris 4192), PD0332991 aka Palbociclib (called ‘Cdk4/6i’ in this study, Sigma PZ0199), PF-4708671 (called ‘p70S6Ki’ in this study, MedChemExpress Hy-15773), PF-4800567 (called ‘CK1Ei’ in this study, Cayman 19171), PHA-793887 (called ‘Cdk2/5/7i’ in this study, ApexBio A5459), PND-1186 (called ‘FAKi’ in this study, MedChemExpress Hy-13917), Purvalanol A (called ‘Cdk1/2/4i’ in this study, Santa Cruz sc-224244), P505-15 (called ‘SYKi’ in this study, Adooq Bioscence A11952), Roscovitine (called ‘Cdk1/2/5i in this study, Santa Cruz sc-24002), RO-3306 (called ‘Cdk1i’ in this study, Cayman 15149), SCH772984 (called ‘ERKi’ in this study, Sellekchem S7101), Staurosporine (called ‘broad kinases’ in this study, Alomone Labs AM-2282), STO609 (called ‘CaMKK1/2ii’ in this study, Cayman 15325), TAK-632 (called ‘panRAFi’ in this study, Selleckchem S7291), Torin 1 (called ‘mTORC1i’ in this study, Tocris 4247), VX-745 (called ‘p38i’ in this study, MedChemExpress Hy-10328) and ZM 447439 (called ‘AurA/AurBi’ in this study, Cayman 13601).