gsk3 inhibitor 3 Search Results


gsk3 inhibitor 3  (MedChemExpress)
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NUAK1 regulation of PLK4 is mediated by GSK3β. (A) Quantification of centrosome number by γ‐tubulin IF staining in synchronised Mia PaCa‐2 cells transfected with MYPT1, or non‐targeting (siC), siRNAs. Fifty cells scored per condition per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc t ‐test. (B) Immunoblot of total PLK4 in Mia PaCa‐2 cells transfected with MYPT1, versus non‐targeting (siCtrl), siRNA. Representative of three independent experiments. (C) Immunoblot of Ser9 phospho‐GSK3β in Mia PaCa‐2 cells transfected with NUAK1, versus non‐targeting, siRNA. Representative of three independent experiments. (D) Immunoblot of Ser9 phospho‐GSK3β in Mia PaCa‐2 cells treated with 10 μ m HTH‐01‐015 or DMSO vehicle for 4 h. Representative of three independent experiments. (E) Immunoblot of total PLK4 in Mia PaCa‐2 cells transiently transfected with constitutively active (S9A) or kinase‐dead (K85R) mutant GSK3β expression vector, compared with empty vector (EV). Representative of three independent experiments. (F) Immunoblots for endogenously expressed PLK4, NUAK1, and GSK3β in lysates and anti‐PLK4 immunoprecipitates, or IgG control IPs, of untreated asynchronous Mia PaCa‐2 cells. Representative of two independent experiments. (G) Immunoblot of total PLK4 in Mia PaCA‐2 cells pre‐treated for 1 h with 3 μ m CHIR‐99021 (GSK3i) or DMSO vehicle, followed by 10 μ m HTH‐01‐015 ± 3 μ m CHIR‐99021 for 1 h immediately prior to harvest. Representative of three independent experiments. (H) Quantification of centrosome number by γ‐tubulin IF in mitotic Mia PaCa‐2 cells treated with CHIR‐99021 (GSK3i), HTH‐01‐015 (HTH), both, or vehicle ctrl, from time of release from thymidine block. Cells were fixed for analysis at 10.5 h post‐release. Fifty cells were scored per treatment condition per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc Tukey's test. (I) Quantification of incidence of nuclear aberrations in Mia PaCa‐2 cells treated with CHIR‐99021 (GSK3i), HTH‐01‐015 (HTH), both, or vehicle ctrl, from time of release from thymidine block. HTH‐01‐015 and ctrl values are the same as Fig. as experiment was performed simultaneously. Cells were fixed for analysis at 13 h post‐release. One hundred cells were scored per treatment group per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc Tukey's test. For all panels, P value; ** P < 0.01; *** P < 0.001; **** P < 0.0001.
Gsk3 Inhibitor 3, supplied by MedChemExpress, 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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gsk 3 inhibitor ix  (TargetMol)
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NUAK1 regulation of PLK4 is mediated by GSK3β. (A) Quantification of centrosome number by γ‐tubulin IF staining in synchronised Mia PaCa‐2 cells transfected with MYPT1, or non‐targeting (siC), siRNAs. Fifty cells scored per condition per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc t ‐test. (B) Immunoblot of total PLK4 in Mia PaCa‐2 cells transfected with MYPT1, versus non‐targeting (siCtrl), siRNA. Representative of three independent experiments. (C) Immunoblot of Ser9 phospho‐GSK3β in Mia PaCa‐2 cells transfected with NUAK1, versus non‐targeting, siRNA. Representative of three independent experiments. (D) Immunoblot of Ser9 phospho‐GSK3β in Mia PaCa‐2 cells treated with 10 μ m HTH‐01‐015 or DMSO vehicle for 4 h. Representative of three independent experiments. (E) Immunoblot of total PLK4 in Mia PaCa‐2 cells transiently transfected with constitutively active (S9A) or kinase‐dead (K85R) mutant GSK3β expression vector, compared with empty vector (EV). Representative of three independent experiments. (F) Immunoblots for endogenously expressed PLK4, NUAK1, and GSK3β in lysates and anti‐PLK4 immunoprecipitates, or IgG control IPs, of untreated asynchronous Mia PaCa‐2 cells. Representative of two independent experiments. (G) Immunoblot of total PLK4 in Mia PaCA‐2 cells pre‐treated for 1 h with 3 μ m CHIR‐99021 (GSK3i) or DMSO vehicle, followed by 10 μ m HTH‐01‐015 ± 3 μ m CHIR‐99021 for 1 h immediately prior to harvest. Representative of three independent experiments. (H) Quantification of centrosome number by γ‐tubulin IF in mitotic Mia PaCa‐2 cells treated with CHIR‐99021 (GSK3i), HTH‐01‐015 (HTH), both, or vehicle ctrl, from time of release from thymidine block. Cells were fixed for analysis at 10.5 h post‐release. Fifty cells were scored per treatment condition per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc Tukey's test. (I) Quantification of incidence of nuclear aberrations in Mia PaCa‐2 cells treated with CHIR‐99021 (GSK3i), HTH‐01‐015 (HTH), both, or vehicle ctrl, from time of release from thymidine block. HTH‐01‐015 and ctrl values are the same as Fig. as experiment was performed simultaneously. Cells were fixed for analysis at 13 h post‐release. One hundred cells were scored per treatment group per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc Tukey's test. For all panels, P value; ** P < 0.01; *** P < 0.001; **** P < 0.0001.
Gsk 3 Inhibitor Ix, supplied by TargetMol, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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gsk 3 inhibitor ix  (MedChemExpress)
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NUAK1 regulation of PLK4 is mediated by GSK3β. (A) Quantification of centrosome number by γ‐tubulin IF staining in synchronised Mia PaCa‐2 cells transfected with MYPT1, or non‐targeting (siC), siRNAs. Fifty cells scored per condition per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc t ‐test. (B) Immunoblot of total PLK4 in Mia PaCa‐2 cells transfected with MYPT1, versus non‐targeting (siCtrl), siRNA. Representative of three independent experiments. (C) Immunoblot of Ser9 phospho‐GSK3β in Mia PaCa‐2 cells transfected with NUAK1, versus non‐targeting, siRNA. Representative of three independent experiments. (D) Immunoblot of Ser9 phospho‐GSK3β in Mia PaCa‐2 cells treated with 10 μ m HTH‐01‐015 or DMSO vehicle for 4 h. Representative of three independent experiments. (E) Immunoblot of total PLK4 in Mia PaCa‐2 cells transiently transfected with constitutively active (S9A) or kinase‐dead (K85R) mutant GSK3β expression vector, compared with empty vector (EV). Representative of three independent experiments. (F) Immunoblots for endogenously expressed PLK4, NUAK1, and GSK3β in lysates and anti‐PLK4 immunoprecipitates, or IgG control IPs, of untreated asynchronous Mia PaCa‐2 cells. Representative of two independent experiments. (G) Immunoblot of total PLK4 in Mia PaCA‐2 cells pre‐treated for 1 h with 3 μ m CHIR‐99021 (GSK3i) or DMSO vehicle, followed by 10 μ m HTH‐01‐015 ± 3 μ m CHIR‐99021 for 1 h immediately prior to harvest. Representative of three independent experiments. (H) Quantification of centrosome number by γ‐tubulin IF in mitotic Mia PaCa‐2 cells treated with CHIR‐99021 (GSK3i), HTH‐01‐015 (HTH), both, or vehicle ctrl, from time of release from thymidine block. Cells were fixed for analysis at 10.5 h post‐release. Fifty cells were scored per treatment condition per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc Tukey's test. (I) Quantification of incidence of nuclear aberrations in Mia PaCa‐2 cells treated with CHIR‐99021 (GSK3i), HTH‐01‐015 (HTH), both, or vehicle ctrl, from time of release from thymidine block. HTH‐01‐015 and ctrl values are the same as Fig. as experiment was performed simultaneously. Cells were fixed for analysis at 13 h post‐release. One hundred cells were scored per treatment group per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc Tukey's test. For all panels, P value; ** P < 0.01; *** P < 0.001; **** P < 0.0001.
Gsk 3 Inhibitor Ix, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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NUAK1 regulation of PLK4 is mediated by GSK3β. (A) Quantification of centrosome number by γ‐tubulin IF staining in synchronised Mia PaCa‐2 cells transfected with MYPT1, or non‐targeting (siC), siRNAs. Fifty cells scored per condition per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc t ‐test. (B) Immunoblot of total PLK4 in Mia PaCa‐2 cells transfected with MYPT1, versus non‐targeting (siCtrl), siRNA. Representative of three independent experiments. (C) Immunoblot of Ser9 phospho‐GSK3β in Mia PaCa‐2 cells transfected with NUAK1, versus non‐targeting, siRNA. Representative of three independent experiments. (D) Immunoblot of Ser9 phospho‐GSK3β in Mia PaCa‐2 cells treated with 10 μ m HTH‐01‐015 or DMSO vehicle for 4 h. Representative of three independent experiments. (E) Immunoblot of total PLK4 in Mia PaCa‐2 cells transiently transfected with constitutively active (S9A) or kinase‐dead (K85R) mutant GSK3β expression vector, compared with empty vector (EV). Representative of three independent experiments. (F) Immunoblots for endogenously expressed PLK4, NUAK1, and GSK3β in lysates and anti‐PLK4 immunoprecipitates, or IgG control IPs, of untreated asynchronous Mia PaCa‐2 cells. Representative of two independent experiments. (G) Immunoblot of total PLK4 in Mia PaCA‐2 cells pre‐treated for 1 h with 3 μ m CHIR‐99021 (GSK3i) or DMSO vehicle, followed by 10 μ m HTH‐01‐015 ± 3 μ m CHIR‐99021 for 1 h immediately prior to harvest. Representative of three independent experiments. (H) Quantification of centrosome number by γ‐tubulin IF in mitotic Mia PaCa‐2 cells treated with CHIR‐99021 (GSK3i), HTH‐01‐015 (HTH), both, or vehicle ctrl, from time of release from thymidine block. Cells were fixed for analysis at 10.5 h post‐release. Fifty cells were scored per treatment condition per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc Tukey's test. (I) Quantification of incidence of nuclear aberrations in Mia PaCa‐2 cells treated with CHIR‐99021 (GSK3i), HTH‐01‐015 (HTH), both, or vehicle ctrl, from time of release from thymidine block. HTH‐01‐015 and ctrl values are the same as Fig. as experiment was performed simultaneously. Cells were fixed for analysis at 13 h post‐release. One hundred cells were scored per treatment group per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc Tukey's test. For all panels, P value; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Journal: Molecular Oncology

Article Title: NUAK1 governs centrosome replication in pancreatic cancer via MYPT1 / PP1β and GSK3β ‐dependent regulation of PLK4

doi: 10.1002/1878-0261.13425

Figure Lengend Snippet: NUAK1 regulation of PLK4 is mediated by GSK3β. (A) Quantification of centrosome number by γ‐tubulin IF staining in synchronised Mia PaCa‐2 cells transfected with MYPT1, or non‐targeting (siC), siRNAs. Fifty cells scored per condition per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc t ‐test. (B) Immunoblot of total PLK4 in Mia PaCa‐2 cells transfected with MYPT1, versus non‐targeting (siCtrl), siRNA. Representative of three independent experiments. (C) Immunoblot of Ser9 phospho‐GSK3β in Mia PaCa‐2 cells transfected with NUAK1, versus non‐targeting, siRNA. Representative of three independent experiments. (D) Immunoblot of Ser9 phospho‐GSK3β in Mia PaCa‐2 cells treated with 10 μ m HTH‐01‐015 or DMSO vehicle for 4 h. Representative of three independent experiments. (E) Immunoblot of total PLK4 in Mia PaCa‐2 cells transiently transfected with constitutively active (S9A) or kinase‐dead (K85R) mutant GSK3β expression vector, compared with empty vector (EV). Representative of three independent experiments. (F) Immunoblots for endogenously expressed PLK4, NUAK1, and GSK3β in lysates and anti‐PLK4 immunoprecipitates, or IgG control IPs, of untreated asynchronous Mia PaCa‐2 cells. Representative of two independent experiments. (G) Immunoblot of total PLK4 in Mia PaCA‐2 cells pre‐treated for 1 h with 3 μ m CHIR‐99021 (GSK3i) or DMSO vehicle, followed by 10 μ m HTH‐01‐015 ± 3 μ m CHIR‐99021 for 1 h immediately prior to harvest. Representative of three independent experiments. (H) Quantification of centrosome number by γ‐tubulin IF in mitotic Mia PaCa‐2 cells treated with CHIR‐99021 (GSK3i), HTH‐01‐015 (HTH), both, or vehicle ctrl, from time of release from thymidine block. Cells were fixed for analysis at 10.5 h post‐release. Fifty cells were scored per treatment condition per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc Tukey's test. (I) Quantification of incidence of nuclear aberrations in Mia PaCa‐2 cells treated with CHIR‐99021 (GSK3i), HTH‐01‐015 (HTH), both, or vehicle ctrl, from time of release from thymidine block. HTH‐01‐015 and ctrl values are the same as Fig. as experiment was performed simultaneously. Cells were fixed for analysis at 13 h post‐release. One hundred cells were scored per treatment group per experiment. Mean ± SEM of three independent experiments shown. One‐way ANOVA with post hoc Tukey's test. For all panels, P value; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: Cells in log phase growth were treated with the indicated concentrations of 5 or 10 μ m of NUAK1 inhibitor (HTH‐01‐015, Tocris, Bristol, UK), GSK3 inhibitor 3 μ m – (CHIR99021, Tocris), PLK4 inhibitor 100 n m (Centrinone, MedChem Express, Monmouth Junction, NJ, USA) throughout the study.

Techniques: Staining, Transfection, Western Blot, Mutagenesis, Expressing, Plasmid Preparation, Control, Blocking Assay