pgsk3β Search Results


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Becton Dickinson pgsk3 β (y216
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TGR BioSciences reaction buffer for pgsk3β assay tgrgbs10k
Reaction Buffer For Pgsk3β Assay Tgrgbs10k, supplied by TGR BioSciences, 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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ImmunoWay Biotechnology Company rabbit anti-p-gsk-3b (ser9) antibody
Rabbit Anti P Gsk 3b (Ser9) Antibody, supplied by ImmunoWay Biotechnology Company, 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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Signalway Antibody rabbit anti-pgsk3 α/β (tyr279/tyr216)
Rabbit Anti Pgsk3 α/β (Tyr279/Tyr216), supplied by Signalway Antibody, 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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Upstate Biotechnology Inc pgsk3β
Neuronal insulin resistance causes Tau hyperphosphorylation in vivo. (A) Western blot analysis of brain extracts derived from individual randomly fed mice with antibodies against Akt or pAkt (Ser-473). (Lower) The densitometric quantification as mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least eight animals of each genotype is shown (**, P < 0.01 by unpaired Student's t test). (B) Western blot analysis of brain extracts derived from individual randomly fed mice with antibodies against GSK3β or <t>pGSK3β</t> (Ser-9). (Lower) The densitometric quantification as mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least eight animals of each genotype (**, P < 0.01 by unpaired Student's t test). (C) Immunohistochemistry of layer V of the frontal cortex (Left) and the pyramidal cells of the CA1 region of the hippocampus (Right) with antiserum specific for pGSK3β (4′,6-diamidino-2-phenylindole counterstaining). (D) Immunoblotting of protein extracts from whole brain lysates of control and NIRKO mice with the AT180 (paired helical filament-Tau phosphorylated at Thr-231) and AT8 (paired helical filament-Tau phosphorylated at Ser-202) antibodies. Data represent mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least six animals of each genotype (**, P < 0.01 unpaired Student's t test).
Pgsk3β, supplied by Upstate Biotechnology Inc, 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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OSI Pharmaceuticals proteomic biomarker analysis of pgsk-3β
Neuronal insulin resistance causes Tau hyperphosphorylation in vivo. (A) Western blot analysis of brain extracts derived from individual randomly fed mice with antibodies against Akt or pAkt (Ser-473). (Lower) The densitometric quantification as mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least eight animals of each genotype is shown (**, P < 0.01 by unpaired Student's t test). (B) Western blot analysis of brain extracts derived from individual randomly fed mice with antibodies against GSK3β or <t>pGSK3β</t> (Ser-9). (Lower) The densitometric quantification as mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least eight animals of each genotype (**, P < 0.01 by unpaired Student's t test). (C) Immunohistochemistry of layer V of the frontal cortex (Left) and the pyramidal cells of the CA1 region of the hippocampus (Right) with antiserum specific for pGSK3β (4′,6-diamidino-2-phenylindole counterstaining). (D) Immunoblotting of protein extracts from whole brain lysates of control and NIRKO mice with the AT180 (paired helical filament-Tau phosphorylated at Thr-231) and AT8 (paired helical filament-Tau phosphorylated at Ser-202) antibodies. Data represent mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least six animals of each genotype (**, P < 0.01 unpaired Student's t test).
Proteomic Biomarker Analysis Of Pgsk 3β, supplied by OSI Pharmaceuticals, 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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Becton Dickinson anti-pgsk-3β
Neuronal insulin resistance causes Tau hyperphosphorylation in vivo. (A) Western blot analysis of brain extracts derived from individual randomly fed mice with antibodies against Akt or pAkt (Ser-473). (Lower) The densitometric quantification as mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least eight animals of each genotype is shown (**, P < 0.01 by unpaired Student's t test). (B) Western blot analysis of brain extracts derived from individual randomly fed mice with antibodies against GSK3β or <t>pGSK3β</t> (Ser-9). (Lower) The densitometric quantification as mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least eight animals of each genotype (**, P < 0.01 by unpaired Student's t test). (C) Immunohistochemistry of layer V of the frontal cortex (Left) and the pyramidal cells of the CA1 region of the hippocampus (Right) with antiserum specific for pGSK3β (4′,6-diamidino-2-phenylindole counterstaining). (D) Immunoblotting of protein extracts from whole brain lysates of control and NIRKO mice with the AT180 (paired helical filament-Tau phosphorylated at Thr-231) and AT8 (paired helical filament-Tau phosphorylated at Ser-202) antibodies. Data represent mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least six animals of each genotype (**, P < 0.01 unpaired Student's t test).
Anti Pgsk 3β, supplied by Becton Dickinson, 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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Affinity Biosciences pgsk 3β antibody
Effects on the phosphorylation of phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), and glycogen synthase kinase <t>3</t> (GSK 3β). After pretreated with MPTP for seven days, the C57BL/6 mice were administrated with MA or different concentrations of OP for the followed seven days. ( A ): Original bands of pPI3K, PI3K, pAkt, Akt, <t>pGsk</t> 3β, Gsk 3β, and β-actin. ( B ): Quantitative density of pGsk 3β, Gsk 3β, and the ratio of pGsk 3β/Gsk 3β. ( C ): Quantitative density of pPI3K, PI3K, and the ratio of pPI3K/PI3K. ( D ): Quantiative density of pAkt, Akt, and the ratio of pAkt/Akt. ( E ): Examation about whether OP affected GSK-3β (Ser9) phosphorylation. ## p < 0.01 compared with the control group; * p < 0.05 and ** p < 0.01 compared with the MPTP-induced group. Data are represented as mean ± SEM, n = 12 mice in each group.
Pgsk 3β Antibody, supplied by Affinity Biosciences, 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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Signalway Antibody anti-pgsk3β 9336
Effects on the phosphorylation of phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), and glycogen synthase kinase <t>3</t> (GSK 3β). After pretreated with MPTP for seven days, the C57BL/6 mice were administrated with MA or different concentrations of OP for the followed seven days. ( A ): Original bands of pPI3K, PI3K, pAkt, Akt, <t>pGsk</t> 3β, Gsk 3β, and β-actin. ( B ): Quantitative density of pGsk 3β, Gsk 3β, and the ratio of pGsk 3β/Gsk 3β. ( C ): Quantitative density of pPI3K, PI3K, and the ratio of pPI3K/PI3K. ( D ): Quantiative density of pAkt, Akt, and the ratio of pAkt/Akt. ( E ): Examation about whether OP affected GSK-3β (Ser9) phosphorylation. ## p < 0.01 compared with the control group; * p < 0.05 and ** p < 0.01 compared with the MPTP-induced group. Data are represented as mean ± SEM, n = 12 mice in each group.
Anti Pgsk3β 9336, supplied by Signalway Antibody, 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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MyBiosource Biotechnology pgsk3β
Effects on the phosphorylation of phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), and glycogen synthase kinase <t>3</t> (GSK 3β). After pretreated with MPTP for seven days, the C57BL/6 mice were administrated with MA or different concentrations of OP for the followed seven days. ( A ): Original bands of pPI3K, PI3K, pAkt, Akt, <t>pGsk</t> 3β, Gsk 3β, and β-actin. ( B ): Quantitative density of pGsk 3β, Gsk 3β, and the ratio of pGsk 3β/Gsk 3β. ( C ): Quantitative density of pPI3K, PI3K, and the ratio of pPI3K/PI3K. ( D ): Quantiative density of pAkt, Akt, and the ratio of pAkt/Akt. ( E ): Examation about whether OP affected GSK-3β (Ser9) phosphorylation. ## p < 0.01 compared with the control group; * p < 0.05 and ** p < 0.01 compared with the MPTP-induced group. Data are represented as mean ± SEM, n = 12 mice in each group.
Pgsk3β, supplied by MyBiosource Biotechnology, 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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Brickell Biotech pgsk3β s9
Adiponectin (APN) could improve Aβ31‐35‐induced abnormal Bmal1 mRNA/protein expression by inhibiting the activity of GSK3β. (A) Real‐time PCR was used to measure Bmal1 mRNA expression in HT22 cells of the control group, Aβ31‐35 group, and LiCl +Aβ31‐35 group at different time points. (B, C) mRNA levels of Bmal1 at CT12 and CT20 in each group. (D, E) Western blotting analysis showing the protein expression of BMAL1 at CT20. (F) The protein expression of <t>PGSK3β</t> S9 and GSK3β in the control group, Aβ31‐35 group, APN +Aβ31‐35 group and APN alone group was detected by western blotting. (G) Quantitative analysis of the PGSK3β S9 /GSK3β ratio in each group. Data are expressed as the mean ± SEM ( n = 6 per group). * p <0.05 compared to the control group; # p < 0.05 compared to the Aβ31‐35 group
Pgsk3β S9, supplied by Brickell Biotech, 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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Beyotime anti-pgsk3β(ser9) af5830
Adiponectin (APN) could improve Aβ31‐35‐induced abnormal Bmal1 mRNA/protein expression by inhibiting the activity of GSK3β. (A) Real‐time PCR was used to measure Bmal1 mRNA expression in HT22 cells of the control group, Aβ31‐35 group, and LiCl +Aβ31‐35 group at different time points. (B, C) mRNA levels of Bmal1 at CT12 and CT20 in each group. (D, E) Western blotting analysis showing the protein expression of BMAL1 at CT20. (F) The protein expression of <t>PGSK3β</t> S9 and GSK3β in the control group, Aβ31‐35 group, APN +Aβ31‐35 group and APN alone group was detected by western blotting. (G) Quantitative analysis of the PGSK3β S9 /GSK3β ratio in each group. Data are expressed as the mean ± SEM ( n = 6 per group). * p <0.05 compared to the control group; # p < 0.05 compared to the Aβ31‐35 group
Anti Pgsk3β(Ser9) Af5830, supplied by Beyotime, 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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Image Search Results


Neuronal insulin resistance causes Tau hyperphosphorylation in vivo. (A) Western blot analysis of brain extracts derived from individual randomly fed mice with antibodies against Akt or pAkt (Ser-473). (Lower) The densitometric quantification as mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least eight animals of each genotype is shown (**, P < 0.01 by unpaired Student's t test). (B) Western blot analysis of brain extracts derived from individual randomly fed mice with antibodies against GSK3β or pGSK3β (Ser-9). (Lower) The densitometric quantification as mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least eight animals of each genotype (**, P < 0.01 by unpaired Student's t test). (C) Immunohistochemistry of layer V of the frontal cortex (Left) and the pyramidal cells of the CA1 region of the hippocampus (Right) with antiserum specific for pGSK3β (4′,6-diamidino-2-phenylindole counterstaining). (D) Immunoblotting of protein extracts from whole brain lysates of control and NIRKO mice with the AT180 (paired helical filament-Tau phosphorylated at Thr-231) and AT8 (paired helical filament-Tau phosphorylated at Ser-202) antibodies. Data represent mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least six animals of each genotype (**, P < 0.01 unpaired Student's t test).

Journal:

Article Title: Role for neuronal insulin resistance in neurodegenerative diseases

doi: 10.1073/pnas.0308724101

Figure Lengend Snippet: Neuronal insulin resistance causes Tau hyperphosphorylation in vivo. (A) Western blot analysis of brain extracts derived from individual randomly fed mice with antibodies against Akt or pAkt (Ser-473). (Lower) The densitometric quantification as mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least eight animals of each genotype is shown (**, P < 0.01 by unpaired Student's t test). (B) Western blot analysis of brain extracts derived from individual randomly fed mice with antibodies against GSK3β or pGSK3β (Ser-9). (Lower) The densitometric quantification as mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least eight animals of each genotype (**, P < 0.01 by unpaired Student's t test). (C) Immunohistochemistry of layer V of the frontal cortex (Left) and the pyramidal cells of the CA1 region of the hippocampus (Right) with antiserum specific for pGSK3β (4′,6-diamidino-2-phenylindole counterstaining). (D) Immunoblotting of protein extracts from whole brain lysates of control and NIRKO mice with the AT180 (paired helical filament-Tau phosphorylated at Thr-231) and AT8 (paired helical filament-Tau phosphorylated at Ser-202) antibodies. Data represent mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least six animals of each genotype (**, P < 0.01 unpaired Student's t test).

Article Snippet: Primary antibodies against the IR β-subunit, insulin-like growth factor (IGF)-IR β-subunit, and Tau (Santa Cruz Biotechnology); Akt, pAkt, glycogen synthase kinase (GSK)3β, and pGSK3β (Upstate Biotechnology, Lake Placid, NY); and AT8 and AT180 (Innogenetic, Ghent, Belgium) were used.

Techniques: In Vivo, Western Blot, Derivative Assay, Immunohistochemistry

Effects on the phosphorylation of phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), and glycogen synthase kinase 3 (GSK 3β). After pretreated with MPTP for seven days, the C57BL/6 mice were administrated with MA or different concentrations of OP for the followed seven days. ( A ): Original bands of pPI3K, PI3K, pAkt, Akt, pGsk 3β, Gsk 3β, and β-actin. ( B ): Quantitative density of pGsk 3β, Gsk 3β, and the ratio of pGsk 3β/Gsk 3β. ( C ): Quantitative density of pPI3K, PI3K, and the ratio of pPI3K/PI3K. ( D ): Quantiative density of pAkt, Akt, and the ratio of pAkt/Akt. ( E ): Examation about whether OP affected GSK-3β (Ser9) phosphorylation. ## p < 0.01 compared with the control group; * p < 0.05 and ** p < 0.01 compared with the MPTP-induced group. Data are represented as mean ± SEM, n = 12 mice in each group.

Journal: Marine Drugs

Article Title: Oligo-Porphyran Ameliorates Neurobehavioral Deficits in Parkinsonian Mice by Regulating the PI3K/Akt/Bcl-2 Pathway

doi: 10.3390/md16030082

Figure Lengend Snippet: Effects on the phosphorylation of phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), and glycogen synthase kinase 3 (GSK 3β). After pretreated with MPTP for seven days, the C57BL/6 mice were administrated with MA or different concentrations of OP for the followed seven days. ( A ): Original bands of pPI3K, PI3K, pAkt, Akt, pGsk 3β, Gsk 3β, and β-actin. ( B ): Quantitative density of pGsk 3β, Gsk 3β, and the ratio of pGsk 3β/Gsk 3β. ( C ): Quantitative density of pPI3K, PI3K, and the ratio of pPI3K/PI3K. ( D ): Quantiative density of pAkt, Akt, and the ratio of pAkt/Akt. ( E ): Examation about whether OP affected GSK-3β (Ser9) phosphorylation. ## p < 0.01 compared with the control group; * p < 0.05 and ** p < 0.01 compared with the MPTP-induced group. Data are represented as mean ± SEM, n = 12 mice in each group.

Article Snippet: pGSK 3β , Rabbit , WB/IHC , Affinity Biosciences , 1:1000.

Techniques: Phospho-proteomics, Control

Antibody information.

Journal: Marine Drugs

Article Title: Oligo-Porphyran Ameliorates Neurobehavioral Deficits in Parkinsonian Mice by Regulating the PI3K/Akt/Bcl-2 Pathway

doi: 10.3390/md16030082

Figure Lengend Snippet: Antibody information.

Article Snippet: pGSK 3β , Rabbit , WB/IHC , Affinity Biosciences , 1:1000.

Techniques:

Adiponectin (APN) could improve Aβ31‐35‐induced abnormal Bmal1 mRNA/protein expression by inhibiting the activity of GSK3β. (A) Real‐time PCR was used to measure Bmal1 mRNA expression in HT22 cells of the control group, Aβ31‐35 group, and LiCl +Aβ31‐35 group at different time points. (B, C) mRNA levels of Bmal1 at CT12 and CT20 in each group. (D, E) Western blotting analysis showing the protein expression of BMAL1 at CT20. (F) The protein expression of PGSK3β S9 and GSK3β in the control group, Aβ31‐35 group, APN +Aβ31‐35 group and APN alone group was detected by western blotting. (G) Quantitative analysis of the PGSK3β S9 /GSK3β ratio in each group. Data are expressed as the mean ± SEM ( n = 6 per group). * p <0.05 compared to the control group; # p < 0.05 compared to the Aβ31‐35 group

Journal: Journal of Cellular and Molecular Medicine

Article Title: Adiponectin improves amyloid‐β 31‐35‐induced circadian rhythm disorder in mice

doi: 10.1111/jcmm.16932

Figure Lengend Snippet: Adiponectin (APN) could improve Aβ31‐35‐induced abnormal Bmal1 mRNA/protein expression by inhibiting the activity of GSK3β. (A) Real‐time PCR was used to measure Bmal1 mRNA expression in HT22 cells of the control group, Aβ31‐35 group, and LiCl +Aβ31‐35 group at different time points. (B, C) mRNA levels of Bmal1 at CT12 and CT20 in each group. (D, E) Western blotting analysis showing the protein expression of BMAL1 at CT20. (F) The protein expression of PGSK3β S9 and GSK3β in the control group, Aβ31‐35 group, APN +Aβ31‐35 group and APN alone group was detected by western blotting. (G) Quantitative analysis of the PGSK3β S9 /GSK3β ratio in each group. Data are expressed as the mean ± SEM ( n = 6 per group). * p <0.05 compared to the control group; # p < 0.05 compared to the Aβ31‐35 group

Article Snippet: The membrane was blocked with 5% skimmed milk at room temperature for 2 h and then incubated with primary antibodies against BMAL1 (Abcam), pGSK3β S9 (BBI), GSK3β (BBI), β‐actin and GAPDH overnight at 4°C.

Techniques: Expressing, Activity Assay, Real-time Polymerase Chain Reaction, Western Blot