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Cell Signaling Technology Inc protein kinase b akt
miR-136-3p-induced increase in glucose uptake is independent of changes in canonical GLUT4 signaling pathways. The mRNA expression of GLUT4, TBC1D4, and AMPKα in primary human myotubes (A) transfected with miR-136-3p. Representative immunoblot and quantification of (B) AMPKα, (C) TBC1D4, (D) P-TBC1D4, (E) <t>AKT,</t> and (F) P-AKT in primary human myotubes transfected with miR-136-3p and subsequently incubated under basal or insulin-stimulated (120 nM, 1 h) conditions. Insets show representative Western blot image and total ponceau staining for loading control. Results are expressed as mean ± standard error of the mean. * p < 0.05, ** p < 0.005. AKT = protein kinase B; AMPKα = AMP-activated protein kinase α; GLUT4 = glucose transporter 4; miR = microRNA; NC = negative control; ns = no significance; P-AKT = phosphorylated AKT; P-TBC1D4 = phosphorylated TBC1D4; TBC1D4 = Tre-2/BUB2/CDC16 domain family member 4.
Protein Kinase B Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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miR-136-3p-induced increase in glucose uptake is independent of changes in canonical GLUT4 signaling pathways. The mRNA expression of GLUT4, TBC1D4, and AMPKα in primary human myotubes (A) transfected with miR-136-3p. Representative immunoblot and quantification of (B) AMPKα, (C) TBC1D4, (D) P-TBC1D4, (E) <t>AKT,</t> and (F) P-AKT in primary human myotubes transfected with miR-136-3p and subsequently incubated under basal or insulin-stimulated (120 nM, 1 h) conditions. Insets show representative Western blot image and total ponceau staining for loading control. Results are expressed as mean ± standard error of the mean. * p < 0.05, ** p < 0.005. AKT = protein kinase B; AMPKα = AMP-activated protein kinase α; GLUT4 = glucose transporter 4; miR = microRNA; NC = negative control; ns = no significance; P-AKT = phosphorylated AKT; P-TBC1D4 = phosphorylated TBC1D4; TBC1D4 = Tre-2/BUB2/CDC16 domain family member 4.
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Aktin Chemicals Inc p akt protein levels
miR-136-3p-induced increase in glucose uptake is independent of changes in canonical GLUT4 signaling pathways. The mRNA expression of GLUT4, TBC1D4, and AMPKα in primary human myotubes (A) transfected with miR-136-3p. Representative immunoblot and quantification of (B) AMPKα, (C) TBC1D4, (D) P-TBC1D4, (E) <t>AKT,</t> and (F) P-AKT in primary human myotubes transfected with miR-136-3p and subsequently incubated under basal or insulin-stimulated (120 nM, 1 h) conditions. Insets show representative Western blot image and total ponceau staining for loading control. Results are expressed as mean ± standard error of the mean. * p < 0.05, ** p < 0.005. AKT = protein kinase B; AMPKα = AMP-activated protein kinase α; GLUT4 = glucose transporter 4; miR = microRNA; NC = negative control; ns = no significance; P-AKT = phosphorylated AKT; P-TBC1D4 = phosphorylated TBC1D4; TBC1D4 = Tre-2/BUB2/CDC16 domain family member 4.
P Akt Protein Levels, supplied by Aktin Chemicals Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Novus Biologicals experiment novus biologicals nbp2 34971 mk2206 akt
miR-136-3p-induced increase in glucose uptake is independent of changes in canonical GLUT4 signaling pathways. The mRNA expression of GLUT4, TBC1D4, and AMPKα in primary human myotubes (A) transfected with miR-136-3p. Representative immunoblot and quantification of (B) AMPKα, (C) TBC1D4, (D) P-TBC1D4, (E) <t>AKT,</t> and (F) P-AKT in primary human myotubes transfected with miR-136-3p and subsequently incubated under basal or insulin-stimulated (120 nM, 1 h) conditions. Insets show representative Western blot image and total ponceau staining for loading control. Results are expressed as mean ± standard error of the mean. * p < 0.05, ** p < 0.005. AKT = protein kinase B; AMPKα = AMP-activated protein kinase α; GLUT4 = glucose transporter 4; miR = microRNA; NC = negative control; ns = no significance; P-AKT = phosphorylated AKT; P-TBC1D4 = phosphorylated TBC1D4; TBC1D4 = Tre-2/BUB2/CDC16 domain family member 4.
Experiment Novus Biologicals Nbp2 34971 Mk2206 Akt, supplied by Novus Biologicals, 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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Elabscience Biotechnology akt
(A–H) PNN neuroprotective role in mitigating EBRO-induced alterations in levels of cellular <t>and</t> <t>molecular</t> targets in MS rat model: GDNF (A) , GFRA1 (B) , <t>AKT</t> (C) , ERK1/2 (D) , GSK3-Beta (E) , in brain homogenates, and GDNF, GFRA1, AKT, ERK1/2, GSK3-Beta in CSF levels (F–H) . Statistical analysis was performed using a one-way ANOVA followed by Tukey’s post hoc test to determine significant differences among groups (A–H) . Data were presented as mean ± standard deviation (SD), with statistical significance set at p < 0.01. Each experimental group consisted of eight wistar rats (n = 8). β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50. To identify significant differences between groups, a one-way ANOVA and Tukey’s post hoc test were used for statistical analysis (A–H) . The statistical significance level was set at p < 0.01, and the data were displayed as mean ± standard deviation (SD). There were eight wistar rats (n = 8) in each experimental group. β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50.
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Cell Signaling Technology Inc rac alpha serine threonine protein kinase
(A–H) PNN neuroprotective role in mitigating EBRO-induced alterations in levels of cellular <t>and</t> <t>molecular</t> targets in MS rat model: GDNF (A) , GFRA1 (B) , <t>AKT</t> (C) , ERK1/2 (D) , GSK3-Beta (E) , in brain homogenates, and GDNF, GFRA1, AKT, ERK1/2, GSK3-Beta in CSF levels (F–H) . Statistical analysis was performed using a one-way ANOVA followed by Tukey’s post hoc test to determine significant differences among groups (A–H) . Data were presented as mean ± standard deviation (SD), with statistical significance set at p < 0.01. Each experimental group consisted of eight wistar rats (n = 8). β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50. To identify significant differences between groups, a one-way ANOVA and Tukey’s post hoc test were used for statistical analysis (A–H) . The statistical significance level was set at p < 0.01, and the data were displayed as mean ± standard deviation (SD). There were eight wistar rats (n = 8) in each experimental group. β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50.
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(A–H) PNN neuroprotective role in mitigating EBRO-induced alterations in levels of cellular <t>and</t> <t>molecular</t> targets in MS rat model: GDNF (A) , GFRA1 (B) , <t>AKT</t> (C) , ERK1/2 (D) , GSK3-Beta (E) , in brain homogenates, and GDNF, GFRA1, AKT, ERK1/2, GSK3-Beta in CSF levels (F–H) . Statistical analysis was performed using a one-way ANOVA followed by Tukey’s post hoc test to determine significant differences among groups (A–H) . Data were presented as mean ± standard deviation (SD), with statistical significance set at p < 0.01. Each experimental group consisted of eight wistar rats (n = 8). β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50. To identify significant differences between groups, a one-way ANOVA and Tukey’s post hoc test were used for statistical analysis (A–H) . The statistical significance level was set at p < 0.01, and the data were displayed as mean ± standard deviation (SD). There were eight wistar rats (n = 8) in each experimental group. β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50.
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(A–H) PNN neuroprotective role in mitigating EBRO-induced alterations in levels of cellular <t>and</t> <t>molecular</t> targets in MS rat model: GDNF (A) , GFRA1 (B) , <t>AKT</t> (C) , ERK1/2 (D) , GSK3-Beta (E) , in brain homogenates, and GDNF, GFRA1, AKT, ERK1/2, GSK3-Beta in CSF levels (F–H) . Statistical analysis was performed using a one-way ANOVA followed by Tukey’s post hoc test to determine significant differences among groups (A–H) . Data were presented as mean ± standard deviation (SD), with statistical significance set at p < 0.01. Each experimental group consisted of eight wistar rats (n = 8). β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50. To identify significant differences between groups, a one-way ANOVA and Tukey’s post hoc test were used for statistical analysis (A–H) . The statistical significance level was set at p < 0.01, and the data were displayed as mean ± standard deviation (SD). There were eight wistar rats (n = 8) in each experimental group. β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50.
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(A–H) PNN neuroprotective role in mitigating EBRO-induced alterations in levels of cellular <t>and</t> <t>molecular</t> targets in MS rat model: GDNF (A) , GFRA1 (B) , <t>AKT</t> (C) , ERK1/2 (D) , GSK3-Beta (E) , in brain homogenates, and GDNF, GFRA1, AKT, ERK1/2, GSK3-Beta in CSF levels (F–H) . Statistical analysis was performed using a one-way ANOVA followed by Tukey’s post hoc test to determine significant differences among groups (A–H) . Data were presented as mean ± standard deviation (SD), with statistical significance set at p < 0.01. Each experimental group consisted of eight wistar rats (n = 8). β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50. To identify significant differences between groups, a one-way ANOVA and Tukey’s post hoc test were used for statistical analysis (A–H) . The statistical significance level was set at p < 0.01, and the data were displayed as mean ± standard deviation (SD). There were eight wistar rats (n = 8) in each experimental group. β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50.
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(A–H) PNN neuroprotective role in mitigating EBRO-induced alterations in levels of cellular <t>and</t> <t>molecular</t> targets in MS rat model: GDNF (A) , GFRA1 (B) , <t>AKT</t> (C) , ERK1/2 (D) , GSK3-Beta (E) , in brain homogenates, and GDNF, GFRA1, AKT, ERK1/2, GSK3-Beta in CSF levels (F–H) . Statistical analysis was performed using a one-way ANOVA followed by Tukey’s post hoc test to determine significant differences among groups (A–H) . Data were presented as mean ± standard deviation (SD), with statistical significance set at p < 0.01. Each experimental group consisted of eight wistar rats (n = 8). β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50. To identify significant differences between groups, a one-way ANOVA and Tukey’s post hoc test were used for statistical analysis (A–H) . The statistical significance level was set at p < 0.01, and the data were displayed as mean ± standard deviation (SD). There were eight wistar rats (n = 8) in each experimental group. β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50.
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Image Search Results


miR-136-3p-induced increase in glucose uptake is independent of changes in canonical GLUT4 signaling pathways. The mRNA expression of GLUT4, TBC1D4, and AMPKα in primary human myotubes (A) transfected with miR-136-3p. Representative immunoblot and quantification of (B) AMPKα, (C) TBC1D4, (D) P-TBC1D4, (E) AKT, and (F) P-AKT in primary human myotubes transfected with miR-136-3p and subsequently incubated under basal or insulin-stimulated (120 nM, 1 h) conditions. Insets show representative Western blot image and total ponceau staining for loading control. Results are expressed as mean ± standard error of the mean. * p < 0.05, ** p < 0.005. AKT = protein kinase B; AMPKα = AMP-activated protein kinase α; GLUT4 = glucose transporter 4; miR = microRNA; NC = negative control; ns = no significance; P-AKT = phosphorylated AKT; P-TBC1D4 = phosphorylated TBC1D4; TBC1D4 = Tre-2/BUB2/CDC16 domain family member 4.

Journal: Journal of Sport and Health Science

Article Title: Exercise training-induced extracellular miR-136-3p modulates glucose uptake and myogenesis through targeting of NRDC in human skeletal muscle

doi: 10.1016/j.jshs.2025.101091

Figure Lengend Snippet: miR-136-3p-induced increase in glucose uptake is independent of changes in canonical GLUT4 signaling pathways. The mRNA expression of GLUT4, TBC1D4, and AMPKα in primary human myotubes (A) transfected with miR-136-3p. Representative immunoblot and quantification of (B) AMPKα, (C) TBC1D4, (D) P-TBC1D4, (E) AKT, and (F) P-AKT in primary human myotubes transfected with miR-136-3p and subsequently incubated under basal or insulin-stimulated (120 nM, 1 h) conditions. Insets show representative Western blot image and total ponceau staining for loading control. Results are expressed as mean ± standard error of the mean. * p < 0.05, ** p < 0.005. AKT = protein kinase B; AMPKα = AMP-activated protein kinase α; GLUT4 = glucose transporter 4; miR = microRNA; NC = negative control; ns = no significance; P-AKT = phosphorylated AKT; P-TBC1D4 = phosphorylated TBC1D4; TBC1D4 = Tre-2/BUB2/CDC16 domain family member 4.

Article Snippet: Membranes were incubated with primary antibodies directed to NRDC (sc-137199; Santa Cruz Biotechnology, Dallas, TX, USA), AMP-activated protein kinase α (AMPKα) (#2532; Cell Signaling Technology, Danvers, MA, USA), Akt substrate of 160 kDa (AS160) (#2670; Cell Signaling Technology), phospho-AS160 (#8730; Cell Signaling Technology), protein kinase B (AKT) (#9272; Cell Signaling Technology), phospho-AKT (Ser473) (#9271; Cell Signaling Technology), or puromycin (MABE343; Merck Burlington, MA, USA).

Techniques: Protein-Protein interactions, Expressing, Transfection, Western Blot, Incubation, Staining, Control, Negative Control

(A–H) PNN neuroprotective role in mitigating EBRO-induced alterations in levels of cellular and molecular targets in MS rat model: GDNF (A) , GFRA1 (B) , AKT (C) , ERK1/2 (D) , GSK3-Beta (E) , in brain homogenates, and GDNF, GFRA1, AKT, ERK1/2, GSK3-Beta in CSF levels (F–H) . Statistical analysis was performed using a one-way ANOVA followed by Tukey’s post hoc test to determine significant differences among groups (A–H) . Data were presented as mean ± standard deviation (SD), with statistical significance set at p < 0.01. Each experimental group consisted of eight wistar rats (n = 8). β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50. To identify significant differences between groups, a one-way ANOVA and Tukey’s post hoc test were used for statistical analysis (A–H) . The statistical significance level was set at p < 0.01, and the data were displayed as mean ± standard deviation (SD). There were eight wistar rats (n = 8) in each experimental group. β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50.

Journal: Frontiers in Pharmacology

Article Title: Enhanced therapeutic potential of paeoniflorin and vitamin B12 in intracerebropeduncle ethidium bromide-induced multiple sclerosis-like pathology

doi: 10.3389/fphar.2026.1792674

Figure Lengend Snippet: (A–H) PNN neuroprotective role in mitigating EBRO-induced alterations in levels of cellular and molecular targets in MS rat model: GDNF (A) , GFRA1 (B) , AKT (C) , ERK1/2 (D) , GSK3-Beta (E) , in brain homogenates, and GDNF, GFRA1, AKT, ERK1/2, GSK3-Beta in CSF levels (F–H) . Statistical analysis was performed using a one-way ANOVA followed by Tukey’s post hoc test to determine significant differences among groups (A–H) . Data were presented as mean ± standard deviation (SD), with statistical significance set at p < 0.01. Each experimental group consisted of eight wistar rats (n = 8). β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50. To identify significant differences between groups, a one-way ANOVA and Tukey’s post hoc test were used for statistical analysis (A–H) . The statistical significance level was set at p < 0.01, and the data were displayed as mean ± standard deviation (SD). There were eight wistar rats (n = 8) in each experimental group. β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50.

Article Snippet: The ELISA kits for evaluating cellular and molecular targets included GDNF [E-EL-H1495; Elabscience GFRA1 [PKSH033670; Elabscience]; RET [AN00810P; Elabscience], AKT [E-EL-R0807 98T, Elabscience, Wuhan, China] ( ); ERK1/2 [E-AB-70292; Elabscience] ( ); and GSK3-Beta [KLR0989, KRISHGEN, Maharashtra, India] ( ).

Techniques: Standard Deviation, Control