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protein kinase b akt  (Cell Signaling Technology Inc)


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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 44749 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/protein kinase b akt/product/Cell Signaling Technology Inc
    Average 99 stars, based on 44749 article reviews
    protein kinase b akt - by Bioz Stars, 2026-06
    99/100 stars

    Images

    1) Product Images from "Exercise training-induced extracellular miR-136-3p modulates glucose uptake and myogenesis through targeting of NRDC in human skeletal muscle"

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

    Journal: Journal of Sport and Health Science

    doi: 10.1016/j.jshs.2025.101091

    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.
    Figure Legend 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.

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



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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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    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