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α p foxo1 thr24  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc α p foxo1 thr24
    α P Foxo1 Thr24, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1425 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/α p foxo1 thr24/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1425 article reviews
    α p foxo1 thr24 - by Bioz Stars, 2026-06
    96/100 stars

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    PDK1 suppresses <t>FoxO1</t> via activating Akt signaling in the carotid artery of diabetic mice. (A–C) Western blotting analysis of (A) PDK1, (B) FoxO1, <t>p‐FoxO1,</t> (C) Akt, and p‐Akt in carotid arteries from mice. Protein expression was normalized to housekeeping protein GAPDH; the numbers indicate the relative densities of the indicated protein bands normalized to GAPDH. The normalized protein expression data for PDK1, FoxO1, p‐FoxO1, AKT, and p‐AKT in carotid arteries were presented as mean ± SD. * p < 0.05, ** p < 0.01. Con: Control, DM: Diabetic mice, DM + AE: Diabetic mice with exercise.
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    PDK1 suppresses <t>FoxO1</t> via activating Akt signaling in the carotid artery of diabetic mice. (A–C) Western blotting analysis of (A) PDK1, (B) FoxO1, <t>p‐FoxO1,</t> (C) Akt, and p‐Akt in carotid arteries from mice. Protein expression was normalized to housekeeping protein GAPDH; the numbers indicate the relative densities of the indicated protein bands normalized to GAPDH. The normalized protein expression data for PDK1, FoxO1, p‐FoxO1, AKT, and p‐AKT in carotid arteries were presented as mean ± SD. * p < 0.05, ** p < 0.01. Con: Control, DM: Diabetic mice, DM + AE: Diabetic mice with exercise.
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    Cell Signaling Technology Inc p foxo1 ser256
    BCAA increased the p-Akt in DFO-treated myotubes after 45 min of BCAA treatment, but had no statistically significant effects on other signaling molecules at the same time point. Representative blots for quantification of (A) p-Akt (F (3, 8) = 6.166, p = 0.018, η 2 = 0.6981), p-mTOR, p-p70S6K, p-4E-BP1, and p-eEF2, (B) p-AMPK, and p-ACC, and (C) <t>p-FOXO1,</t> and p–NF–κB p65. Protein was extracted at 45 min after BCCA treatment. Data are presented as the mean ± SD (error bars) from three independent experiments (N = 3), and were analyzed using one-way analysis of variance (ANOVA) with eta squared (η 2 ) used to measure effect sizes, followed by a post hoc Tukey–Kramer test. ∗p < 0.05.
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    Cell Signaling Technology Inc phospho jo urn al pr e p roo f foxo1
    BCAA increased the p-Akt in DFO-treated myotubes after 45 min of BCAA treatment, but had no statistically significant effects on other signaling molecules at the same time point. Representative blots for quantification of (A) p-Akt (F (3, 8) = 6.166, p = 0.018, η 2 = 0.6981), p-mTOR, p-p70S6K, p-4E-BP1, and p-eEF2, (B) p-AMPK, and p-ACC, and (C) <t>p-FOXO1,</t> and p–NF–κB p65. Protein was extracted at 45 min after BCCA treatment. Data are presented as the mean ± SD (error bars) from three independent experiments (N = 3), and were analyzed using one-way analysis of variance (ANOVA) with eta squared (η 2 ) used to measure effect sizes, followed by a post hoc Tukey–Kramer test. ∗p < 0.05.
    Phospho Jo Urn Al Pr E P Roo F Foxo1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti p foxo1
    BCAA increased the p-Akt in DFO-treated myotubes after 45 min of BCAA treatment, but had no statistically significant effects on other signaling molecules at the same time point. Representative blots for quantification of (A) p-Akt (F (3, 8) = 6.166, p = 0.018, η 2 = 0.6981), p-mTOR, p-p70S6K, p-4E-BP1, and p-eEF2, (B) p-AMPK, and p-ACC, and (C) <t>p-FOXO1,</t> and p–NF–κB p65. Protein was extracted at 45 min after BCCA treatment. Data are presented as the mean ± SD (error bars) from three independent experiments (N = 3), and were analyzed using one-way analysis of variance (ANOVA) with eta squared (η 2 ) used to measure effect sizes, followed by a post hoc Tukey–Kramer test. ∗p < 0.05.
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    Proteintech p foxo1
    BCAA increased the p-Akt in DFO-treated myotubes after 45 min of BCAA treatment, but had no statistically significant effects on other signaling molecules at the same time point. Representative blots for quantification of (A) p-Akt (F (3, 8) = 6.166, p = 0.018, η 2 = 0.6981), p-mTOR, p-p70S6K, p-4E-BP1, and p-eEF2, (B) p-AMPK, and p-ACC, and (C) <t>p-FOXO1,</t> and p–NF–κB p65. Protein was extracted at 45 min after BCCA treatment. Data are presented as the mean ± SD (error bars) from three independent experiments (N = 3), and were analyzed using one-way analysis of variance (ANOVA) with eta squared (η 2 ) used to measure effect sizes, followed by a post hoc Tukey–Kramer test. ∗p < 0.05.
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    Image Search Results


    PDK1 suppresses FoxO1 via activating Akt signaling in the carotid artery of diabetic mice. (A–C) Western blotting analysis of (A) PDK1, (B) FoxO1, p‐FoxO1, (C) Akt, and p‐Akt in carotid arteries from mice. Protein expression was normalized to housekeeping protein GAPDH; the numbers indicate the relative densities of the indicated protein bands normalized to GAPDH. The normalized protein expression data for PDK1, FoxO1, p‐FoxO1, AKT, and p‐AKT in carotid arteries were presented as mean ± SD. * p < 0.05, ** p < 0.01. Con: Control, DM: Diabetic mice, DM + AE: Diabetic mice with exercise.

    Journal: The FASEB Journal

    Article Title: Aerobic Exercise Ameliorates Adverse Vascular Remodeling in Diabetes via PDK1 / FoxO1 Axis

    doi: 10.1096/fj.202504631R

    Figure Lengend Snippet: PDK1 suppresses FoxO1 via activating Akt signaling in the carotid artery of diabetic mice. (A–C) Western blotting analysis of (A) PDK1, (B) FoxO1, p‐FoxO1, (C) Akt, and p‐Akt in carotid arteries from mice. Protein expression was normalized to housekeeping protein GAPDH; the numbers indicate the relative densities of the indicated protein bands normalized to GAPDH. The normalized protein expression data for PDK1, FoxO1, p‐FoxO1, AKT, and p‐AKT in carotid arteries were presented as mean ± SD. * p < 0.05, ** p < 0.01. Con: Control, DM: Diabetic mice, DM + AE: Diabetic mice with exercise.

    Article Snippet: The primary antibodies used in the experiment included rat anti‐PECAM‐1 (1:2000, B&D), NLRP3 (1:1000, Abclonal), ASC (1:1000, Abclonal), NF‐kB1 (1:1000, Cell Signaling Technology), NF‐kB p65 (1:1000, Abcam), CCR2(1:500, Boster), IL‐18 (1:500, Abclonal), VCAM‐1 (1:2000, Abcam), α‐SMA (1:1000, Cell Signaling Technology), SM‐MHC (1:2000, Abcam), Calponin (1:1000, Abcam), MMP2 (1:500, Abclonal), MMP9 (1:1000, Cell Signaling Technology), PDK1 (1:1000, Abcam), p‐PDK1 (1:1000, Cell Signaling Technology), FoxO1 (1:1000, Sigma‐Aldrich), p‐FoxO1 (1:1000, Cell Signaling Technology), AKT (1:1000, Cell Signaling Technology), p‐AKT (1:1000, Cell Signaling Technology), Caspase‐3 (1:1000, Cell Signaling Technology), Bax (1:1000, Abclonal) and mouse anti‐SMN/Gemin (1:500, Abcam), GAPDH (1:4000, Proteintech).

    Techniques: Western Blot, Expressing, Control

    PDK1 inhibits FoxO1 expression under HG conditions in SV40. (A, B) Western blotting analysis of PDK1 expression from SV40 under high glucose with PS48 (PDK1 activator). Protein expression was normalized to the housekeeping protein GAPDH. (C–G) Western blot analysis of PDK1, FoxO1, p‐FoxO1, and α‐SMA expression from SV40 under HG with/without PS48 or infected with FoxO1‐shRNA. Protein expression was normalized to housekeeping protein GAPDH; the numbers indicate the relative densities of the indicated protein bands normalized to GAPDH. The normalized protein expression data for PDK1, FoxO1, p‐FoxO1, and α‐SMA were presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001. Con: Human aortic smooth muscle cells (SV40) in the culture medium. HG: SV40 in HG medium (30 mM D‐glucose). HG + FoxO1‐shRNA: SV40 in HG medium (with infection of FoxO1‐shRNA). HG + PS48: SV40 in HG medium (with treatment of PS48, 20 μM). HG + FoxO1‐shRNA+ PS48: SV40 in HG medium (with infection of FoxO1‐shRNA and treatment of PS48).

    Journal: The FASEB Journal

    Article Title: Aerobic Exercise Ameliorates Adverse Vascular Remodeling in Diabetes via PDK1 / FoxO1 Axis

    doi: 10.1096/fj.202504631R

    Figure Lengend Snippet: PDK1 inhibits FoxO1 expression under HG conditions in SV40. (A, B) Western blotting analysis of PDK1 expression from SV40 under high glucose with PS48 (PDK1 activator). Protein expression was normalized to the housekeeping protein GAPDH. (C–G) Western blot analysis of PDK1, FoxO1, p‐FoxO1, and α‐SMA expression from SV40 under HG with/without PS48 or infected with FoxO1‐shRNA. Protein expression was normalized to housekeeping protein GAPDH; the numbers indicate the relative densities of the indicated protein bands normalized to GAPDH. The normalized protein expression data for PDK1, FoxO1, p‐FoxO1, and α‐SMA were presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001. Con: Human aortic smooth muscle cells (SV40) in the culture medium. HG: SV40 in HG medium (30 mM D‐glucose). HG + FoxO1‐shRNA: SV40 in HG medium (with infection of FoxO1‐shRNA). HG + PS48: SV40 in HG medium (with treatment of PS48, 20 μM). HG + FoxO1‐shRNA+ PS48: SV40 in HG medium (with infection of FoxO1‐shRNA and treatment of PS48).

    Article Snippet: The primary antibodies used in the experiment included rat anti‐PECAM‐1 (1:2000, B&D), NLRP3 (1:1000, Abclonal), ASC (1:1000, Abclonal), NF‐kB1 (1:1000, Cell Signaling Technology), NF‐kB p65 (1:1000, Abcam), CCR2(1:500, Boster), IL‐18 (1:500, Abclonal), VCAM‐1 (1:2000, Abcam), α‐SMA (1:1000, Cell Signaling Technology), SM‐MHC (1:2000, Abcam), Calponin (1:1000, Abcam), MMP2 (1:500, Abclonal), MMP9 (1:1000, Cell Signaling Technology), PDK1 (1:1000, Abcam), p‐PDK1 (1:1000, Cell Signaling Technology), FoxO1 (1:1000, Sigma‐Aldrich), p‐FoxO1 (1:1000, Cell Signaling Technology), AKT (1:1000, Cell Signaling Technology), p‐AKT (1:1000, Cell Signaling Technology), Caspase‐3 (1:1000, Cell Signaling Technology), Bax (1:1000, Abclonal) and mouse anti‐SMN/Gemin (1:500, Abcam), GAPDH (1:4000, Proteintech).

    Techniques: Expressing, Western Blot, Infection, shRNA

    BCAA increased the p-Akt in DFO-treated myotubes after 45 min of BCAA treatment, but had no statistically significant effects on other signaling molecules at the same time point. Representative blots for quantification of (A) p-Akt (F (3, 8) = 6.166, p = 0.018, η 2 = 0.6981), p-mTOR, p-p70S6K, p-4E-BP1, and p-eEF2, (B) p-AMPK, and p-ACC, and (C) p-FOXO1, and p–NF–κB p65. Protein was extracted at 45 min after BCCA treatment. Data are presented as the mean ± SD (error bars) from three independent experiments (N = 3), and were analyzed using one-way analysis of variance (ANOVA) with eta squared (η 2 ) used to measure effect sizes, followed by a post hoc Tukey–Kramer test. ∗p < 0.05.

    Journal: Biochemistry and Biophysics Reports

    Article Title: Effects of branched-chain amino acids on iron deficiency-induced muscle atrophy

    doi: 10.1016/j.bbrep.2026.102451

    Figure Lengend Snippet: BCAA increased the p-Akt in DFO-treated myotubes after 45 min of BCAA treatment, but had no statistically significant effects on other signaling molecules at the same time point. Representative blots for quantification of (A) p-Akt (F (3, 8) = 6.166, p = 0.018, η 2 = 0.6981), p-mTOR, p-p70S6K, p-4E-BP1, and p-eEF2, (B) p-AMPK, and p-ACC, and (C) p-FOXO1, and p–NF–κB p65. Protein was extracted at 45 min after BCCA treatment. Data are presented as the mean ± SD (error bars) from three independent experiments (N = 3), and were analyzed using one-way analysis of variance (ANOVA) with eta squared (η 2 ) used to measure effect sizes, followed by a post hoc Tukey–Kramer test. ∗p < 0.05.

    Article Snippet: p-FoxO1 (Ser256) , Rabbit , 84192 , 1:1000 , Cell Signaling Technology.

    Techniques: