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Cell Signaling Technology Inc p gsk3β
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Cell Signaling Technology Inc anti p gsk3β
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Cell Signaling Technology Inc anti phospho synapsin 1 ser9
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Cell Signaling Technology Inc phospho gsk 3β ser9
(A) Schematic overview of the canonical signaling events modulating muscle insulin action and its interaction with mTORC1 signaling. (B to D) Canonical insulin signaling as determined by phosphorylation of Akt2 on Ser473 and Thr308, and phosphorylation of the Akt substrates GSK3β on <t>Ser9</t> and TBC1D4 on Thr 642 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the hyperinsulinemic-euglycemic (HE) clamp. Levels of total Akt2, GSK3β, and TBC1D4 were comparable across groups and unaffected by insulin. (E and F) mTORC1 signaling as determined by phosphorylation of p70 S6 kinase (p70S6K) on Thr389 and S6 on Ser235/236 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the HE clamp. Levels of total p70S6K and S6 were comparable across groups and unaffected by insulin. Linear mixed models were used to estimate within– and between-group differences. Data are presented as observed individual values (with lines connecting individually matched participants) and estimated means ± 95% confidence limits, unless otherwise stated. For m.3243A>G carriers, individual datapoints are color-shaded to indicate muscle mtDNA heteroplasmy (light red = low, dark red = high). *Different from Basal ( P < 0.05). Basal, n = 30; Insulin, n = 27 (13 in m.3243A>G, 14 in Controls). Illustrations in (A) were created with BioRender.com.
Phospho Gsk 3β Ser9, 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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Proteintech gsk3b monoclo nal antibody
(A) Schematic overview of the canonical signaling events modulating muscle insulin action and its interaction with mTORC1 signaling. (B to D) Canonical insulin signaling as determined by phosphorylation of Akt2 on Ser473 and Thr308, and phosphorylation of the Akt substrates GSK3β on <t>Ser9</t> and TBC1D4 on Thr 642 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the hyperinsulinemic-euglycemic (HE) clamp. Levels of total Akt2, GSK3β, and TBC1D4 were comparable across groups and unaffected by insulin. (E and F) mTORC1 signaling as determined by phosphorylation of p70 S6 kinase (p70S6K) on Thr389 and S6 on Ser235/236 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the HE clamp. Levels of total p70S6K and S6 were comparable across groups and unaffected by insulin. Linear mixed models were used to estimate within– and between-group differences. Data are presented as observed individual values (with lines connecting individually matched participants) and estimated means ± 95% confidence limits, unless otherwise stated. For m.3243A>G carriers, individual datapoints are color-shaded to indicate muscle mtDNA heteroplasmy (light red = low, dark red = high). *Different from Basal ( P < 0.05). Basal, n = 30; Insulin, n = 27 (13 in m.3243A>G, 14 in Controls). Illustrations in (A) were created with BioRender.com.
Gsk3b Monoclo Nal Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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R&D Systems anti gsk3 β s9
(A) Schematic overview of the canonical signaling events modulating muscle insulin action and its interaction with mTORC1 signaling. (B to D) Canonical insulin signaling as determined by phosphorylation of Akt2 on Ser473 and Thr308, and phosphorylation of the Akt substrates GSK3β on <t>Ser9</t> and TBC1D4 on Thr 642 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the hyperinsulinemic-euglycemic (HE) clamp. Levels of total Akt2, GSK3β, and TBC1D4 were comparable across groups and unaffected by insulin. (E and F) mTORC1 signaling as determined by phosphorylation of p70 S6 kinase (p70S6K) on Thr389 and S6 on Ser235/236 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the HE clamp. Levels of total p70S6K and S6 were comparable across groups and unaffected by insulin. Linear mixed models were used to estimate within– and between-group differences. Data are presented as observed individual values (with lines connecting individually matched participants) and estimated means ± 95% confidence limits, unless otherwise stated. For m.3243A>G carriers, individual datapoints are color-shaded to indicate muscle mtDNA heteroplasmy (light red = low, dark red = high). *Different from Basal ( P < 0.05). Basal, n = 30; Insulin, n = 27 (13 in m.3243A>G, 14 in Controls). Illustrations in (A) were created with BioRender.com.
Anti Gsk3 β S9, supplied by R&D Systems, 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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Cell Signaling Technology Inc cell signaling rrid ab 331470
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Cell Signaling Rrid Ab 331470, supplied by Cell Signaling Technology Inc, 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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Novus Biologicals rabbit anti synapsin1
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Cell Signaling Technology Inc d85e12 xp rabbit mab pacific blue tm conjugate cst
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Cell Signaling Technology Inc mouse
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Mouse, supplied by Cell Signaling Technology Inc, 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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Cell Signaling Technology Inc pathscan phospho gsk 3b ser9 sandwich elisa kit
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Image Search Results


(A) Schematic overview of the canonical signaling events modulating muscle insulin action and its interaction with mTORC1 signaling. (B to D) Canonical insulin signaling as determined by phosphorylation of Akt2 on Ser473 and Thr308, and phosphorylation of the Akt substrates GSK3β on Ser9 and TBC1D4 on Thr 642 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the hyperinsulinemic-euglycemic (HE) clamp. Levels of total Akt2, GSK3β, and TBC1D4 were comparable across groups and unaffected by insulin. (E and F) mTORC1 signaling as determined by phosphorylation of p70 S6 kinase (p70S6K) on Thr389 and S6 on Ser235/236 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the HE clamp. Levels of total p70S6K and S6 were comparable across groups and unaffected by insulin. Linear mixed models were used to estimate within– and between-group differences. Data are presented as observed individual values (with lines connecting individually matched participants) and estimated means ± 95% confidence limits, unless otherwise stated. For m.3243A>G carriers, individual datapoints are color-shaded to indicate muscle mtDNA heteroplasmy (light red = low, dark red = high). *Different from Basal ( P < 0.05). Basal, n = 30; Insulin, n = 27 (13 in m.3243A>G, 14 in Controls). Illustrations in (A) were created with BioRender.com.

Journal: medRxiv

Article Title: Physiological and molecular characterization of individuals carrying a diabetogenic mtDNA mutation establishes a mitochondrial basis for insulin resistance in humans

doi: 10.64898/2025.12.17.25342274

Figure Lengend Snippet: (A) Schematic overview of the canonical signaling events modulating muscle insulin action and its interaction with mTORC1 signaling. (B to D) Canonical insulin signaling as determined by phosphorylation of Akt2 on Ser473 and Thr308, and phosphorylation of the Akt substrates GSK3β on Ser9 and TBC1D4 on Thr 642 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the hyperinsulinemic-euglycemic (HE) clamp. Levels of total Akt2, GSK3β, and TBC1D4 were comparable across groups and unaffected by insulin. (E and F) mTORC1 signaling as determined by phosphorylation of p70 S6 kinase (p70S6K) on Thr389 and S6 on Ser235/236 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the HE clamp. Levels of total p70S6K and S6 were comparable across groups and unaffected by insulin. Linear mixed models were used to estimate within– and between-group differences. Data are presented as observed individual values (with lines connecting individually matched participants) and estimated means ± 95% confidence limits, unless otherwise stated. For m.3243A>G carriers, individual datapoints are color-shaded to indicate muscle mtDNA heteroplasmy (light red = low, dark red = high). *Different from Basal ( P < 0.05). Basal, n = 30; Insulin, n = 27 (13 in m.3243A>G, 14 in Controls). Illustrations in (A) were created with BioRender.com.

Article Snippet: The following antibodies were used: Phospho-Akt (Thr308) (Cell Signaling, catalog no. 9275); Phospho-Akt (Ser473) (Cell Signaling, catalog no. 9271); Akt2 (Cell Signaling, catalog no. 3063); Phospho-GSK-3β (Ser9) (Cell Signaling, catalog no. 5558); GSK-3β (BD Transduction Laboratories, catalog no. 610202); Phospho-TBC1D4 (Thr642) (Cell Signaling, catalog no. 8881); TBC1D4 (Abcam, catalog no. ab189890); Phospho-p70S6K (Thr389) (Cell Signaling, catalog no. 9205); p70S6K (Cell Signaling, catalog no. 9202); Phospho-S6 (Ser235/236) (Cell Signaling, catalog no. 4858); S6 (Cell Signaling, catalog no. 2217); PRDX2 (Abcam, catalog no. ab109367); PRDX3 (Abcam, catalog no. ab73349).

Techniques: Phospho-proteomics

KEY RESOURCES TABLE

Journal: Molecular cell

Article Title: Condensed-phase signaling can expand kinase specificity and respond to macromolecular crowding

doi: 10.1016/j.molcel.2022.08.016

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: anti-p-P53(S9) , 9288 , Cell signaling; RRID: AB_331470.

Techniques: Virus, Recombinant, Software, Concentration Assay