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anti phospho-akt (thr308)  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho-akt (thr308)
    Anti Phospho Akt (Thr308), supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 5238 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/thr308/Phospho-Akt+(Thr308)+Antibody/pmc12765182-83-18-33
    Average 96 stars, based on 5238 article reviews
    anti phospho-akt (thr308) - by Bioz Stars, 2026-09
    96/100 stars

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    other:

    Article Title: Metabolic effects of 3-hydroxybutyrate infusion in individuals with type 1 diabetes compared with healthy control participants: a randomised crossover trial showing intact feedback suppression of lipolysis.
    Article Snippet: The following primary antibodies were used: hormone-sensitive lipase phosphorylated at Ser563, Ser565 or Ser660 (pHSL) (4139, 4137 and 4126; Cell Signaling Technology, MA, USA), HSL (PA5-17196; Cell Signaling Technology), phospho-PKA substrate (9624; Cell Signaling Technology), perilipin (PLIN1; 9349; Cell Signaling Technology), Akt phosphorylated at Ser473 or Thr308 (4060 and 9275; Cell Signaling Technology), pan Akt (ma5-14916; Thermo Fisher) and the phosphatase and tensin homologue (PTEN; 9188; Cell Signaling Technology).

    Article Title: Arrestin-3-assisted activation of JNK3 mediates dopaminergic behavioral sensitization
    Article Snippet: Akt phosphorylated at Thr308 was visualized with rabbit anti-Akt(T308) antibody (Cell Signaling, # 9275), phosphorylated at Ser473 - with anti-Akt(S473) rabbit antibody (Cell Signaling, # 4060), and total Akt was detected with a rabbit antibody (Cell Signaling, # 9272), all at 1:1,000 dilution.

    Article Title: Formation of a giant unilocular vacuole via macropinocytosis-like process confers anoikis resistance
    Article Snippet: Antibodies to BCL2 (15,071T), Bim (2933T), phospho- Akt (Ser473, 4060S; Thr308, 13038S), cleaved caspase- 3 (9664S), Na,K- ATPase 1 (3010S), Vinculin (13901S), and VPS34 (4263S) were obtained from Cell Signaling Technology; those to CHC (ab21679), LAMP1 (ab25630), LC3B (ab192890), glyceraldehyde- 3- phosphate dehydrogenase (GAPDH) (ab8245), and GFP (ab13970) were from Abcam; those to dynamin 2 (sc- 166669) and PI3K- C2α (sc- 365290) were from Santa Cruz Biotechnology; those to EEA1 (610457) were from BD Biosciences; those to Transferrin receptor (13- 6800) were from Invitrogen; and those to β-actin (A5316) were from Sigma- Aldrich.

    Article Title: IGF-1 impacts neocortical interneuron connectivity in epileptic spasm generation and resolution
    Article Snippet: Membranes were probed with anti-GAPDH (Millipore, CB1001-500; 1:10,000); rabbit-anti Thr308-phosphorylated-AKT (Cell Signaling, 2965S; 1:1000); and rabbit anti-pan-AKT (Cell Signaling, 4691; 1:1000).

    Article Title: Metabolic effects of 3-hydroxybutyrate infusion in individuals with type 1 diabetes compared with healthy control participants: a randomised crossover trial showing intact feedback suppression of lipolysis
    Article Snippet: The following primary antibodies were used: hormone-sensitive lipase phosphorylated at Ser563, Ser565 or Ser660 (pHSL) (4139, 4137 and 4126; Cell Signaling Technology, MA, USA), HSL (PA5-17196; Cell Signaling Technology), phospho-PKA substrate (9624; Cell Signaling Technology), perilipin (PLIN1; 9349; Cell Signaling Technology), Akt phosphorylated at Ser473 or Thr308 (4060 and 9275; Cell Signaling Technology), pan Akt (ma5-14916; Thermo Fisher) and the phosphatase and tensin homologue (PTEN; 9188; Cell Signaling Technology).

    Article Title: IGF-1 IMPACTS NEOCORTICAL INTERNEURON CONNECTIVITY IN EPILEPTIC SPASM GENERATION AND RESOLUTION
    Article Snippet: Membranes were probed with anti-GAPDH (Millipore, CB1001-500; 1:10,000); rabbit-anti Thr308-phosphorylated-AKT (Cell Signaling, 2965S; 1:1,000); and rabbit anti-pan-AKT (Cell Signaling, 4691; 1:1,000).

    Western Blot:

    Article Title: De Novo Gene Transcription of Connexin Mediates Cytoplasmic Fluid Exchange and Flocking Transitions in Physiological and Cancerous Epithelial Systems
    Article Snippet: AKT , Cell Signaling , , #9272 , WB , 1:1000. .. pAKT , Cell Signaling , Thr308 , #9275 , WB , 1:500. .. STAT3 , Cell Signaling , , 9139 , WB , 1:500.

    Binding Assay:

    Article Title: Anti-oxidative stress and cognitive improvement of a semi-synthetic isoorientin-based GSK-3β inhibitor in rat pheochromocytoma cell PC12 and scopolamine-induced AD model mice via AKT/GSK-3β/Nrf2 pathway.
    Article Snippet: Background.. Alzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive cognitive deficits.. Although the pathogenesis of AD is unclear, oxidative stress has been implicated to play a dominant role in its development.



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    MYCT1 limits endothelial mTORC1 signaling, related to Figs. 3 and 4. (A) Flow cytometry gating strategy (CD45 neg CD31 + ) for sorting of ECs from mesenteric fat for scRNA-seq. (B) Dot plot of markers for the indicated clusters. Color code: scaled average expression level in each cluster; the dot size denotes the percent of cells in each cluster expressing the given gene. (C) Number of differentially expressed genes (DEGs) between wild-type and Myct1 ecKO cell clusters. (D) Volcano plot of DEGs between the wild-type and Myct1 ecKO mice in the BEC cluster. Mat2a gene was selected for scRNA-seq validation. Mat2a, methionine adenosyltransferase 2A. (E) MYCT1 protein levels in human primary ECs. Western blot analysis for the indicated proteins. HPMECs, human pulmonary ECs; HUVECs, human umbilical vein ECs; HIECs, human intestinal ECs. (F and G) MYCT1 antibody and siRNAs validation for identification of endogenous human MYCT1 protein. Human primary ECs were transfected with two different MYCT1 targeting siRNAs. (F) Staining of ECs for MYCT1 (black) and DAPI (blue). Arrow, not transfected EC. Scale bar, 50 μm. (G) Western blot analysis showing MYCT1 migration profile and siRNA specificity. (H) MYCT1 knockdown increases phosphorylation of S6 but does not affect AKT and ERK1/2 phosphorylation status. Western blot analysis for the indicated proteins. (I) Quantification of p-S6 Ser240/244 levels normalized to total S6 (tot-S6). P = 0.037 (*). (J) Quantification of p-AKT Ser473 levels normalized to total AKT (tot-AKT). P > 0.05. (K) Quantification of p-AKT <t>Thr308</t> levels normalized to total AKT (tot-AKT). P > 0.05. (L) Quantification of p-ERK1/2 Thr202/Tyr204 levels normalized to total ERK1/2 (tot-ERK1/2). P > 0.05. (M) Quantification of MYCT1 levels normalized to vinculin. P = 0.001 (*). (I–M) n = 5 independent experiments; paired t tests. (N) MYCT1 knockdown increases phosphorylation of p70/S6 kinase (p70/S6K), a key downstream effector of mTORC1 signaling, in response to amino acids. Western blot for the indicated proteins. (O) Quantification of data shown in N. n = 2 independent experiments; mean ± SD; two-way ANOVA with Tukey’s multiple comparison test, P = 0.0194 (*). (P) MYCT1 knockdown hyperactivates mTORC1 signaling in response to amino acids. 2 days after siRNA transfection, confluent ECs were serum- and growth factor–starved overnight, then starved in PBS for 1 h before 30-min stimulation with amino acids, glucose, growth factors, FBS, their combination, or PBS as control. Staining of ECs for p-S6 (gray), VE-cadherin (magenta), and DAPI (blue). Scale bar, 50 μm. Source data are available for this figure: .
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    primary antibodies against phospho akt thr308  (Cell Signaling Technology Inc)
    96
    Cell Signaling Technology Inc primary antibodies against phospho akt thr308
    MYCT1 limits endothelial mTORC1 signaling, related to Figs. 3 and 4. (A) Flow cytometry gating strategy (CD45 neg CD31 + ) for sorting of ECs from mesenteric fat for scRNA-seq. (B) Dot plot of markers for the indicated clusters. Color code: scaled average expression level in each cluster; the dot size denotes the percent of cells in each cluster expressing the given gene. (C) Number of differentially expressed genes (DEGs) between wild-type and Myct1 ecKO cell clusters. (D) Volcano plot of DEGs between the wild-type and Myct1 ecKO mice in the BEC cluster. Mat2a gene was selected for scRNA-seq validation. Mat2a, methionine adenosyltransferase 2A. (E) MYCT1 protein levels in human primary ECs. Western blot analysis for the indicated proteins. HPMECs, human pulmonary ECs; HUVECs, human umbilical vein ECs; HIECs, human intestinal ECs. (F and G) MYCT1 antibody and siRNAs validation for identification of endogenous human MYCT1 protein. Human primary ECs were transfected with two different MYCT1 targeting siRNAs. (F) Staining of ECs for MYCT1 (black) and DAPI (blue). Arrow, not transfected EC. Scale bar, 50 μm. (G) Western blot analysis showing MYCT1 migration profile and siRNA specificity. (H) MYCT1 knockdown increases phosphorylation of S6 but does not affect AKT and ERK1/2 phosphorylation status. Western blot analysis for the indicated proteins. (I) Quantification of p-S6 Ser240/244 levels normalized to total S6 (tot-S6). P = 0.037 (*). (J) Quantification of p-AKT Ser473 levels normalized to total AKT (tot-AKT). P > 0.05. (K) Quantification of p-AKT <t>Thr308</t> levels normalized to total AKT (tot-AKT). P > 0.05. (L) Quantification of p-ERK1/2 Thr202/Tyr204 levels normalized to total ERK1/2 (tot-ERK1/2). P > 0.05. (M) Quantification of MYCT1 levels normalized to vinculin. P = 0.001 (*). (I–M) n = 5 independent experiments; paired t tests. (N) MYCT1 knockdown increases phosphorylation of p70/S6 kinase (p70/S6K), a key downstream effector of mTORC1 signaling, in response to amino acids. Western blot for the indicated proteins. (O) Quantification of data shown in N. n = 2 independent experiments; mean ± SD; two-way ANOVA with Tukey’s multiple comparison test, P = 0.0194 (*). (P) MYCT1 knockdown hyperactivates mTORC1 signaling in response to amino acids. 2 days after siRNA transfection, confluent ECs were serum- and growth factor–starved overnight, then starved in PBS for 1 h before 30-min stimulation with amino acids, glucose, growth factors, FBS, their combination, or PBS as control. Staining of ECs for p-S6 (gray), VE-cadherin (magenta), and DAPI (blue). Scale bar, 50 μm. Source data are available for this figure: .
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    MYCT1 limits endothelial mTORC1 signaling, related to Figs. 3 and 4. (A) Flow cytometry gating strategy (CD45 neg CD31 + ) for sorting of ECs from mesenteric fat for scRNA-seq. (B) Dot plot of markers for the indicated clusters. Color code: scaled average expression level in each cluster; the dot size denotes the percent of cells in each cluster expressing the given gene. (C) Number of differentially expressed genes (DEGs) between wild-type and Myct1 ecKO cell clusters. (D) Volcano plot of DEGs between the wild-type and Myct1 ecKO mice in the BEC cluster. Mat2a gene was selected for scRNA-seq validation. Mat2a, methionine adenosyltransferase 2A. (E) MYCT1 protein levels in human primary ECs. Western blot analysis for the indicated proteins. HPMECs, human pulmonary ECs; HUVECs, human umbilical vein ECs; HIECs, human intestinal ECs. (F and G) MYCT1 antibody and siRNAs validation for identification of endogenous human MYCT1 protein. Human primary ECs were transfected with two different MYCT1 targeting siRNAs. (F) Staining of ECs for MYCT1 (black) and DAPI (blue). Arrow, not transfected EC. Scale bar, 50 μm. (G) Western blot analysis showing MYCT1 migration profile and siRNA specificity. (H) MYCT1 knockdown increases phosphorylation of S6 but does not affect AKT and ERK1/2 phosphorylation status. Western blot analysis for the indicated proteins. (I) Quantification of p-S6 Ser240/244 levels normalized to total S6 (tot-S6). P = 0.037 (*). (J) Quantification of p-AKT Ser473 levels normalized to total AKT (tot-AKT). P > 0.05. (K) Quantification of p-AKT Thr308 levels normalized to total AKT (tot-AKT). P > 0.05. (L) Quantification of p-ERK1/2 Thr202/Tyr204 levels normalized to total ERK1/2 (tot-ERK1/2). P > 0.05. (M) Quantification of MYCT1 levels normalized to vinculin. P = 0.001 (*). (I–M) n = 5 independent experiments; paired t tests. (N) MYCT1 knockdown increases phosphorylation of p70/S6 kinase (p70/S6K), a key downstream effector of mTORC1 signaling, in response to amino acids. Western blot for the indicated proteins. (O) Quantification of data shown in N. n = 2 independent experiments; mean ± SD; two-way ANOVA with Tukey’s multiple comparison test, P = 0.0194 (*). (P) MYCT1 knockdown hyperactivates mTORC1 signaling in response to amino acids. 2 days after siRNA transfection, confluent ECs were serum- and growth factor–starved overnight, then starved in PBS for 1 h before 30-min stimulation with amino acids, glucose, growth factors, FBS, their combination, or PBS as control. Staining of ECs for p-S6 (gray), VE-cadherin (magenta), and DAPI (blue). Scale bar, 50 μm. Source data are available for this figure: .

    Journal: The Journal of Experimental Medicine

    Article Title: MYCT1–IFITM2/3 interaction links endothelial endolysosomal trafficking to white adipose tissue expansion

    doi: 10.1084/jem.20251497

    Figure Lengend Snippet: MYCT1 limits endothelial mTORC1 signaling, related to Figs. 3 and 4. (A) Flow cytometry gating strategy (CD45 neg CD31 + ) for sorting of ECs from mesenteric fat for scRNA-seq. (B) Dot plot of markers for the indicated clusters. Color code: scaled average expression level in each cluster; the dot size denotes the percent of cells in each cluster expressing the given gene. (C) Number of differentially expressed genes (DEGs) between wild-type and Myct1 ecKO cell clusters. (D) Volcano plot of DEGs between the wild-type and Myct1 ecKO mice in the BEC cluster. Mat2a gene was selected for scRNA-seq validation. Mat2a, methionine adenosyltransferase 2A. (E) MYCT1 protein levels in human primary ECs. Western blot analysis for the indicated proteins. HPMECs, human pulmonary ECs; HUVECs, human umbilical vein ECs; HIECs, human intestinal ECs. (F and G) MYCT1 antibody and siRNAs validation for identification of endogenous human MYCT1 protein. Human primary ECs were transfected with two different MYCT1 targeting siRNAs. (F) Staining of ECs for MYCT1 (black) and DAPI (blue). Arrow, not transfected EC. Scale bar, 50 μm. (G) Western blot analysis showing MYCT1 migration profile and siRNA specificity. (H) MYCT1 knockdown increases phosphorylation of S6 but does not affect AKT and ERK1/2 phosphorylation status. Western blot analysis for the indicated proteins. (I) Quantification of p-S6 Ser240/244 levels normalized to total S6 (tot-S6). P = 0.037 (*). (J) Quantification of p-AKT Ser473 levels normalized to total AKT (tot-AKT). P > 0.05. (K) Quantification of p-AKT Thr308 levels normalized to total AKT (tot-AKT). P > 0.05. (L) Quantification of p-ERK1/2 Thr202/Tyr204 levels normalized to total ERK1/2 (tot-ERK1/2). P > 0.05. (M) Quantification of MYCT1 levels normalized to vinculin. P = 0.001 (*). (I–M) n = 5 independent experiments; paired t tests. (N) MYCT1 knockdown increases phosphorylation of p70/S6 kinase (p70/S6K), a key downstream effector of mTORC1 signaling, in response to amino acids. Western blot for the indicated proteins. (O) Quantification of data shown in N. n = 2 independent experiments; mean ± SD; two-way ANOVA with Tukey’s multiple comparison test, P = 0.0194 (*). (P) MYCT1 knockdown hyperactivates mTORC1 signaling in response to amino acids. 2 days after siRNA transfection, confluent ECs were serum- and growth factor–starved overnight, then starved in PBS for 1 h before 30-min stimulation with amino acids, glucose, growth factors, FBS, their combination, or PBS as control. Staining of ECs for p-S6 (gray), VE-cadherin (magenta), and DAPI (blue). Scale bar, 50 μm. Source data are available for this figure: .

    Article Snippet: Rabbit monoclonal anti-phospho-Akt (Thr308) , Cell Signaling Technology , Cat# 13038, RRID:AB_2629447.

    Techniques: Flow Cytometry, Expressing, Biomarker Discovery, Western Blot, Transfection, Staining, Migration, Knockdown, Phospho-proteomics, Comparison, Control