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pten  (ATCC)
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ATCC pten
Compound screening <t>in</t> <t>SH-SY5Y</t> <t>PTEN</t> −/− cells (A) Schematic of the PI3K/Akt/mTOR signaling cascade. PTEN counterbalances PI3K activity and loss of PTEN function leads to increased phosphorylation of AKT and downstream activity of mTOR. (B) Using a CRIPSR-based approach, we generated a PTEN −/− SH-SY5Y cell line. Compared to the control SH-SY5Y cells, the newly generated line shows loss of PTEN and concomitant increase of pAKT (Ser473). Loading control, GAPDH. (C–E) Highlighted are three example experiments, using different compounds. The different readouts are labeled in dark (pAKT (Ser473)) and light blue (pS6 (Ser240/244)). (C) Buparlisib similarly reduced both targets with low micromolar IC50. (D) Sapanisertib is effective at even lower concentrations. (E) SCH772984 only modestly decreases pS6 at high concentrations; however, increases pAKT levels. In all three graphs, LDH curves (orange and red) indicate the general viability. None of the displayed compounds shows sign of toxicity, even though LDH levels rise ∼15% in (C). n = 6 for each compound (2 independent experiments with 3 replicates each). Shown are mean and SEM.
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Compound screening <t>in</t> <t>SH-SY5Y</t> <t>PTEN</t> −/− cells (A) Schematic of the PI3K/Akt/mTOR signaling cascade. PTEN counterbalances PI3K activity and loss of PTEN function leads to increased phosphorylation of AKT and downstream activity of mTOR. (B) Using a CRIPSR-based approach, we generated a PTEN −/− SH-SY5Y cell line. Compared to the control SH-SY5Y cells, the newly generated line shows loss of PTEN and concomitant increase of pAKT (Ser473). Loading control, GAPDH. (C–E) Highlighted are three example experiments, using different compounds. The different readouts are labeled in dark (pAKT (Ser473)) and light blue (pS6 (Ser240/244)). (C) Buparlisib similarly reduced both targets with low micromolar IC50. (D) Sapanisertib is effective at even lower concentrations. (E) SCH772984 only modestly decreases pS6 at high concentrations; however, increases pAKT levels. In all three graphs, LDH curves (orange and red) indicate the general viability. None of the displayed compounds shows sign of toxicity, even though LDH levels rise ∼15% in (C). n = 6 for each compound (2 independent experiments with 3 replicates each). Shown are mean and SEM.
Anti Pten, 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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Compound screening <t>in</t> <t>SH-SY5Y</t> <t>PTEN</t> −/− cells (A) Schematic of the PI3K/Akt/mTOR signaling cascade. PTEN counterbalances PI3K activity and loss of PTEN function leads to increased phosphorylation of AKT and downstream activity of mTOR. (B) Using a CRIPSR-based approach, we generated a PTEN −/− SH-SY5Y cell line. Compared to the control SH-SY5Y cells, the newly generated line shows loss of PTEN and concomitant increase of pAKT (Ser473). Loading control, GAPDH. (C–E) Highlighted are three example experiments, using different compounds. The different readouts are labeled in dark (pAKT (Ser473)) and light blue (pS6 (Ser240/244)). (C) Buparlisib similarly reduced both targets with low micromolar IC50. (D) Sapanisertib is effective at even lower concentrations. (E) SCH772984 only modestly decreases pS6 at high concentrations; however, increases pAKT levels. In all three graphs, LDH curves (orange and red) indicate the general viability. None of the displayed compounds shows sign of toxicity, even though LDH levels rise ∼15% in (C). n = 6 for each compound (2 independent experiments with 3 replicates each). Shown are mean and SEM.
Pten 588, 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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Compound screening <t>in</t> <t>SH-SY5Y</t> <t>PTEN</t> −/− cells (A) Schematic of the PI3K/Akt/mTOR signaling cascade. PTEN counterbalances PI3K activity and loss of PTEN function leads to increased phosphorylation of AKT and downstream activity of mTOR. (B) Using a CRIPSR-based approach, we generated a PTEN −/− SH-SY5Y cell line. Compared to the control SH-SY5Y cells, the newly generated line shows loss of PTEN and concomitant increase of pAKT (Ser473). Loading control, GAPDH. (C–E) Highlighted are three example experiments, using different compounds. The different readouts are labeled in dark (pAKT (Ser473)) and light blue (pS6 (Ser240/244)). (C) Buparlisib similarly reduced both targets with low micromolar IC50. (D) Sapanisertib is effective at even lower concentrations. (E) SCH772984 only modestly decreases pS6 at high concentrations; however, increases pAKT levels. In all three graphs, LDH curves (orange and red) indicate the general viability. None of the displayed compounds shows sign of toxicity, even though LDH levels rise ∼15% in (C). n = 6 for each compound (2 independent experiments with 3 replicates each). Shown are mean and SEM.
Rabbit Anti Pten, 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 anti pten induced putative kinase 1
Compound screening <t>in</t> <t>SH-SY5Y</t> <t>PTEN</t> −/− cells (A) Schematic of the PI3K/Akt/mTOR signaling cascade. PTEN counterbalances PI3K activity and loss of PTEN function leads to increased phosphorylation of AKT and downstream activity of mTOR. (B) Using a CRIPSR-based approach, we generated a PTEN −/− SH-SY5Y cell line. Compared to the control SH-SY5Y cells, the newly generated line shows loss of PTEN and concomitant increase of pAKT (Ser473). Loading control, GAPDH. (C–E) Highlighted are three example experiments, using different compounds. The different readouts are labeled in dark (pAKT (Ser473)) and light blue (pS6 (Ser240/244)). (C) Buparlisib similarly reduced both targets with low micromolar IC50. (D) Sapanisertib is effective at even lower concentrations. (E) SCH772984 only modestly decreases pS6 at high concentrations; however, increases pAKT levels. In all three graphs, LDH curves (orange and red) indicate the general viability. None of the displayed compounds shows sign of toxicity, even though LDH levels rise ∼15% in (C). n = 6 for each compound (2 independent experiments with 3 replicates each). Shown are mean and SEM.
Anti Pten Induced Putative Kinase 1, supplied by Proteintech, 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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Compound screening <t>in</t> <t>SH-SY5Y</t> <t>PTEN</t> −/− cells (A) Schematic of the PI3K/Akt/mTOR signaling cascade. PTEN counterbalances PI3K activity and loss of PTEN function leads to increased phosphorylation of AKT and downstream activity of mTOR. (B) Using a CRIPSR-based approach, we generated a PTEN −/− SH-SY5Y cell line. Compared to the control SH-SY5Y cells, the newly generated line shows loss of PTEN and concomitant increase of pAKT (Ser473). Loading control, GAPDH. (C–E) Highlighted are three example experiments, using different compounds. The different readouts are labeled in dark (pAKT (Ser473)) and light blue (pS6 (Ser240/244)). (C) Buparlisib similarly reduced both targets with low micromolar IC50. (D) Sapanisertib is effective at even lower concentrations. (E) SCH772984 only modestly decreases pS6 at high concentrations; however, increases pAKT levels. In all three graphs, LDH curves (orange and red) indicate the general viability. None of the displayed compounds shows sign of toxicity, even though LDH levels rise ∼15% in (C). n = 6 for each compound (2 independent experiments with 3 replicates each). Shown are mean and SEM.
Pten Cap8 Cells, supplied by ATCC, 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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Addgene inc mcherry fkbp pten
Compound screening <t>in</t> <t>SH-SY5Y</t> <t>PTEN</t> −/− cells (A) Schematic of the PI3K/Akt/mTOR signaling cascade. PTEN counterbalances PI3K activity and loss of PTEN function leads to increased phosphorylation of AKT and downstream activity of mTOR. (B) Using a CRIPSR-based approach, we generated a PTEN −/− SH-SY5Y cell line. Compared to the control SH-SY5Y cells, the newly generated line shows loss of PTEN and concomitant increase of pAKT (Ser473). Loading control, GAPDH. (C–E) Highlighted are three example experiments, using different compounds. The different readouts are labeled in dark (pAKT (Ser473)) and light blue (pS6 (Ser240/244)). (C) Buparlisib similarly reduced both targets with low micromolar IC50. (D) Sapanisertib is effective at even lower concentrations. (E) SCH772984 only modestly decreases pS6 at high concentrations; however, increases pAKT levels. In all three graphs, LDH curves (orange and red) indicate the general viability. None of the displayed compounds shows sign of toxicity, even though LDH levels rise ∼15% in (C). n = 6 for each compound (2 independent experiments with 3 replicates each). Shown are mean and SEM.
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Compound screening <t>in</t> <t>SH-SY5Y</t> <t>PTEN</t> −/− cells (A) Schematic of the PI3K/Akt/mTOR signaling cascade. PTEN counterbalances PI3K activity and loss of PTEN function leads to increased phosphorylation of AKT and downstream activity of mTOR. (B) Using a CRIPSR-based approach, we generated a PTEN −/− SH-SY5Y cell line. Compared to the control SH-SY5Y cells, the newly generated line shows loss of PTEN and concomitant increase of pAKT (Ser473). Loading control, GAPDH. (C–E) Highlighted are three example experiments, using different compounds. The different readouts are labeled in dark (pAKT (Ser473)) and light blue (pS6 (Ser240/244)). (C) Buparlisib similarly reduced both targets with low micromolar IC50. (D) Sapanisertib is effective at even lower concentrations. (E) SCH772984 only modestly decreases pS6 at high concentrations; however, increases pAKT levels. In all three graphs, LDH curves (orange and red) indicate the general viability. None of the displayed compounds shows sign of toxicity, even though LDH levels rise ∼15% in (C). n = 6 for each compound (2 independent experiments with 3 replicates each). Shown are mean and SEM.
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Compound screening <t>in</t> <t>SH-SY5Y</t> <t>PTEN</t> −/− cells (A) Schematic of the PI3K/Akt/mTOR signaling cascade. PTEN counterbalances PI3K activity and loss of PTEN function leads to increased phosphorylation of AKT and downstream activity of mTOR. (B) Using a CRIPSR-based approach, we generated a PTEN −/− SH-SY5Y cell line. Compared to the control SH-SY5Y cells, the newly generated line shows loss of PTEN and concomitant increase of pAKT (Ser473). Loading control, GAPDH. (C–E) Highlighted are three example experiments, using different compounds. The different readouts are labeled in dark (pAKT (Ser473)) and light blue (pS6 (Ser240/244)). (C) Buparlisib similarly reduced both targets with low micromolar IC50. (D) Sapanisertib is effective at even lower concentrations. (E) SCH772984 only modestly decreases pS6 at high concentrations; however, increases pAKT levels. In all three graphs, LDH curves (orange and red) indicate the general viability. None of the displayed compounds shows sign of toxicity, even though LDH levels rise ∼15% in (C). n = 6 for each compound (2 independent experiments with 3 replicates each). Shown are mean and SEM.
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Image Search Results


Compound screening in SH-SY5Y PTEN −/− cells (A) Schematic of the PI3K/Akt/mTOR signaling cascade. PTEN counterbalances PI3K activity and loss of PTEN function leads to increased phosphorylation of AKT and downstream activity of mTOR. (B) Using a CRIPSR-based approach, we generated a PTEN −/− SH-SY5Y cell line. Compared to the control SH-SY5Y cells, the newly generated line shows loss of PTEN and concomitant increase of pAKT (Ser473). Loading control, GAPDH. (C–E) Highlighted are three example experiments, using different compounds. The different readouts are labeled in dark (pAKT (Ser473)) and light blue (pS6 (Ser240/244)). (C) Buparlisib similarly reduced both targets with low micromolar IC50. (D) Sapanisertib is effective at even lower concentrations. (E) SCH772984 only modestly decreases pS6 at high concentrations; however, increases pAKT levels. In all three graphs, LDH curves (orange and red) indicate the general viability. None of the displayed compounds shows sign of toxicity, even though LDH levels rise ∼15% in (C). n = 6 for each compound (2 independent experiments with 3 replicates each). Shown are mean and SEM.

Journal: iScience

Article Title: Repurposing drugs for treating the neurobehavioral manifestations of PTEN hamartoma tumor syndrome

doi: 10.1016/j.isci.2026.115428

Figure Lengend Snippet: Compound screening in SH-SY5Y PTEN −/− cells (A) Schematic of the PI3K/Akt/mTOR signaling cascade. PTEN counterbalances PI3K activity and loss of PTEN function leads to increased phosphorylation of AKT and downstream activity of mTOR. (B) Using a CRIPSR-based approach, we generated a PTEN −/− SH-SY5Y cell line. Compared to the control SH-SY5Y cells, the newly generated line shows loss of PTEN and concomitant increase of pAKT (Ser473). Loading control, GAPDH. (C–E) Highlighted are three example experiments, using different compounds. The different readouts are labeled in dark (pAKT (Ser473)) and light blue (pS6 (Ser240/244)). (C) Buparlisib similarly reduced both targets with low micromolar IC50. (D) Sapanisertib is effective at even lower concentrations. (E) SCH772984 only modestly decreases pS6 at high concentrations; however, increases pAKT levels. In all three graphs, LDH curves (orange and red) indicate the general viability. None of the displayed compounds shows sign of toxicity, even though LDH levels rise ∼15% in (C). n = 6 for each compound (2 independent experiments with 3 replicates each). Shown are mean and SEM.

Article Snippet: Knockout of PTEN in the SH-SY5Y line (ATCC, CRL-2266) was generated using CRISPR technology.

Techniques: Activity Assay, Phospho-proteomics, Generated, Control, Labeling