mtor Search Results


anti mtor  (Epizyme Inc)
86
Epizyme Inc anti mtor
Anti Mtor, supplied by Epizyme Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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phosphorylated mtor  (Cell Signaling Technology Inc)
86
Cell Signaling Technology Inc phosphorylated mtor
Phosphorylated Mtor, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mtor antibody  (Cell Signaling Technology Inc)
86
Cell Signaling Technology Inc mtor antibody
Mtor Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti phospho mtor s2481 rabbit polyclonal  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc anti phospho mtor s2481 rabbit polyclonal
(A) Schematic overview of the mTORC1 pathway comprising an insulin (Ins)-sensing module (AKT-TSC-Rheb) and an amino acid (AA)–sensing module (Ragulator/LAMTOR-Rag). Red arrows indicate activatory phosphorylation, blue arrows indicate inhibitory phosphorylation, and black lines indicate inhibitory reactions. GAP: GTPase-activating protein. (B) Phosphorylation levels of AKT at T308 and S473, TSC2 at S939 and T1462, mTOR at <t>S2481,</t> S6K at T389, and GSK3β at S9 monitored when HEK293 (left), and p18 re-expressing p18-KO (p18Rev) (middle) and MEF cells (right) were exposed to AA deprivation and subsequently treated with AA and Ins. Cells were cultured in minimal medium without AA and Ins for 1 h, then incubated with medium containing AA and Ins (10 μg/ml) for the indicated times. Cell lysates were analyzed by Western blotting using the indicated antibodies. *: nonspecific band. (C, D) Phosphorylation levels of AKT at T308 and S473, TSC2 at S939 and T1462, S6K at T389, and GSK3β at S9 monitored in p18Rev cells treated with Ins and AA alone or in combination as indicated. p18Rev cells were treated with AA and/or Ins, as shown in (B). Cell lysates were analyzed by Western blotting using the indicated antibodies. (E) Immunofluorescence analysis of p18Rev cells treated with AA and/or Ins for 20 min, as indicated. The areas in the small squares in the top panels are enlarged and shown in the middle panels. mTOR, green; LAMP1, red. Scale bars, 10 μm. Line scans of mTOR (green) and LAMP1 (red) are shown at the bottom of the panel. (E, F) mTOR-LAMP1 colocalization in (E) was measured. The mean values of Pearson’s correlation coefficient from four cells and the SEM are shown. P -values were assessed using one-way ANOVA with Tukey’s multiple comparison test. NS, not significant.
Anti Phospho Mtor S2481 Rabbit Polyclonal, 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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rabbit monoclonal anti phospho mtor pmtor  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc rabbit monoclonal anti phospho mtor pmtor
(A) Schematic overview of the mTORC1 pathway comprising an insulin (Ins)-sensing module (AKT-TSC-Rheb) and an amino acid (AA)–sensing module (Ragulator/LAMTOR-Rag). Red arrows indicate activatory phosphorylation, blue arrows indicate inhibitory phosphorylation, and black lines indicate inhibitory reactions. GAP: GTPase-activating protein. (B) Phosphorylation levels of AKT at T308 and S473, TSC2 at S939 and T1462, mTOR at <t>S2481,</t> S6K at T389, and GSK3β at S9 monitored when HEK293 (left), and p18 re-expressing p18-KO (p18Rev) (middle) and MEF cells (right) were exposed to AA deprivation and subsequently treated with AA and Ins. Cells were cultured in minimal medium without AA and Ins for 1 h, then incubated with medium containing AA and Ins (10 μg/ml) for the indicated times. Cell lysates were analyzed by Western blotting using the indicated antibodies. *: nonspecific band. (C, D) Phosphorylation levels of AKT at T308 and S473, TSC2 at S939 and T1462, S6K at T389, and GSK3β at S9 monitored in p18Rev cells treated with Ins and AA alone or in combination as indicated. p18Rev cells were treated with AA and/or Ins, as shown in (B). Cell lysates were analyzed by Western blotting using the indicated antibodies. (E) Immunofluorescence analysis of p18Rev cells treated with AA and/or Ins for 20 min, as indicated. The areas in the small squares in the top panels are enlarged and shown in the middle panels. mTOR, green; LAMP1, red. Scale bars, 10 μm. Line scans of mTOR (green) and LAMP1 (red) are shown at the bottom of the panel. (E, F) mTOR-LAMP1 colocalization in (E) was measured. The mean values of Pearson’s correlation coefficient from four cells and the SEM are shown. P -values were assessed using one-way ANOVA with Tukey’s multiple comparison test. NS, not significant.
Rabbit Monoclonal Anti Phospho Mtor Pmtor, 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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mtor sirna  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc mtor sirna
(A) Schematic overview of the mTORC1 pathway comprising an insulin (Ins)-sensing module (AKT-TSC-Rheb) and an amino acid (AA)–sensing module (Ragulator/LAMTOR-Rag). Red arrows indicate activatory phosphorylation, blue arrows indicate inhibitory phosphorylation, and black lines indicate inhibitory reactions. GAP: GTPase-activating protein. (B) Phosphorylation levels of AKT at T308 and S473, TSC2 at S939 and T1462, mTOR at <t>S2481,</t> S6K at T389, and GSK3β at S9 monitored when HEK293 (left), and p18 re-expressing p18-KO (p18Rev) (middle) and MEF cells (right) were exposed to AA deprivation and subsequently treated with AA and Ins. Cells were cultured in minimal medium without AA and Ins for 1 h, then incubated with medium containing AA and Ins (10 μg/ml) for the indicated times. Cell lysates were analyzed by Western blotting using the indicated antibodies. *: nonspecific band. (C, D) Phosphorylation levels of AKT at T308 and S473, TSC2 at S939 and T1462, S6K at T389, and GSK3β at S9 monitored in p18Rev cells treated with Ins and AA alone or in combination as indicated. p18Rev cells were treated with AA and/or Ins, as shown in (B). Cell lysates were analyzed by Western blotting using the indicated antibodies. (E) Immunofluorescence analysis of p18Rev cells treated with AA and/or Ins for 20 min, as indicated. The areas in the small squares in the top panels are enlarged and shown in the middle panels. mTOR, green; LAMP1, red. Scale bars, 10 μm. Line scans of mTOR (green) and LAMP1 (red) are shown at the bottom of the panel. (E, F) mTOR-LAMP1 colocalization in (E) was measured. The mean values of Pearson’s correlation coefficient from four cells and the SEM are shown. P -values were assessed using one-way ANOVA with Tukey’s multiple comparison test. NS, not significant.
Mtor Sirna, 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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phospho mtor ser2448  (Cell Signaling Technology Inc)
97
Cell Signaling Technology Inc phospho mtor ser2448
(A) Schematic overview of the mTORC1 pathway comprising an insulin (Ins)-sensing module (AKT-TSC-Rheb) and an amino acid (AA)–sensing module (Ragulator/LAMTOR-Rag). Red arrows indicate activatory phosphorylation, blue arrows indicate inhibitory phosphorylation, and black lines indicate inhibitory reactions. GAP: GTPase-activating protein. (B) Phosphorylation levels of AKT at T308 and S473, TSC2 at S939 and T1462, mTOR at <t>S2481,</t> S6K at T389, and GSK3β at S9 monitored when HEK293 (left), and p18 re-expressing p18-KO (p18Rev) (middle) and MEF cells (right) were exposed to AA deprivation and subsequently treated with AA and Ins. Cells were cultured in minimal medium without AA and Ins for 1 h, then incubated with medium containing AA and Ins (10 μg/ml) for the indicated times. Cell lysates were analyzed by Western blotting using the indicated antibodies. *: nonspecific band. (C, D) Phosphorylation levels of AKT at T308 and S473, TSC2 at S939 and T1462, S6K at T389, and GSK3β at S9 monitored in p18Rev cells treated with Ins and AA alone or in combination as indicated. p18Rev cells were treated with AA and/or Ins, as shown in (B). Cell lysates were analyzed by Western blotting using the indicated antibodies. (E) Immunofluorescence analysis of p18Rev cells treated with AA and/or Ins for 20 min, as indicated. The areas in the small squares in the top panels are enlarged and shown in the middle panels. mTOR, green; LAMP1, red. Scale bars, 10 μm. Line scans of mTOR (green) and LAMP1 (red) are shown at the bottom of the panel. (E, F) mTOR-LAMP1 colocalization in (E) was measured. The mean values of Pearson’s correlation coefficient from four cells and the SEM are shown. P -values were assessed using one-way ANOVA with Tukey’s multiple comparison test. NS, not significant.
Phospho Mtor Ser2448, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mtor  (Santa Cruz Biotechnology)
96
Santa Cruz Biotechnology mtor
Figure 5. CANE abolishes autophagy in A549DR. (A) CANE was treated to A549DR cells for 24 h and autophagic protein levels detected such as LC-3, p62, Beclin-1, <t>mTOR,</t> <t>ATG5</t> and ATG7. Densitometry analysis of the respective proteins was evaluated by Image J software, and results were normalized with b-actin with respect to controls. (B) For further confirmation, autophagic vacoule formation detected with the help of fluorogenic dye LysoTracker V R Red, DAPI was used as counter stain to stain nucleus. Acridine orange was used to detect the autopaghic vacoule formation. Image J software was used for quantification of oxidative stress. Images were taken at 40 magnification [scale bar¼ 0.1 mm]. Each value in the graph represents as the mean ± SD of three independent experiments. Values with different superscripts differ significantly from each other (p < .05).
Mtor, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mtor/product/Santa Cruz Biotechnology
Average 96 stars, based on 1 article reviews
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mtor  (Proteintech)
96
Proteintech mtor
<t>KIN17</t> positively regulates <t>PI3K/AKT/mTOR</t> expression in RCC and PF-04691502 can reverse the pathway protein expression and biological function. ( A ) Predict effects of KIN17 knockdown on the pathways of RCC cells (ACHN and 786–0) in vitro by kegg and GSEA. ( B ) p-mTOR, mTOR, p-AKT, AKT, p-PI3K and PI3K protein levels were measured by WB using the paired RCC cells (ACHN and 786–0) group and knockdown KIN17 group. ( C ) p-mTOR, mTOR, p-AKT, AKT, p-PI3K and PI3K protein levels were measured by WB using the paired RCC vector cells group (VE groups), overexpression KIN17 group (OE groups), VE groups + PF-04691502 and OE groups + PF-04691502. ( D ) N-cadherin and Vimentin protein levels were measured by WB using the paired RCC cells (ACHN and 786–0) in knockdown KIN17 group and different using PF-04691502 groups.
Mtor, 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
https://www.bioz.com/result/mtor/product/Proteintech
Average 96 stars, based on 1 article reviews
mtor - by Bioz Stars, 2026-05
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addgene pcdna3 au1 mtor e2419k  (Addgene inc)
93
Addgene inc addgene pcdna3 au1 mtor e2419k
<t>KIN17</t> positively regulates <t>PI3K/AKT/mTOR</t> expression in RCC and PF-04691502 can reverse the pathway protein expression and biological function. ( A ) Predict effects of KIN17 knockdown on the pathways of RCC cells (ACHN and 786–0) in vitro by kegg and GSEA. ( B ) p-mTOR, mTOR, p-AKT, AKT, p-PI3K and PI3K protein levels were measured by WB using the paired RCC cells (ACHN and 786–0) group and knockdown KIN17 group. ( C ) p-mTOR, mTOR, p-AKT, AKT, p-PI3K and PI3K protein levels were measured by WB using the paired RCC vector cells group (VE groups), overexpression KIN17 group (OE groups), VE groups + PF-04691502 and OE groups + PF-04691502. ( D ) N-cadherin and Vimentin protein levels were measured by WB using the paired RCC cells (ACHN and 786–0) in knockdown KIN17 group and different using PF-04691502 groups.
Addgene Pcdna3 Au1 Mtor E2419k, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/addgene pcdna3 au1 mtor e2419k/product/Addgene inc
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id  (Addgene inc)
93
Addgene inc id
<t>KIN17</t> positively regulates <t>PI3K/AKT/mTOR</t> expression in RCC and PF-04691502 can reverse the pathway protein expression and biological function. ( A ) Predict effects of KIN17 knockdown on the pathways of RCC cells (ACHN and 786–0) in vitro by kegg and GSEA. ( B ) p-mTOR, mTOR, p-AKT, AKT, p-PI3K and PI3K protein levels were measured by WB using the paired RCC cells (ACHN and 786–0) group and knockdown KIN17 group. ( C ) p-mTOR, mTOR, p-AKT, AKT, p-PI3K and PI3K protein levels were measured by WB using the paired RCC vector cells group (VE groups), overexpression KIN17 group (OE groups), VE groups + PF-04691502 and OE groups + PF-04691502. ( D ) N-cadherin and Vimentin protein levels were measured by WB using the paired RCC cells (ACHN and 786–0) in knockdown KIN17 group and different using PF-04691502 groups.
Id, supplied by Addgene 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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Average 93 stars, based on 1 article reviews
id - by Bioz Stars, 2026-05
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p mtor  (Santa Cruz Biotechnology)
96
Santa Cruz Biotechnology p mtor
SNCG induces ovarian cancer progression via activating the PI3K/AKT signaling pathway. a-b A phospho-kinase array kit was performed on protein lysates of SKOV3-sh1 and control cells. Thirteen proteins were obvious changes in their phosphorylation status and highlighted by boxes. c Western blot analysis of the levels of Akt, p-Akt (Sec473), p70S6 kinase, p-p70S6 kinase (Thr389), <t>mTOR,</t> and p-mTOR <t>(Sec2448)</t> in SKOV3 and HO-8901 PM cells transfected with SNCG-shRNA or Scr, and OVCAR3 cells transfected with SNCG-Ove or Ctrl. d Expression levels of Akt, p-Akt (Sec473), p70S6 kinase, p-p70S6 kinase (Thr389), mTOR, and p-mTOR (Sec2448) in cells transfected with SNCG shRNA, Scr, SNCG Ove, Ctrl, IGF-1, and DMSO were determined by Western blot. e Expression levels of Akt, p-Akt (Sec473), p70S6 kinase, p-p70S6 kinase (Thr389), mTOR, and p-mTOR (Sec2448) in cells transfected with SNCG shRNA, Scr, SNCG Ove, Ctrl, LY294002, and DMSO were determined by Western blot. f Wound healing assay (upper, original magnification × 40) and cell colony formation (lower) of cells transfected with SNCG shRNA, Scr, SNCG Ove, Ctrl, IGF-1, LY294002, and DMSO confirmed the effect of SNCG on the PI3K/AKT signaling pathway. ▲ , P < 0.05. *, P < 0.001. IGF-1: insulin-like growth factor 1; sh-SNCG: small hairpin RNAs of SNCG
P Mtor, supplied by Santa Cruz Biotechnology, 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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Image Search Results


(A) Schematic overview of the mTORC1 pathway comprising an insulin (Ins)-sensing module (AKT-TSC-Rheb) and an amino acid (AA)–sensing module (Ragulator/LAMTOR-Rag). Red arrows indicate activatory phosphorylation, blue arrows indicate inhibitory phosphorylation, and black lines indicate inhibitory reactions. GAP: GTPase-activating protein. (B) Phosphorylation levels of AKT at T308 and S473, TSC2 at S939 and T1462, mTOR at S2481, S6K at T389, and GSK3β at S9 monitored when HEK293 (left), and p18 re-expressing p18-KO (p18Rev) (middle) and MEF cells (right) were exposed to AA deprivation and subsequently treated with AA and Ins. Cells were cultured in minimal medium without AA and Ins for 1 h, then incubated with medium containing AA and Ins (10 μg/ml) for the indicated times. Cell lysates were analyzed by Western blotting using the indicated antibodies. *: nonspecific band. (C, D) Phosphorylation levels of AKT at T308 and S473, TSC2 at S939 and T1462, S6K at T389, and GSK3β at S9 monitored in p18Rev cells treated with Ins and AA alone or in combination as indicated. p18Rev cells were treated with AA and/or Ins, as shown in (B). Cell lysates were analyzed by Western blotting using the indicated antibodies. (E) Immunofluorescence analysis of p18Rev cells treated with AA and/or Ins for 20 min, as indicated. The areas in the small squares in the top panels are enlarged and shown in the middle panels. mTOR, green; LAMP1, red. Scale bars, 10 μm. Line scans of mTOR (green) and LAMP1 (red) are shown at the bottom of the panel. (E, F) mTOR-LAMP1 colocalization in (E) was measured. The mean values of Pearson’s correlation coefficient from four cells and the SEM are shown. P -values were assessed using one-way ANOVA with Tukey’s multiple comparison test. NS, not significant.

Journal: Life Science Alliance

Article Title: Amino acid–dependent TSC2 dephosphorylation by lysosome–PP2A regulates mTORC1 signaling transduction

doi: 10.26508/lsa.202503206

Figure Lengend Snippet: (A) Schematic overview of the mTORC1 pathway comprising an insulin (Ins)-sensing module (AKT-TSC-Rheb) and an amino acid (AA)–sensing module (Ragulator/LAMTOR-Rag). Red arrows indicate activatory phosphorylation, blue arrows indicate inhibitory phosphorylation, and black lines indicate inhibitory reactions. GAP: GTPase-activating protein. (B) Phosphorylation levels of AKT at T308 and S473, TSC2 at S939 and T1462, mTOR at S2481, S6K at T389, and GSK3β at S9 monitored when HEK293 (left), and p18 re-expressing p18-KO (p18Rev) (middle) and MEF cells (right) were exposed to AA deprivation and subsequently treated with AA and Ins. Cells were cultured in minimal medium without AA and Ins for 1 h, then incubated with medium containing AA and Ins (10 μg/ml) for the indicated times. Cell lysates were analyzed by Western blotting using the indicated antibodies. *: nonspecific band. (C, D) Phosphorylation levels of AKT at T308 and S473, TSC2 at S939 and T1462, S6K at T389, and GSK3β at S9 monitored in p18Rev cells treated with Ins and AA alone or in combination as indicated. p18Rev cells were treated with AA and/or Ins, as shown in (B). Cell lysates were analyzed by Western blotting using the indicated antibodies. (E) Immunofluorescence analysis of p18Rev cells treated with AA and/or Ins for 20 min, as indicated. The areas in the small squares in the top panels are enlarged and shown in the middle panels. mTOR, green; LAMP1, red. Scale bars, 10 μm. Line scans of mTOR (green) and LAMP1 (red) are shown at the bottom of the panel. (E, F) mTOR-LAMP1 colocalization in (E) was measured. The mean values of Pearson’s correlation coefficient from four cells and the SEM are shown. P -values were assessed using one-way ANOVA with Tukey’s multiple comparison test. NS, not significant.

Article Snippet: The following antibodies were used: anti-phospho-S6K (T389) rabbit monoclonal (108D2) (#9234; Cell Signaling Technology); anti-phospho-mTOR (S2481) rabbit polyclonal (#2974; Cell Signaling Technology); anti-phospho-AKT (T308) rabbit monoclonal (244F9) (#4056; Cell Signaling Technology); anti-phospho-AKT (S473) rabbit monoclonal (D9E) (#4060; Cell Signaling Technology); anti-phospho-TSC2 (T1462) rabbit monoclonal (5B12) (#3617; Cell Signaling Technology); anti-phospho-TSC2 (S664) rabbit monoclonal (D3B9Z) (#40729; Cell Signaling Technology); anti-phospho-TSC2 (S939) rabbit polyclonal (#3615; Cell Signaling Technology); anti-phospho-S6 (S235/S236) rabbit monoclonal (D57.2.2E) (#4858; Cell Signaling Technology); anti-phospho-ERK (T202/Y204) rabbit polyclonal (#9101; Cell Signaling Technology); anti-phospho-eIF2α (S51) rabbit polyclonal (#9721; Cell Signaling Technology); anti-phospho-GSK3β (S9) rabbit monoclonal (D85E12) (#5558; Cell Signaling Technology); anti-S6K rabbit polyclonal (#9202; Cell Signaling Technology); anti-mTOR rabbit polyclonal (#2972; Cell Signaling Technology); anti-AKT1 rabbit monoclonal (C73H10) (#2938; Cell Signaling Technology); anti-AKT rabbit monoclonal (C67E7) (#4691; Cell Signaling Technology); anti-TSC2 rabbit polyclonal (#3612; Cell Signaling Technology); anti-TSC2 rabbit monoclonal (D93F12) (#4308; Cell Signaling Technology); anti-p18/LAMTOR1/C11orf59 rabbit monoclonal (D11H6) (#8975; Cell Signaling Technology); anti-p53 mouse monoclonal (1C12) (#2524; Cell Signaling Technology); anti-ERK1/2 mouse monoclonal (C-9) (sc-514302; Santa Cruz Biotechnology); anti-eIF2α mouse monoclonal (D-3) (sc-133132; Santa Cruz Biotechnology); anti-PP2A-Aα/β mouse monoclonal (4G7) (sc-13600; Santa Cruz Biotechnology); anti-p70 S6K α mouse monoclonal (H9) (sc-8418; Santa Cruz Biotechnology); anti-S6 mouse monoclonal (C8) (sc-74459; Santa Cruz Biotechnology); anti-Rheb mouse monoclonal (B12) (sc-271509; Santa Cruz Biotechnology); anti-Myc mouse monoclonal (9E10) (sc-40; Santa Cruz Biotechnology); anti-PP2A-Cα mouse monoclonal (46/PP2A; Catalytic a) (610555; BD Transduction Laboratories); anti-β-actin mouse monoclonal (6D1) (010-27841; Fujifilm Wako); anti-Flag mouse monoclonal (M2) antibody (F3165; Sigma-Aldrich).

Techniques: Phospho-proteomics, Expressing, Cell Culture, Incubation, Western Blot, Immunofluorescence, Comparison

(A) Schematic representation of reactions involved in the spatiotemporal regulation of the mTORC1 pathway. A mathematical model of the AKT-TSC1/2-Rheb axis consisting of 25 equations was defined based on available mathematical models. A mathematical model of the AA-sensing (Ragulator/LAMTOR-Rag) axis was defined based on a standard reaction network system with nine equations. Reactions depicting mTORC1 activation on the lysosomal surface, mediated by the active forms of Rag GTP and Rheb GTP , were defined using six equations. k (solid-line arrow) and l (dotted line arrow) represent the rate constants, whereas Φ represents the degradation of the insulin receptor (IR). (B) Comparison of the phosphorylation levels of mTOR at S2481, S6K at T389, AKT at T308, and TSC2 at T1462 between simulation and experimental values under AA(+) Ins(+) stimulation. The solid black lines indicate the values obtained from the simulation, whereas the blue dots indicate the values measured during the experiment. Error bars indicate the SEM (n = 3).

Journal: Life Science Alliance

Article Title: Amino acid–dependent TSC2 dephosphorylation by lysosome–PP2A regulates mTORC1 signaling transduction

doi: 10.26508/lsa.202503206

Figure Lengend Snippet: (A) Schematic representation of reactions involved in the spatiotemporal regulation of the mTORC1 pathway. A mathematical model of the AKT-TSC1/2-Rheb axis consisting of 25 equations was defined based on available mathematical models. A mathematical model of the AA-sensing (Ragulator/LAMTOR-Rag) axis was defined based on a standard reaction network system with nine equations. Reactions depicting mTORC1 activation on the lysosomal surface, mediated by the active forms of Rag GTP and Rheb GTP , were defined using six equations. k (solid-line arrow) and l (dotted line arrow) represent the rate constants, whereas Φ represents the degradation of the insulin receptor (IR). (B) Comparison of the phosphorylation levels of mTOR at S2481, S6K at T389, AKT at T308, and TSC2 at T1462 between simulation and experimental values under AA(+) Ins(+) stimulation. The solid black lines indicate the values obtained from the simulation, whereas the blue dots indicate the values measured during the experiment. Error bars indicate the SEM (n = 3).

Article Snippet: The following antibodies were used: anti-phospho-S6K (T389) rabbit monoclonal (108D2) (#9234; Cell Signaling Technology); anti-phospho-mTOR (S2481) rabbit polyclonal (#2974; Cell Signaling Technology); anti-phospho-AKT (T308) rabbit monoclonal (244F9) (#4056; Cell Signaling Technology); anti-phospho-AKT (S473) rabbit monoclonal (D9E) (#4060; Cell Signaling Technology); anti-phospho-TSC2 (T1462) rabbit monoclonal (5B12) (#3617; Cell Signaling Technology); anti-phospho-TSC2 (S664) rabbit monoclonal (D3B9Z) (#40729; Cell Signaling Technology); anti-phospho-TSC2 (S939) rabbit polyclonal (#3615; Cell Signaling Technology); anti-phospho-S6 (S235/S236) rabbit monoclonal (D57.2.2E) (#4858; Cell Signaling Technology); anti-phospho-ERK (T202/Y204) rabbit polyclonal (#9101; Cell Signaling Technology); anti-phospho-eIF2α (S51) rabbit polyclonal (#9721; Cell Signaling Technology); anti-phospho-GSK3β (S9) rabbit monoclonal (D85E12) (#5558; Cell Signaling Technology); anti-S6K rabbit polyclonal (#9202; Cell Signaling Technology); anti-mTOR rabbit polyclonal (#2972; Cell Signaling Technology); anti-AKT1 rabbit monoclonal (C73H10) (#2938; Cell Signaling Technology); anti-AKT rabbit monoclonal (C67E7) (#4691; Cell Signaling Technology); anti-TSC2 rabbit polyclonal (#3612; Cell Signaling Technology); anti-TSC2 rabbit monoclonal (D93F12) (#4308; Cell Signaling Technology); anti-p18/LAMTOR1/C11orf59 rabbit monoclonal (D11H6) (#8975; Cell Signaling Technology); anti-p53 mouse monoclonal (1C12) (#2524; Cell Signaling Technology); anti-ERK1/2 mouse monoclonal (C-9) (sc-514302; Santa Cruz Biotechnology); anti-eIF2α mouse monoclonal (D-3) (sc-133132; Santa Cruz Biotechnology); anti-PP2A-Aα/β mouse monoclonal (4G7) (sc-13600; Santa Cruz Biotechnology); anti-p70 S6K α mouse monoclonal (H9) (sc-8418; Santa Cruz Biotechnology); anti-S6 mouse monoclonal (C8) (sc-74459; Santa Cruz Biotechnology); anti-Rheb mouse monoclonal (B12) (sc-271509; Santa Cruz Biotechnology); anti-Myc mouse monoclonal (9E10) (sc-40; Santa Cruz Biotechnology); anti-PP2A-Cα mouse monoclonal (46/PP2A; Catalytic a) (610555; BD Transduction Laboratories); anti-β-actin mouse monoclonal (6D1) (010-27841; Fujifilm Wako); anti-Flag mouse monoclonal (M2) antibody (F3165; Sigma-Aldrich).

Techniques: Activation Assay, Comparison, Phospho-proteomics

(A, B, C, D) (Left) Comparison of the levels of (mTOR+Ragulator-Rag GTP ) (A), (mTOR+Ragulator-Rag GTP +Rheb GTP ) (B), P-mTOR (P-S2481) (P-mTOR+Ragulator-Rag GTP +Rheb GTP ) (C), and P-S6K (P-T389) (D). Solid black lines indicate the values obtained from the simulation, whereas the blue dots indicate the values measured during the experiment. Error bars indicate the SEM (n = 3). (Right) Schematic representation of reactions depicting mTORC1 activation on the lysosomal surface, mediated by the active forms of Rag GTP and Rheb GTP .

Journal: Life Science Alliance

Article Title: Amino acid–dependent TSC2 dephosphorylation by lysosome–PP2A regulates mTORC1 signaling transduction

doi: 10.26508/lsa.202503206

Figure Lengend Snippet: (A, B, C, D) (Left) Comparison of the levels of (mTOR+Ragulator-Rag GTP ) (A), (mTOR+Ragulator-Rag GTP +Rheb GTP ) (B), P-mTOR (P-S2481) (P-mTOR+Ragulator-Rag GTP +Rheb GTP ) (C), and P-S6K (P-T389) (D). Solid black lines indicate the values obtained from the simulation, whereas the blue dots indicate the values measured during the experiment. Error bars indicate the SEM (n = 3). (Right) Schematic representation of reactions depicting mTORC1 activation on the lysosomal surface, mediated by the active forms of Rag GTP and Rheb GTP .

Article Snippet: The following antibodies were used: anti-phospho-S6K (T389) rabbit monoclonal (108D2) (#9234; Cell Signaling Technology); anti-phospho-mTOR (S2481) rabbit polyclonal (#2974; Cell Signaling Technology); anti-phospho-AKT (T308) rabbit monoclonal (244F9) (#4056; Cell Signaling Technology); anti-phospho-AKT (S473) rabbit monoclonal (D9E) (#4060; Cell Signaling Technology); anti-phospho-TSC2 (T1462) rabbit monoclonal (5B12) (#3617; Cell Signaling Technology); anti-phospho-TSC2 (S664) rabbit monoclonal (D3B9Z) (#40729; Cell Signaling Technology); anti-phospho-TSC2 (S939) rabbit polyclonal (#3615; Cell Signaling Technology); anti-phospho-S6 (S235/S236) rabbit monoclonal (D57.2.2E) (#4858; Cell Signaling Technology); anti-phospho-ERK (T202/Y204) rabbit polyclonal (#9101; Cell Signaling Technology); anti-phospho-eIF2α (S51) rabbit polyclonal (#9721; Cell Signaling Technology); anti-phospho-GSK3β (S9) rabbit monoclonal (D85E12) (#5558; Cell Signaling Technology); anti-S6K rabbit polyclonal (#9202; Cell Signaling Technology); anti-mTOR rabbit polyclonal (#2972; Cell Signaling Technology); anti-AKT1 rabbit monoclonal (C73H10) (#2938; Cell Signaling Technology); anti-AKT rabbit monoclonal (C67E7) (#4691; Cell Signaling Technology); anti-TSC2 rabbit polyclonal (#3612; Cell Signaling Technology); anti-TSC2 rabbit monoclonal (D93F12) (#4308; Cell Signaling Technology); anti-p18/LAMTOR1/C11orf59 rabbit monoclonal (D11H6) (#8975; Cell Signaling Technology); anti-p53 mouse monoclonal (1C12) (#2524; Cell Signaling Technology); anti-ERK1/2 mouse monoclonal (C-9) (sc-514302; Santa Cruz Biotechnology); anti-eIF2α mouse monoclonal (D-3) (sc-133132; Santa Cruz Biotechnology); anti-PP2A-Aα/β mouse monoclonal (4G7) (sc-13600; Santa Cruz Biotechnology); anti-p70 S6K α mouse monoclonal (H9) (sc-8418; Santa Cruz Biotechnology); anti-S6 mouse monoclonal (C8) (sc-74459; Santa Cruz Biotechnology); anti-Rheb mouse monoclonal (B12) (sc-271509; Santa Cruz Biotechnology); anti-Myc mouse monoclonal (9E10) (sc-40; Santa Cruz Biotechnology); anti-PP2A-Cα mouse monoclonal (46/PP2A; Catalytic a) (610555; BD Transduction Laboratories); anti-β-actin mouse monoclonal (6D1) (010-27841; Fujifilm Wako); anti-Flag mouse monoclonal (M2) antibody (F3165; Sigma-Aldrich).

Techniques: Comparison, Activation Assay

Figure 5. CANE abolishes autophagy in A549DR. (A) CANE was treated to A549DR cells for 24 h and autophagic protein levels detected such as LC-3, p62, Beclin-1, mTOR, ATG5 and ATG7. Densitometry analysis of the respective proteins was evaluated by Image J software, and results were normalized with b-actin with respect to controls. (B) For further confirmation, autophagic vacoule formation detected with the help of fluorogenic dye LysoTracker V R Red, DAPI was used as counter stain to stain nucleus. Acridine orange was used to detect the autopaghic vacoule formation. Image J software was used for quantification of oxidative stress. Images were taken at 40 magnification [scale bar¼ 0.1 mm]. Each value in the graph represents as the mean ± SD of three independent experiments. Values with different superscripts differ significantly from each other (p < .05).

Journal: Artificial cells, nanomedicine, and biotechnology

Article Title: Carvacrol nanoemulsion evokes cell cycle arrest, apoptosis induction and autophagy inhibition in doxorubicin resistant-A549 cell line.

doi: 10.1080/21691401.2018.1434187

Figure Lengend Snippet: Figure 5. CANE abolishes autophagy in A549DR. (A) CANE was treated to A549DR cells for 24 h and autophagic protein levels detected such as LC-3, p62, Beclin-1, mTOR, ATG5 and ATG7. Densitometry analysis of the respective proteins was evaluated by Image J software, and results were normalized with b-actin with respect to controls. (B) For further confirmation, autophagic vacoule formation detected with the help of fluorogenic dye LysoTracker V R Red, DAPI was used as counter stain to stain nucleus. Acridine orange was used to detect the autopaghic vacoule formation. Image J software was used for quantification of oxidative stress. Images were taken at 40 magnification [scale bar¼ 0.1 mm]. Each value in the graph represents as the mean ± SD of three independent experiments. Values with different superscripts differ significantly from each other (p < .05).

Article Snippet: Carvacrol, 3-Methyladenine (3-MA), N-acetyl-L-cysteine (NAC), primary antibodies against b-actin, JNK, p-JNK, caspase-3, caspase-9, Bax, Bcl2, cytochrome C, CDK2, CDK4, CDK6, Cyclin E, Cyclin D1, p21, LC-3, ATG5, ATG7, mTOR, p62, Beclin-1 as well as horseradish peroxidase (HRP)-conjugated secondary antibody were purchased from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA).

Techniques: Software, Staining

KIN17 positively regulates PI3K/AKT/mTOR expression in RCC and PF-04691502 can reverse the pathway protein expression and biological function. ( A ) Predict effects of KIN17 knockdown on the pathways of RCC cells (ACHN and 786–0) in vitro by kegg and GSEA. ( B ) p-mTOR, mTOR, p-AKT, AKT, p-PI3K and PI3K protein levels were measured by WB using the paired RCC cells (ACHN and 786–0) group and knockdown KIN17 group. ( C ) p-mTOR, mTOR, p-AKT, AKT, p-PI3K and PI3K protein levels were measured by WB using the paired RCC vector cells group (VE groups), overexpression KIN17 group (OE groups), VE groups + PF-04691502 and OE groups + PF-04691502. ( D ) N-cadherin and Vimentin protein levels were measured by WB using the paired RCC cells (ACHN and 786–0) in knockdown KIN17 group and different using PF-04691502 groups.

Journal: Scientific Reports

Article Title: KIN17 facilitates the initiation and progression of renal tumor progression through the PI3K-AKT-mTOR pathway

doi: 10.1038/s41598-026-35851-5

Figure Lengend Snippet: KIN17 positively regulates PI3K/AKT/mTOR expression in RCC and PF-04691502 can reverse the pathway protein expression and biological function. ( A ) Predict effects of KIN17 knockdown on the pathways of RCC cells (ACHN and 786–0) in vitro by kegg and GSEA. ( B ) p-mTOR, mTOR, p-AKT, AKT, p-PI3K and PI3K protein levels were measured by WB using the paired RCC cells (ACHN and 786–0) group and knockdown KIN17 group. ( C ) p-mTOR, mTOR, p-AKT, AKT, p-PI3K and PI3K protein levels were measured by WB using the paired RCC vector cells group (VE groups), overexpression KIN17 group (OE groups), VE groups + PF-04691502 and OE groups + PF-04691502. ( D ) N-cadherin and Vimentin protein levels were measured by WB using the paired RCC cells (ACHN and 786–0) in knockdown KIN17 group and different using PF-04691502 groups.

Article Snippet: The membranes were then blocked with 5% non-fat milk in TBS/Tween (0.05% Tween-20 in TBS) for 2 h. Membranes were incubated with primary antibodies including KIN17(Santa Cruz, Catalog number: sc-32768, 1:500), AKT (Proteintech, Catalog number: 60203–2-Ig, 1:10,000), mTOR (Proteintech, Catalog number: 66888–1-Ig, 1:10,000), PI3K(CST, Catalog number: 11889, 1:1000), p-AKT(CST, Catalog number: 4060S, 1:2000), p-mTOR(CST, Catalog number: 5536S, 1:1000), p-PI3K(CST, Catalog number: 17366S, 1:1000), N-cadherin (Proteintech, Catalog number: 22018–1-AP, 1:10,000), Vimentin (Proteintech, Catalog number: 10366–1-AP, 1:50,000) and GAPDH (Proteintech, 60,004–1-lg, 1:10,000) overnight at 4°C and then with secondary antibodies (anti-rabbit or anti- mouse; Proteintech) for room temperature.

Techniques: Expressing, Knockdown, In Vitro, Plasmid Preparation, Over Expression

KIN17 promotes tumor growth and suppression of tumor growth by PF-04691502 in vivo ( A ) Representative images of xenograft tumors 786–0 cells with expression of shNC and shKIN17 (n = 7 in each group). Tumor volume and tumor weight were analyzed. ( B ) Representative H&E staining and immunohistochemstry staining of Ki67, TUNEL, KIN17, p-mTOR and p-AKT in the xenograft tumor tissues (× 400 magnification). ( C ) Representative images of xenograft tumors 786–0 cells with expression of Vector, Vector + PF-04691502, OE and OE + PF-04691502 (n = 8 in each group). Tumor volume and tumor weight were analyzed. ( D ) Representative H&E staining and immunohistochemstry staining of Ki67, TUNEL, KIN17, p-mTOR and p-AKT in the xenograft tumor tissues (× 400 magnification). The error bars represent the mean ± SD of triplicate technical replicates. * P < 0.05, ** P < 0.01, ***P < 0.001.

Journal: Scientific Reports

Article Title: KIN17 facilitates the initiation and progression of renal tumor progression through the PI3K-AKT-mTOR pathway

doi: 10.1038/s41598-026-35851-5

Figure Lengend Snippet: KIN17 promotes tumor growth and suppression of tumor growth by PF-04691502 in vivo ( A ) Representative images of xenograft tumors 786–0 cells with expression of shNC and shKIN17 (n = 7 in each group). Tumor volume and tumor weight were analyzed. ( B ) Representative H&E staining and immunohistochemstry staining of Ki67, TUNEL, KIN17, p-mTOR and p-AKT in the xenograft tumor tissues (× 400 magnification). ( C ) Representative images of xenograft tumors 786–0 cells with expression of Vector, Vector + PF-04691502, OE and OE + PF-04691502 (n = 8 in each group). Tumor volume and tumor weight were analyzed. ( D ) Representative H&E staining and immunohistochemstry staining of Ki67, TUNEL, KIN17, p-mTOR and p-AKT in the xenograft tumor tissues (× 400 magnification). The error bars represent the mean ± SD of triplicate technical replicates. * P < 0.05, ** P < 0.01, ***P < 0.001.

Article Snippet: The membranes were then blocked with 5% non-fat milk in TBS/Tween (0.05% Tween-20 in TBS) for 2 h. Membranes were incubated with primary antibodies including KIN17(Santa Cruz, Catalog number: sc-32768, 1:500), AKT (Proteintech, Catalog number: 60203–2-Ig, 1:10,000), mTOR (Proteintech, Catalog number: 66888–1-Ig, 1:10,000), PI3K(CST, Catalog number: 11889, 1:1000), p-AKT(CST, Catalog number: 4060S, 1:2000), p-mTOR(CST, Catalog number: 5536S, 1:1000), p-PI3K(CST, Catalog number: 17366S, 1:1000), N-cadherin (Proteintech, Catalog number: 22018–1-AP, 1:10,000), Vimentin (Proteintech, Catalog number: 10366–1-AP, 1:50,000) and GAPDH (Proteintech, 60,004–1-lg, 1:10,000) overnight at 4°C and then with secondary antibodies (anti-rabbit or anti- mouse; Proteintech) for room temperature.

Techniques: In Vivo, Expressing, Staining, TUNEL Assay, Plasmid Preparation

SNCG induces ovarian cancer progression via activating the PI3K/AKT signaling pathway. a-b A phospho-kinase array kit was performed on protein lysates of SKOV3-sh1 and control cells. Thirteen proteins were obvious changes in their phosphorylation status and highlighted by boxes. c Western blot analysis of the levels of Akt, p-Akt (Sec473), p70S6 kinase, p-p70S6 kinase (Thr389), mTOR, and p-mTOR (Sec2448) in SKOV3 and HO-8901 PM cells transfected with SNCG-shRNA or Scr, and OVCAR3 cells transfected with SNCG-Ove or Ctrl. d Expression levels of Akt, p-Akt (Sec473), p70S6 kinase, p-p70S6 kinase (Thr389), mTOR, and p-mTOR (Sec2448) in cells transfected with SNCG shRNA, Scr, SNCG Ove, Ctrl, IGF-1, and DMSO were determined by Western blot. e Expression levels of Akt, p-Akt (Sec473), p70S6 kinase, p-p70S6 kinase (Thr389), mTOR, and p-mTOR (Sec2448) in cells transfected with SNCG shRNA, Scr, SNCG Ove, Ctrl, LY294002, and DMSO were determined by Western blot. f Wound healing assay (upper, original magnification × 40) and cell colony formation (lower) of cells transfected with SNCG shRNA, Scr, SNCG Ove, Ctrl, IGF-1, LY294002, and DMSO confirmed the effect of SNCG on the PI3K/AKT signaling pathway. ▲ , P < 0.05. *, P < 0.001. IGF-1: insulin-like growth factor 1; sh-SNCG: small hairpin RNAs of SNCG

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: SNCG promotes the progression and metastasis of high-grade serous ovarian cancer via targeting the PI3K/AKT signaling pathway

doi: 10.1186/s13046-020-01589-9

Figure Lengend Snippet: SNCG induces ovarian cancer progression via activating the PI3K/AKT signaling pathway. a-b A phospho-kinase array kit was performed on protein lysates of SKOV3-sh1 and control cells. Thirteen proteins were obvious changes in their phosphorylation status and highlighted by boxes. c Western blot analysis of the levels of Akt, p-Akt (Sec473), p70S6 kinase, p-p70S6 kinase (Thr389), mTOR, and p-mTOR (Sec2448) in SKOV3 and HO-8901 PM cells transfected with SNCG-shRNA or Scr, and OVCAR3 cells transfected with SNCG-Ove or Ctrl. d Expression levels of Akt, p-Akt (Sec473), p70S6 kinase, p-p70S6 kinase (Thr389), mTOR, and p-mTOR (Sec2448) in cells transfected with SNCG shRNA, Scr, SNCG Ove, Ctrl, IGF-1, and DMSO were determined by Western blot. e Expression levels of Akt, p-Akt (Sec473), p70S6 kinase, p-p70S6 kinase (Thr389), mTOR, and p-mTOR (Sec2448) in cells transfected with SNCG shRNA, Scr, SNCG Ove, Ctrl, LY294002, and DMSO were determined by Western blot. f Wound healing assay (upper, original magnification × 40) and cell colony formation (lower) of cells transfected with SNCG shRNA, Scr, SNCG Ove, Ctrl, IGF-1, LY294002, and DMSO confirmed the effect of SNCG on the PI3K/AKT signaling pathway. ▲ , P < 0.05. *, P < 0.001. IGF-1: insulin-like growth factor 1; sh-SNCG: small hairpin RNAs of SNCG

Article Snippet: Antibodies against mTOR (sc-517,464), p-mTOR (Sec2448, sc-293,133), p70S6 kinase (sc-8418), GAPDH (sc-47,724), β-Actin (sc-47,778), Cyclin D1 (sc-8396), MMP9 (sc-393,859, sc-21,733), Vimentin (sc-6260) were purchased from Santa Cruz (CA, USA).

Techniques: Control, Phospho-proteomics, Western Blot, Transfection, shRNA, Expressing, Wound Healing Assay

The schematic diagram summarizing the role of SNCG in promoting HGSOC progression. SNCG promotes the phosphorylation of AKT, mTOR, and p70S6K, which regulating the malignant behaviors in ovarian cancer cells

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: SNCG promotes the progression and metastasis of high-grade serous ovarian cancer via targeting the PI3K/AKT signaling pathway

doi: 10.1186/s13046-020-01589-9

Figure Lengend Snippet: The schematic diagram summarizing the role of SNCG in promoting HGSOC progression. SNCG promotes the phosphorylation of AKT, mTOR, and p70S6K, which regulating the malignant behaviors in ovarian cancer cells

Article Snippet: Antibodies against mTOR (sc-517,464), p-mTOR (Sec2448, sc-293,133), p70S6 kinase (sc-8418), GAPDH (sc-47,724), β-Actin (sc-47,778), Cyclin D1 (sc-8396), MMP9 (sc-393,859, sc-21,733), Vimentin (sc-6260) were purchased from Santa Cruz (CA, USA).

Techniques: Phospho-proteomics