phosphor akt ser473  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphor akt ser473
    Phosphor Akt Ser473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    phosphor akt ser473  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphor akt ser473
    Phosphor Akt Ser473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    akt1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc akt1
    K562 cells with or without ME2 knockdown were lysed with RIPA lysis buffer (50 mM Tris-HCl, pH 8.0, 150 mM NaCl, 1% Triton X-100, 1 mM EGTA) containing 1 mM PMSF and a protease inhibitor cocktail and subjected to centrifugation at 15,000× g for 10 min at 4°C to remove debris. After lysis, equal aliquots of protein lysate were resolved by Western blotting. Western blots were probed with anti-phospho-ERK1/2, anti-ERK1, anti-p-AKT308, anti-AKT472, <t>anti-AKT1/2,</t> anti-GATA-1, anti-vimentin and anti-β-tubulin. A, phospho-ERK1/2 activity in ME2 knockdown K562 cells. B, Phospho-AKT detection in ME2 knockdown K562 cells. C, 10 µM PI3K inhibitor, LY294002, inhibits p-AKT activity. D, LY294002 rescue of differentiation in ME2 knockdown K562 cells. E, The effect of LY294002 on the proliferation of K562 cells with or without ME2 knockdown. F, The expression difference of GATA-1 and vimentin in ME2 knockdown cells. Data are representative of three independent experiments.
    Akt1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Induction of Erythroid Differentiation in Human Erythroleukemia Cells by Depletion of Malic Enzyme 2"

    Article Title: Induction of Erythroid Differentiation in Human Erythroleukemia Cells by Depletion of Malic Enzyme 2

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0012520

    K562 cells with or without ME2 knockdown were lysed with RIPA lysis buffer (50 mM Tris-HCl, pH 8.0, 150 mM NaCl, 1% Triton X-100, 1 mM EGTA) containing 1 mM PMSF and a protease inhibitor cocktail and subjected to centrifugation at 15,000× g for 10 min at 4°C to remove debris. After lysis, equal aliquots of protein lysate were resolved by Western blotting. Western blots were probed with anti-phospho-ERK1/2, anti-ERK1, anti-p-AKT308, anti-AKT472, anti-AKT1/2, anti-GATA-1, anti-vimentin and anti-β-tubulin. A, phospho-ERK1/2 activity in ME2 knockdown K562 cells. B, Phospho-AKT detection in ME2 knockdown K562 cells. C, 10 µM PI3K inhibitor, LY294002, inhibits p-AKT activity. D, LY294002 rescue of differentiation in ME2 knockdown K562 cells. E, The effect of LY294002 on the proliferation of K562 cells with or without ME2 knockdown. F, The expression difference of GATA-1 and vimentin in ME2 knockdown cells. Data are representative of three independent experiments.
    Figure Legend Snippet: K562 cells with or without ME2 knockdown were lysed with RIPA lysis buffer (50 mM Tris-HCl, pH 8.0, 150 mM NaCl, 1% Triton X-100, 1 mM EGTA) containing 1 mM PMSF and a protease inhibitor cocktail and subjected to centrifugation at 15,000× g for 10 min at 4°C to remove debris. After lysis, equal aliquots of protein lysate were resolved by Western blotting. Western blots were probed with anti-phospho-ERK1/2, anti-ERK1, anti-p-AKT308, anti-AKT472, anti-AKT1/2, anti-GATA-1, anti-vimentin and anti-β-tubulin. A, phospho-ERK1/2 activity in ME2 knockdown K562 cells. B, Phospho-AKT detection in ME2 knockdown K562 cells. C, 10 µM PI3K inhibitor, LY294002, inhibits p-AKT activity. D, LY294002 rescue of differentiation in ME2 knockdown K562 cells. E, The effect of LY294002 on the proliferation of K562 cells with or without ME2 knockdown. F, The expression difference of GATA-1 and vimentin in ME2 knockdown cells. Data are representative of three independent experiments.

    Techniques Used: Lysis, Protease Inhibitor, Centrifugation, Western Blot, Activity Assay, Expressing

    akt1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc akt1
    Knock-down of AKT is synergistic with mTORC1/2 inhibition. (A) Knockdown of <t>AKT1</t> and AKT2 in Huh7 cells was confirmed by Western blot, HSC70 served as loading control. (B) Huh7 SCR and AKT1/2 knockdown cells were incubated with DMSO, 2 µM MK-2206, 100 nM AZD8055, or a combination of both over 72h. After 72h cells were trypsinized and counted, and the relative increase in cell number in given in the graph. The Experiments were performed in triplicates. Bars: SD; #, p < 0.01
    Akt1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Vertical Targeting of AKT and mTOR as Well as Dual Targeting of AKT and MEK Signaling Is Synergistic in Hepatocellular Carcinoma"

    Article Title: Vertical Targeting of AKT and mTOR as Well as Dual Targeting of AKT and MEK Signaling Is Synergistic in Hepatocellular Carcinoma

    Journal: Journal of Cancer

    doi: 10.7150/jca.12452

    Knock-down of AKT is synergistic with mTORC1/2 inhibition. (A) Knockdown of AKT1 and AKT2 in Huh7 cells was confirmed by Western blot, HSC70 served as loading control. (B) Huh7 SCR and AKT1/2 knockdown cells were incubated with DMSO, 2 µM MK-2206, 100 nM AZD8055, or a combination of both over 72h. After 72h cells were trypsinized and counted, and the relative increase in cell number in given in the graph. The Experiments were performed in triplicates. Bars: SD; #, p < 0.01
    Figure Legend Snippet: Knock-down of AKT is synergistic with mTORC1/2 inhibition. (A) Knockdown of AKT1 and AKT2 in Huh7 cells was confirmed by Western blot, HSC70 served as loading control. (B) Huh7 SCR and AKT1/2 knockdown cells were incubated with DMSO, 2 µM MK-2206, 100 nM AZD8055, or a combination of both over 72h. After 72h cells were trypsinized and counted, and the relative increase in cell number in given in the graph. The Experiments were performed in triplicates. Bars: SD; #, p < 0.01

    Techniques Used: Inhibition, Western Blot, Incubation

    pakt ser473  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc pakt ser473
    A – B ) Western blot analysis showed that CCl 4 reduced the phosphorylation of eNOS and AMPK, while ADP355 treatment significantly increased the phosphorylation of eNOS ser1177 and AMPK tyr172 residue. C ) Western blot and densitometric ratio of p-AKT <t>ser473/AKT,</t> * p <0.05 (N = 5 mice/cohort).
    Pakt Ser473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Adiponectin Agonist ADP355 Attenuates CCl 4 -Induced Liver Fibrosis in Mice"

    Article Title: Adiponectin Agonist ADP355 Attenuates CCl 4 -Induced Liver Fibrosis in Mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0110405

    A – B ) Western blot analysis showed that CCl 4 reduced the phosphorylation of eNOS and AMPK, while ADP355 treatment significantly increased the phosphorylation of eNOS ser1177 and AMPK tyr172 residue. C ) Western blot and densitometric ratio of p-AKT ser473/AKT, * p <0.05 (N = 5 mice/cohort).
    Figure Legend Snippet: A – B ) Western blot analysis showed that CCl 4 reduced the phosphorylation of eNOS and AMPK, while ADP355 treatment significantly increased the phosphorylation of eNOS ser1177 and AMPK tyr172 residue. C ) Western blot and densitometric ratio of p-AKT ser473/AKT, * p <0.05 (N = 5 mice/cohort).

    Techniques Used: Western Blot

    ser 473  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ser 473
    Ser 473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    akt t akt  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc akt t akt
    (A) The rMC-1 cells were treated with 400 µM H 2 O 2 in the presence of 1 µM SERPINA3K, 250 nM U73122 (PLC inhibitor), 10 µM U0126 (ERK inhibitor), 100 nM Wortmannin (PI3K inhibitor) or 10 µM BAPTA. BSA (1 µM) was used as negative control. Intracellular [Ca 2+ ] was measured using the fluorescence of the probe Fluo-4/AM at different intervals of the treatment (mean±SEM, n = 6). (B) The protective effects of the inhibitors and 1 µM SERPINA3K against the H 2 O 2 -induced cell death with or without 10 µM m-3M3FBS (PLC activator) were quantified by the MTT assay after exposure to H 2 O 2 for 8 h (mean±SEM, n = 3). (C) The rMC-1 cells were treated with 400 µM H 2 O 2 . The cells were harvested at different time points for Western blotting. (D) The cells were exposed to H 2 O 2 for 15 min in the presence of 1 µM SERPINA3K or BSA. The phosphorylated PLC-γ1 (p-PLC), ERK1/2 (p-ERK) and <t>Akt</t> (p-AKT) were blotted with phosphorylation-specific antibodies. The total PLC-γ1 (t-PLC), ERK1/2 (t-ERK) and <t>Akt</t> <t>(t-AKT)</t> were blotted with antibodies for total proteins. (E) Protein levels was quantified using densitometry of the Western blotting results (mean±SEM, n = 3). (F) The reduced phosphorylation level of each kinase was shown as percentages of the maximum phosphorylation levels at 15 min exposure (mean±SEM, n = 3). $ P<0.01, under H 2 O 2 exposure from 1.5 h to 4 h; the U73122 and SERPINA3K-treated cells versus the BSA-treated cells. * P<0.01, versus control cells. # P<0.01, the cells treated with H 2 O 2 , m-3M3FBS and SERPINA3K versus the cells treated with H 2 O 2 and SERPINA3K. & P<0.01, versus control cells exposed to H 2 O 2 for 0 min.
    Akt T Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "SERPINA3K Prevents Oxidative Stress Induced Necrotic Cell Death by Inhibiting Calcium Overload"

    Article Title: SERPINA3K Prevents Oxidative Stress Induced Necrotic Cell Death by Inhibiting Calcium Overload

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0004077

    (A) The rMC-1 cells were treated with 400 µM H 2 O 2 in the presence of 1 µM SERPINA3K, 250 nM U73122 (PLC inhibitor), 10 µM U0126 (ERK inhibitor), 100 nM Wortmannin (PI3K inhibitor) or 10 µM BAPTA. BSA (1 µM) was used as negative control. Intracellular [Ca 2+ ] was measured using the fluorescence of the probe Fluo-4/AM at different intervals of the treatment (mean±SEM, n = 6). (B) The protective effects of the inhibitors and 1 µM SERPINA3K against the H 2 O 2 -induced cell death with or without 10 µM m-3M3FBS (PLC activator) were quantified by the MTT assay after exposure to H 2 O 2 for 8 h (mean±SEM, n = 3). (C) The rMC-1 cells were treated with 400 µM H 2 O 2 . The cells were harvested at different time points for Western blotting. (D) The cells were exposed to H 2 O 2 for 15 min in the presence of 1 µM SERPINA3K or BSA. The phosphorylated PLC-γ1 (p-PLC), ERK1/2 (p-ERK) and Akt (p-AKT) were blotted with phosphorylation-specific antibodies. The total PLC-γ1 (t-PLC), ERK1/2 (t-ERK) and Akt (t-AKT) were blotted with antibodies for total proteins. (E) Protein levels was quantified using densitometry of the Western blotting results (mean±SEM, n = 3). (F) The reduced phosphorylation level of each kinase was shown as percentages of the maximum phosphorylation levels at 15 min exposure (mean±SEM, n = 3). $ P<0.01, under H 2 O 2 exposure from 1.5 h to 4 h; the U73122 and SERPINA3K-treated cells versus the BSA-treated cells. * P<0.01, versus control cells. # P<0.01, the cells treated with H 2 O 2 , m-3M3FBS and SERPINA3K versus the cells treated with H 2 O 2 and SERPINA3K. & P<0.01, versus control cells exposed to H 2 O 2 for 0 min.
    Figure Legend Snippet: (A) The rMC-1 cells were treated with 400 µM H 2 O 2 in the presence of 1 µM SERPINA3K, 250 nM U73122 (PLC inhibitor), 10 µM U0126 (ERK inhibitor), 100 nM Wortmannin (PI3K inhibitor) or 10 µM BAPTA. BSA (1 µM) was used as negative control. Intracellular [Ca 2+ ] was measured using the fluorescence of the probe Fluo-4/AM at different intervals of the treatment (mean±SEM, n = 6). (B) The protective effects of the inhibitors and 1 µM SERPINA3K against the H 2 O 2 -induced cell death with or without 10 µM m-3M3FBS (PLC activator) were quantified by the MTT assay after exposure to H 2 O 2 for 8 h (mean±SEM, n = 3). (C) The rMC-1 cells were treated with 400 µM H 2 O 2 . The cells were harvested at different time points for Western blotting. (D) The cells were exposed to H 2 O 2 for 15 min in the presence of 1 µM SERPINA3K or BSA. The phosphorylated PLC-γ1 (p-PLC), ERK1/2 (p-ERK) and Akt (p-AKT) were blotted with phosphorylation-specific antibodies. The total PLC-γ1 (t-PLC), ERK1/2 (t-ERK) and Akt (t-AKT) were blotted with antibodies for total proteins. (E) Protein levels was quantified using densitometry of the Western blotting results (mean±SEM, n = 3). (F) The reduced phosphorylation level of each kinase was shown as percentages of the maximum phosphorylation levels at 15 min exposure (mean±SEM, n = 3). $ P<0.01, under H 2 O 2 exposure from 1.5 h to 4 h; the U73122 and SERPINA3K-treated cells versus the BSA-treated cells. * P<0.01, versus control cells. # P<0.01, the cells treated with H 2 O 2 , m-3M3FBS and SERPINA3K versus the cells treated with H 2 O 2 and SERPINA3K. & P<0.01, versus control cells exposed to H 2 O 2 for 0 min.

    Techniques Used: Negative Control, Fluorescence, MTT Assay, Western Blot

    anti akt phospho ser473  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti akt phospho ser473
    Anti Akt Phospho Ser473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti pakt ser473 antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti pakt ser473 antibody
    Anti Pakt Ser473 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    phosphorylated akt ser473  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated akt ser473
    Phosphorylated Akt Ser473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    p ser473 akt  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p ser473 akt
    List of Antibodies and Relative Dilutions Used in Western Blot and Immunocytochemistry Experiments
    P Ser473 Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "TM6SF2/PNPLA3/MBOAT7 Loss-of-Function Genetic Variants Impact on NAFLD Development and Progression Both in Patients and in In Vitro Models"

    Article Title: TM6SF2/PNPLA3/MBOAT7 Loss-of-Function Genetic Variants Impact on NAFLD Development and Progression Both in Patients and in In Vitro Models

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    doi: 10.1016/j.jcmgh.2021.11.007

    List of Antibodies and Relative Dilutions Used in Western Blot and Immunocytochemistry Experiments
    Figure Legend Snippet: List of Antibodies and Relative Dilutions Used in Western Blot and Immunocytochemistry Experiments

    Techniques Used: Western Blot, Immunocytochemistry

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    Cell Signaling Technology Inc phosphor akt ser473
    Phosphor Akt Ser473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc akt1
    K562 cells with or without ME2 knockdown were lysed with RIPA lysis buffer (50 mM Tris-HCl, pH 8.0, 150 mM NaCl, 1% Triton X-100, 1 mM EGTA) containing 1 mM PMSF and a protease inhibitor cocktail and subjected to centrifugation at 15,000× g for 10 min at 4°C to remove debris. After lysis, equal aliquots of protein lysate were resolved by Western blotting. Western blots were probed with anti-phospho-ERK1/2, anti-ERK1, anti-p-AKT308, anti-AKT472, <t>anti-AKT1/2,</t> anti-GATA-1, anti-vimentin and anti-β-tubulin. A, phospho-ERK1/2 activity in ME2 knockdown K562 cells. B, Phospho-AKT detection in ME2 knockdown K562 cells. C, 10 µM PI3K inhibitor, LY294002, inhibits p-AKT activity. D, LY294002 rescue of differentiation in ME2 knockdown K562 cells. E, The effect of LY294002 on the proliferation of K562 cells with or without ME2 knockdown. F, The expression difference of GATA-1 and vimentin in ME2 knockdown cells. Data are representative of three independent experiments.
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    Cell Signaling Technology Inc pakt ser473
    A – B ) Western blot analysis showed that CCl 4 reduced the phosphorylation of eNOS and AMPK, while ADP355 treatment significantly increased the phosphorylation of eNOS ser1177 and AMPK tyr172 residue. C ) Western blot and densitometric ratio of p-AKT <t>ser473/AKT,</t> * p <0.05 (N = 5 mice/cohort).
    Pakt Ser473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc ser 473
    A – B ) Western blot analysis showed that CCl 4 reduced the phosphorylation of eNOS and AMPK, while ADP355 treatment significantly increased the phosphorylation of eNOS ser1177 and AMPK tyr172 residue. C ) Western blot and densitometric ratio of p-AKT <t>ser473/AKT,</t> * p <0.05 (N = 5 mice/cohort).
    Ser 473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc akt t akt
    (A) The rMC-1 cells were treated with 400 µM H 2 O 2 in the presence of 1 µM SERPINA3K, 250 nM U73122 (PLC inhibitor), 10 µM U0126 (ERK inhibitor), 100 nM Wortmannin (PI3K inhibitor) or 10 µM BAPTA. BSA (1 µM) was used as negative control. Intracellular [Ca 2+ ] was measured using the fluorescence of the probe Fluo-4/AM at different intervals of the treatment (mean±SEM, n = 6). (B) The protective effects of the inhibitors and 1 µM SERPINA3K against the H 2 O 2 -induced cell death with or without 10 µM m-3M3FBS (PLC activator) were quantified by the MTT assay after exposure to H 2 O 2 for 8 h (mean±SEM, n = 3). (C) The rMC-1 cells were treated with 400 µM H 2 O 2 . The cells were harvested at different time points for Western blotting. (D) The cells were exposed to H 2 O 2 for 15 min in the presence of 1 µM SERPINA3K or BSA. The phosphorylated PLC-γ1 (p-PLC), ERK1/2 (p-ERK) and <t>Akt</t> (p-AKT) were blotted with phosphorylation-specific antibodies. The total PLC-γ1 (t-PLC), ERK1/2 (t-ERK) and <t>Akt</t> <t>(t-AKT)</t> were blotted with antibodies for total proteins. (E) Protein levels was quantified using densitometry of the Western blotting results (mean±SEM, n = 3). (F) The reduced phosphorylation level of each kinase was shown as percentages of the maximum phosphorylation levels at 15 min exposure (mean±SEM, n = 3). $ P<0.01, under H 2 O 2 exposure from 1.5 h to 4 h; the U73122 and SERPINA3K-treated cells versus the BSA-treated cells. * P<0.01, versus control cells. # P<0.01, the cells treated with H 2 O 2 , m-3M3FBS and SERPINA3K versus the cells treated with H 2 O 2 and SERPINA3K. & P<0.01, versus control cells exposed to H 2 O 2 for 0 min.
    Akt T Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti akt phospho ser473
    (A) The rMC-1 cells were treated with 400 µM H 2 O 2 in the presence of 1 µM SERPINA3K, 250 nM U73122 (PLC inhibitor), 10 µM U0126 (ERK inhibitor), 100 nM Wortmannin (PI3K inhibitor) or 10 µM BAPTA. BSA (1 µM) was used as negative control. Intracellular [Ca 2+ ] was measured using the fluorescence of the probe Fluo-4/AM at different intervals of the treatment (mean±SEM, n = 6). (B) The protective effects of the inhibitors and 1 µM SERPINA3K against the H 2 O 2 -induced cell death with or without 10 µM m-3M3FBS (PLC activator) were quantified by the MTT assay after exposure to H 2 O 2 for 8 h (mean±SEM, n = 3). (C) The rMC-1 cells were treated with 400 µM H 2 O 2 . The cells were harvested at different time points for Western blotting. (D) The cells were exposed to H 2 O 2 for 15 min in the presence of 1 µM SERPINA3K or BSA. The phosphorylated PLC-γ1 (p-PLC), ERK1/2 (p-ERK) and <t>Akt</t> (p-AKT) were blotted with phosphorylation-specific antibodies. The total PLC-γ1 (t-PLC), ERK1/2 (t-ERK) and <t>Akt</t> <t>(t-AKT)</t> were blotted with antibodies for total proteins. (E) Protein levels was quantified using densitometry of the Western blotting results (mean±SEM, n = 3). (F) The reduced phosphorylation level of each kinase was shown as percentages of the maximum phosphorylation levels at 15 min exposure (mean±SEM, n = 3). $ P<0.01, under H 2 O 2 exposure from 1.5 h to 4 h; the U73122 and SERPINA3K-treated cells versus the BSA-treated cells. * P<0.01, versus control cells. # P<0.01, the cells treated with H 2 O 2 , m-3M3FBS and SERPINA3K versus the cells treated with H 2 O 2 and SERPINA3K. & P<0.01, versus control cells exposed to H 2 O 2 for 0 min.
    Anti Akt Phospho Ser473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti pakt ser473 antibody
    (A) The rMC-1 cells were treated with 400 µM H 2 O 2 in the presence of 1 µM SERPINA3K, 250 nM U73122 (PLC inhibitor), 10 µM U0126 (ERK inhibitor), 100 nM Wortmannin (PI3K inhibitor) or 10 µM BAPTA. BSA (1 µM) was used as negative control. Intracellular [Ca 2+ ] was measured using the fluorescence of the probe Fluo-4/AM at different intervals of the treatment (mean±SEM, n = 6). (B) The protective effects of the inhibitors and 1 µM SERPINA3K against the H 2 O 2 -induced cell death with or without 10 µM m-3M3FBS (PLC activator) were quantified by the MTT assay after exposure to H 2 O 2 for 8 h (mean±SEM, n = 3). (C) The rMC-1 cells were treated with 400 µM H 2 O 2 . The cells were harvested at different time points for Western blotting. (D) The cells were exposed to H 2 O 2 for 15 min in the presence of 1 µM SERPINA3K or BSA. The phosphorylated PLC-γ1 (p-PLC), ERK1/2 (p-ERK) and <t>Akt</t> (p-AKT) were blotted with phosphorylation-specific antibodies. The total PLC-γ1 (t-PLC), ERK1/2 (t-ERK) and <t>Akt</t> <t>(t-AKT)</t> were blotted with antibodies for total proteins. (E) Protein levels was quantified using densitometry of the Western blotting results (mean±SEM, n = 3). (F) The reduced phosphorylation level of each kinase was shown as percentages of the maximum phosphorylation levels at 15 min exposure (mean±SEM, n = 3). $ P<0.01, under H 2 O 2 exposure from 1.5 h to 4 h; the U73122 and SERPINA3K-treated cells versus the BSA-treated cells. * P<0.01, versus control cells. # P<0.01, the cells treated with H 2 O 2 , m-3M3FBS and SERPINA3K versus the cells treated with H 2 O 2 and SERPINA3K. & P<0.01, versus control cells exposed to H 2 O 2 for 0 min.
    Anti Pakt Ser473 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti pakt ser473 antibody - by Bioz Stars, 2023-01
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    Cell Signaling Technology Inc phosphorylated akt ser473
    (A) The rMC-1 cells were treated with 400 µM H 2 O 2 in the presence of 1 µM SERPINA3K, 250 nM U73122 (PLC inhibitor), 10 µM U0126 (ERK inhibitor), 100 nM Wortmannin (PI3K inhibitor) or 10 µM BAPTA. BSA (1 µM) was used as negative control. Intracellular [Ca 2+ ] was measured using the fluorescence of the probe Fluo-4/AM at different intervals of the treatment (mean±SEM, n = 6). (B) The protective effects of the inhibitors and 1 µM SERPINA3K against the H 2 O 2 -induced cell death with or without 10 µM m-3M3FBS (PLC activator) were quantified by the MTT assay after exposure to H 2 O 2 for 8 h (mean±SEM, n = 3). (C) The rMC-1 cells were treated with 400 µM H 2 O 2 . The cells were harvested at different time points for Western blotting. (D) The cells were exposed to H 2 O 2 for 15 min in the presence of 1 µM SERPINA3K or BSA. The phosphorylated PLC-γ1 (p-PLC), ERK1/2 (p-ERK) and <t>Akt</t> (p-AKT) were blotted with phosphorylation-specific antibodies. The total PLC-γ1 (t-PLC), ERK1/2 (t-ERK) and <t>Akt</t> <t>(t-AKT)</t> were blotted with antibodies for total proteins. (E) Protein levels was quantified using densitometry of the Western blotting results (mean±SEM, n = 3). (F) The reduced phosphorylation level of each kinase was shown as percentages of the maximum phosphorylation levels at 15 min exposure (mean±SEM, n = 3). $ P<0.01, under H 2 O 2 exposure from 1.5 h to 4 h; the U73122 and SERPINA3K-treated cells versus the BSA-treated cells. * P<0.01, versus control cells. # P<0.01, the cells treated with H 2 O 2 , m-3M3FBS and SERPINA3K versus the cells treated with H 2 O 2 and SERPINA3K. & P<0.01, versus control cells exposed to H 2 O 2 for 0 min.
    Phosphorylated Akt Ser473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc p ser473 akt
    List of Antibodies and Relative Dilutions Used in Western Blot and Immunocytochemistry Experiments
    P Ser473 Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    K562 cells with or without ME2 knockdown were lysed with RIPA lysis buffer (50 mM Tris-HCl, pH 8.0, 150 mM NaCl, 1% Triton X-100, 1 mM EGTA) containing 1 mM PMSF and a protease inhibitor cocktail and subjected to centrifugation at 15,000× g for 10 min at 4°C to remove debris. After lysis, equal aliquots of protein lysate were resolved by Western blotting. Western blots were probed with anti-phospho-ERK1/2, anti-ERK1, anti-p-AKT308, anti-AKT472, anti-AKT1/2, anti-GATA-1, anti-vimentin and anti-β-tubulin. A, phospho-ERK1/2 activity in ME2 knockdown K562 cells. B, Phospho-AKT detection in ME2 knockdown K562 cells. C, 10 µM PI3K inhibitor, LY294002, inhibits p-AKT activity. D, LY294002 rescue of differentiation in ME2 knockdown K562 cells. E, The effect of LY294002 on the proliferation of K562 cells with or without ME2 knockdown. F, The expression difference of GATA-1 and vimentin in ME2 knockdown cells. Data are representative of three independent experiments.

    Journal: PLoS ONE

    Article Title: Induction of Erythroid Differentiation in Human Erythroleukemia Cells by Depletion of Malic Enzyme 2

    doi: 10.1371/journal.pone.0012520

    Figure Lengend Snippet: K562 cells with or without ME2 knockdown were lysed with RIPA lysis buffer (50 mM Tris-HCl, pH 8.0, 150 mM NaCl, 1% Triton X-100, 1 mM EGTA) containing 1 mM PMSF and a protease inhibitor cocktail and subjected to centrifugation at 15,000× g for 10 min at 4°C to remove debris. After lysis, equal aliquots of protein lysate were resolved by Western blotting. Western blots were probed with anti-phospho-ERK1/2, anti-ERK1, anti-p-AKT308, anti-AKT472, anti-AKT1/2, anti-GATA-1, anti-vimentin and anti-β-tubulin. A, phospho-ERK1/2 activity in ME2 knockdown K562 cells. B, Phospho-AKT detection in ME2 knockdown K562 cells. C, 10 µM PI3K inhibitor, LY294002, inhibits p-AKT activity. D, LY294002 rescue of differentiation in ME2 knockdown K562 cells. E, The effect of LY294002 on the proliferation of K562 cells with or without ME2 knockdown. F, The expression difference of GATA-1 and vimentin in ME2 knockdown cells. Data are representative of three independent experiments.

    Article Snippet: The anti-GATA-1, phospho-ERK1/2, phospho-AKT308, phospho-AKT473 and AKT1/2 polyclonal antibodies were purchased from Cell Signaling Technology.

    Techniques: Lysis, Protease Inhibitor, Centrifugation, Western Blot, Activity Assay, Expressing

    A – B ) Western blot analysis showed that CCl 4 reduced the phosphorylation of eNOS and AMPK, while ADP355 treatment significantly increased the phosphorylation of eNOS ser1177 and AMPK tyr172 residue. C ) Western blot and densitometric ratio of p-AKT ser473/AKT, * p <0.05 (N = 5 mice/cohort).

    Journal: PLoS ONE

    Article Title: Adiponectin Agonist ADP355 Attenuates CCl 4 -Induced Liver Fibrosis in Mice

    doi: 10.1371/journal.pone.0110405

    Figure Lengend Snippet: A – B ) Western blot analysis showed that CCl 4 reduced the phosphorylation of eNOS and AMPK, while ADP355 treatment significantly increased the phosphorylation of eNOS ser1177 and AMPK tyr172 residue. C ) Western blot and densitometric ratio of p-AKT ser473/AKT, * p <0.05 (N = 5 mice/cohort).

    Article Snippet: The primary antibodies were purchased from following manufacturer; CTGF, TGF-β1and MMP13 (Santa Cruz Biotechnology, Dallas, Texas); p-AMPKα tyr172, AMPKα, p-eNOS ser1177, eNOS, pAKT ser473 and AKT (Cell Signaling, Beverly, MA); anti-actin, α-SMA and anti-desmin (Sigma-Aldrich, St. Louis, MO); anti-mTIMP1 (R&D Systems, Minneapolis, MN).

    Techniques: Western Blot

    (A) The rMC-1 cells were treated with 400 µM H 2 O 2 in the presence of 1 µM SERPINA3K, 250 nM U73122 (PLC inhibitor), 10 µM U0126 (ERK inhibitor), 100 nM Wortmannin (PI3K inhibitor) or 10 µM BAPTA. BSA (1 µM) was used as negative control. Intracellular [Ca 2+ ] was measured using the fluorescence of the probe Fluo-4/AM at different intervals of the treatment (mean±SEM, n = 6). (B) The protective effects of the inhibitors and 1 µM SERPINA3K against the H 2 O 2 -induced cell death with or without 10 µM m-3M3FBS (PLC activator) were quantified by the MTT assay after exposure to H 2 O 2 for 8 h (mean±SEM, n = 3). (C) The rMC-1 cells were treated with 400 µM H 2 O 2 . The cells were harvested at different time points for Western blotting. (D) The cells were exposed to H 2 O 2 for 15 min in the presence of 1 µM SERPINA3K or BSA. The phosphorylated PLC-γ1 (p-PLC), ERK1/2 (p-ERK) and Akt (p-AKT) were blotted with phosphorylation-specific antibodies. The total PLC-γ1 (t-PLC), ERK1/2 (t-ERK) and Akt (t-AKT) were blotted with antibodies for total proteins. (E) Protein levels was quantified using densitometry of the Western blotting results (mean±SEM, n = 3). (F) The reduced phosphorylation level of each kinase was shown as percentages of the maximum phosphorylation levels at 15 min exposure (mean±SEM, n = 3). $ P<0.01, under H 2 O 2 exposure from 1.5 h to 4 h; the U73122 and SERPINA3K-treated cells versus the BSA-treated cells. * P<0.01, versus control cells. # P<0.01, the cells treated with H 2 O 2 , m-3M3FBS and SERPINA3K versus the cells treated with H 2 O 2 and SERPINA3K. & P<0.01, versus control cells exposed to H 2 O 2 for 0 min.

    Journal: PLoS ONE

    Article Title: SERPINA3K Prevents Oxidative Stress Induced Necrotic Cell Death by Inhibiting Calcium Overload

    doi: 10.1371/journal.pone.0004077

    Figure Lengend Snippet: (A) The rMC-1 cells were treated with 400 µM H 2 O 2 in the presence of 1 µM SERPINA3K, 250 nM U73122 (PLC inhibitor), 10 µM U0126 (ERK inhibitor), 100 nM Wortmannin (PI3K inhibitor) or 10 µM BAPTA. BSA (1 µM) was used as negative control. Intracellular [Ca 2+ ] was measured using the fluorescence of the probe Fluo-4/AM at different intervals of the treatment (mean±SEM, n = 6). (B) The protective effects of the inhibitors and 1 µM SERPINA3K against the H 2 O 2 -induced cell death with or without 10 µM m-3M3FBS (PLC activator) were quantified by the MTT assay after exposure to H 2 O 2 for 8 h (mean±SEM, n = 3). (C) The rMC-1 cells were treated with 400 µM H 2 O 2 . The cells were harvested at different time points for Western blotting. (D) The cells were exposed to H 2 O 2 for 15 min in the presence of 1 µM SERPINA3K or BSA. The phosphorylated PLC-γ1 (p-PLC), ERK1/2 (p-ERK) and Akt (p-AKT) were blotted with phosphorylation-specific antibodies. The total PLC-γ1 (t-PLC), ERK1/2 (t-ERK) and Akt (t-AKT) were blotted with antibodies for total proteins. (E) Protein levels was quantified using densitometry of the Western blotting results (mean±SEM, n = 3). (F) The reduced phosphorylation level of each kinase was shown as percentages of the maximum phosphorylation levels at 15 min exposure (mean±SEM, n = 3). $ P<0.01, under H 2 O 2 exposure from 1.5 h to 4 h; the U73122 and SERPINA3K-treated cells versus the BSA-treated cells. * P<0.01, versus control cells. # P<0.01, the cells treated with H 2 O 2 , m-3M3FBS and SERPINA3K versus the cells treated with H 2 O 2 and SERPINA3K. & P<0.01, versus control cells exposed to H 2 O 2 for 0 min.

    Article Snippet: Antibodies for PLCγ1 (t-PLC), phosphorylated PLCγ1 at Tyr783 (p-PLC), ERK1/2 (t-ERK), phosphorylated ERK1/2 at Thr202 and Tyr204 (p-ERK), Akt (t-AKT) and phosphorylated Akt at Ser473 (p-AKT) were purchased from Cell Signaling (Danvers, MA) and used at the 1∶1000 dilution.

    Techniques: Negative Control, Fluorescence, MTT Assay, Western Blot

    List of Antibodies and Relative Dilutions Used in Western Blot and Immunocytochemistry Experiments

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: TM6SF2/PNPLA3/MBOAT7 Loss-of-Function Genetic Variants Impact on NAFLD Development and Progression Both in Patients and in In Vitro Models

    doi: 10.1016/j.jcmgh.2021.11.007

    Figure Lengend Snippet: List of Antibodies and Relative Dilutions Used in Western Blot and Immunocytochemistry Experiments

    Article Snippet: Anti–P-Ser473 Akt, Akt, P(Thr37/46)-4E-BP1, 4E-BP1, P(Ser2448)-mTOR, and mTOR antibodies were acquired from Cell Signaling Technology (Danvers, MA).

    Techniques: Western Blot, Immunocytochemistry