erk1 erk2 Search Results


erk1 2  (MedChemExpress)
96
MedChemExpress erk1 2
<t>Inhibiting</t> <t>ERK1/2</t> signaling decreased the effect of DHA against oxidative stress. AML12 cells were pre-treated with DHA (50 μM) and TUG891 (10 μM) for 12 h, and then treated with H 2 O 2 (400 μM) for another 2 h. ( A ) The protein expression of ERK1/2, P-ERK1/2, AMPK, and P-AMPK was determined by Western-blotting. ( B ) The protein expression of ERK1/2 and P-ERK1/2 in AML12 cells after treated with U0126. ( C ) Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12h followed with H 2 O 2 (400 μM) 2h challenge. Cellular ROS was stained with DCFH-DA fluorescent probe and detected by Flow cytometry. ( D ) The cell viability of AML12 cells. All data were expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).
Erk1 2, supplied by MedChemExpress, 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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phospho erk1  (R&D Systems)
93
R&D Systems phospho erk1
<t>Inhibiting</t> <t>ERK1/2</t> signaling decreased the effect of DHA against oxidative stress. AML12 cells were pre-treated with DHA (50 μM) and TUG891 (10 μM) for 12 h, and then treated with H 2 O 2 (400 μM) for another 2 h. ( A ) The protein expression of ERK1/2, P-ERK1/2, AMPK, and P-AMPK was determined by Western-blotting. ( B ) The protein expression of ERK1/2 and P-ERK1/2 in AML12 cells after treated with U0126. ( C ) Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12h followed with H 2 O 2 (400 μM) 2h challenge. Cellular ROS was stained with DCFH-DA fluorescent probe and detected by Flow cytometry. ( D ) The cell viability of AML12 cells. All data were expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).
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dyc1018b  (R&D Systems)
94
R&D Systems dyc1018b
<t>Inhibiting</t> <t>ERK1/2</t> signaling decreased the effect of DHA against oxidative stress. AML12 cells were pre-treated with DHA (50 μM) and TUG891 (10 μM) for 12 h, and then treated with H 2 O 2 (400 μM) for another 2 h. ( A ) The protein expression of ERK1/2, P-ERK1/2, AMPK, and P-AMPK was determined by Western-blotting. ( B ) The protein expression of ERK1/2 and P-ERK1/2 in AML12 cells after treated with U0126. ( C ) Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12h followed with H 2 O 2 (400 μM) 2h challenge. Cellular ROS was stained with DCFH-DA fluorescent probe and detected by Flow cytometry. ( D ) The cell viability of AML12 cells. All data were expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).
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anti erk1 erk2  (R&D Systems)
93
R&D Systems anti erk1 erk2
<t>Inhibiting</t> <t>ERK1/2</t> signaling decreased the effect of DHA against oxidative stress. AML12 cells were pre-treated with DHA (50 μM) and TUG891 (10 μM) for 12 h, and then treated with H 2 O 2 (400 μM) for another 2 h. ( A ) The protein expression of ERK1/2, P-ERK1/2, AMPK, and P-AMPK was determined by Western-blotting. ( B ) The protein expression of ERK1/2 and P-ERK1/2 in AML12 cells after treated with U0126. ( C ) Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12h followed with H 2 O 2 (400 μM) 2h challenge. Cellular ROS was stained with DCFH-DA fluorescent probe and detected by Flow cytometry. ( D ) The cell viability of AML12 cells. All data were expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).
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p erk1 erk2  (R&D Systems)
90
R&D Systems p erk1 erk2
<t>Inhibiting</t> <t>ERK1/2</t> signaling decreased the effect of DHA against oxidative stress. AML12 cells were pre-treated with DHA (50 μM) and TUG891 (10 μM) for 12 h, and then treated with H 2 O 2 (400 μM) for another 2 h. ( A ) The protein expression of ERK1/2, P-ERK1/2, AMPK, and P-AMPK was determined by Western-blotting. ( B ) The protein expression of ERK1/2 and P-ERK1/2 in AML12 cells after treated with U0126. ( C ) Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12h followed with H 2 O 2 (400 μM) 2h challenge. Cellular ROS was stained with DCFH-DA fluorescent probe and detected by Flow cytometry. ( D ) The cell viability of AML12 cells. All data were expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).
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rabbit monoclonal  (Danaher Inc)
99
Danaher Inc rabbit monoclonal
<t>Inhibiting</t> <t>ERK1/2</t> signaling decreased the effect of DHA against oxidative stress. AML12 cells were pre-treated with DHA (50 μM) and TUG891 (10 μM) for 12 h, and then treated with H 2 O 2 (400 μM) for another 2 h. ( A ) The protein expression of ERK1/2, P-ERK1/2, AMPK, and P-AMPK was determined by Western-blotting. ( B ) The protein expression of ERK1/2 and P-ERK1/2 in AML12 cells after treated with U0126. ( C ) Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12h followed with H 2 O 2 (400 μM) 2h challenge. Cellular ROS was stained with DCFH-DA fluorescent probe and detected by Flow cytometry. ( D ) The cell viability of AML12 cells. All data were expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).
Rabbit Monoclonal, supplied by Danaher 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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mouse anti phospho erk1 2 tyr204 tyr187 igg  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc mouse anti phospho erk1 2 tyr204 tyr187 igg
<t>Inhibiting</t> <t>ERK1/2</t> signaling decreased the effect of DHA against oxidative stress. AML12 cells were pre-treated with DHA (50 μM) and TUG891 (10 μM) for 12 h, and then treated with H 2 O 2 (400 μM) for another 2 h. ( A ) The protein expression of ERK1/2, P-ERK1/2, AMPK, and P-AMPK was determined by Western-blotting. ( B ) The protein expression of ERK1/2 and P-ERK1/2 in AML12 cells after treated with U0126. ( C ) Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12h followed with H 2 O 2 (400 μM) 2h challenge. Cellular ROS was stained with DCFH-DA fluorescent probe and detected by Flow cytometry. ( D ) The cell viability of AML12 cells. All data were expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).
Mouse Anti Phospho Erk1 2 Tyr204 Tyr187 Igg, 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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erk  (Proteintech)
96
Proteintech erk
<t>Inhibiting</t> <t>ERK1/2</t> signaling decreased the effect of DHA against oxidative stress. AML12 cells were pre-treated with DHA (50 μM) and TUG891 (10 μM) for 12 h, and then treated with H 2 O 2 (400 μM) for another 2 h. ( A ) The protein expression of ERK1/2, P-ERK1/2, AMPK, and P-AMPK was determined by Western-blotting. ( B ) The protein expression of ERK1/2 and P-ERK1/2 in AML12 cells after treated with U0126. ( C ) Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12h followed with H 2 O 2 (400 μM) 2h challenge. Cellular ROS was stained with DCFH-DA fluorescent probe and detected by Flow cytometry. ( D ) The cell viability of AML12 cells. All data were expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).
Erk, 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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cell based human mouse erk1 2  (RayBiotech inc)
90
RayBiotech inc cell based human mouse erk1 2
<t>Inhibiting</t> <t>ERK1/2</t> signaling decreased the effect of DHA against oxidative stress. AML12 cells were pre-treated with DHA (50 μM) and TUG891 (10 μM) for 12 h, and then treated with H 2 O 2 (400 μM) for another 2 h. ( A ) The protein expression of ERK1/2, P-ERK1/2, AMPK, and P-AMPK was determined by Western-blotting. ( B ) The protein expression of ERK1/2 and P-ERK1/2 in AML12 cells after treated with U0126. ( C ) Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12h followed with H 2 O 2 (400 μM) 2h challenge. Cellular ROS was stained with DCFH-DA fluorescent probe and detected by Flow cytometry. ( D ) The cell viability of AML12 cells. All data were expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).
Cell Based Human Mouse Erk1 2, supplied by RayBiotech inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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p erk1 2 rb  (ABclonal Biotechnology)
95
ABclonal Biotechnology p erk1 2 rb
<t>Inhibiting</t> <t>ERK1/2</t> signaling decreased the effect of DHA against oxidative stress. AML12 cells were pre-treated with DHA (50 μM) and TUG891 (10 μM) for 12 h, and then treated with H 2 O 2 (400 μM) for another 2 h. ( A ) The protein expression of ERK1/2, P-ERK1/2, AMPK, and P-AMPK was determined by Western-blotting. ( B ) The protein expression of ERK1/2 and P-ERK1/2 in AML12 cells after treated with U0126. ( C ) Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12h followed with H 2 O 2 (400 μM) 2h challenge. Cellular ROS was stained with DCFH-DA fluorescent probe and detected by Flow cytometry. ( D ) The cell viability of AML12 cells. All data were expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).
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rabbit anti erk1 2  (ABclonal Biotechnology)
96
ABclonal Biotechnology rabbit anti erk1 2
<t>Inhibiting</t> <t>ERK1/2</t> signaling decreased the effect of DHA against oxidative stress. AML12 cells were pre-treated with DHA (50 μM) and TUG891 (10 μM) for 12 h, and then treated with H 2 O 2 (400 μM) for another 2 h. ( A ) The protein expression of ERK1/2, P-ERK1/2, AMPK, and P-AMPK was determined by Western-blotting. ( B ) The protein expression of ERK1/2 and P-ERK1/2 in AML12 cells after treated with U0126. ( C ) Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12h followed with H 2 O 2 (400 μM) 2h challenge. Cellular ROS was stained with DCFH-DA fluorescent probe and detected by Flow cytometry. ( D ) The cell viability of AML12 cells. All data were expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).
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anti erk1 2 rb a16686 abclonal  (ABclonal Biotechnology)
95
ABclonal Biotechnology anti erk1 2 rb a16686 abclonal
<t>Inhibiting</t> <t>ERK1/2</t> signaling decreased the effect of DHA against oxidative stress. AML12 cells were pre-treated with DHA (50 μM) and TUG891 (10 μM) for 12 h, and then treated with H 2 O 2 (400 μM) for another 2 h. ( A ) The protein expression of ERK1/2, P-ERK1/2, AMPK, and P-AMPK was determined by Western-blotting. ( B ) The protein expression of ERK1/2 and P-ERK1/2 in AML12 cells after treated with U0126. ( C ) Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12h followed with H 2 O 2 (400 μM) 2h challenge. Cellular ROS was stained with DCFH-DA fluorescent probe and detected by Flow cytometry. ( D ) The cell viability of AML12 cells. All data were expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).
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Image Search Results


Inhibiting ERK1/2 signaling decreased the effect of DHA against oxidative stress. AML12 cells were pre-treated with DHA (50 μM) and TUG891 (10 μM) for 12 h, and then treated with H 2 O 2 (400 μM) for another 2 h. ( A ) The protein expression of ERK1/2, P-ERK1/2, AMPK, and P-AMPK was determined by Western-blotting. ( B ) The protein expression of ERK1/2 and P-ERK1/2 in AML12 cells after treated with U0126. ( C ) Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12h followed with H 2 O 2 (400 μM) 2h challenge. Cellular ROS was stained with DCFH-DA fluorescent probe and detected by Flow cytometry. ( D ) The cell viability of AML12 cells. All data were expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).

Journal: International Journal of Molecular Sciences

Article Title: DHA Protects Hepatocytes from Oxidative Injury through GPR120/ERK-Mediated Mitophagy

doi: 10.3390/ijms22115675

Figure Lengend Snippet: Inhibiting ERK1/2 signaling decreased the effect of DHA against oxidative stress. AML12 cells were pre-treated with DHA (50 μM) and TUG891 (10 μM) for 12 h, and then treated with H 2 O 2 (400 μM) for another 2 h. ( A ) The protein expression of ERK1/2, P-ERK1/2, AMPK, and P-AMPK was determined by Western-blotting. ( B ) The protein expression of ERK1/2 and P-ERK1/2 in AML12 cells after treated with U0126. ( C ) Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12h followed with H 2 O 2 (400 μM) 2h challenge. Cellular ROS was stained with DCFH-DA fluorescent probe and detected by Flow cytometry. ( D ) The cell viability of AML12 cells. All data were expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).

Article Snippet: Therefore, we inhibited the expression of ERK1/2 with the specific inhibitor U0126 (HY-12031A, MCE, Shanghai, China).

Techniques: Expressing, Western Blot, Staining, Flow Cytometry

The inhibition of ERK1/2 signaling blocked DHA-mediated mitophagy. Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12 h followed with H 2 O 2 (400 μM) 2h challenge. ( A ) The protein expression of Beclin1, P62/SOSTM1, LC3B, PINK, and Parkin was determined by Western-blotting. ( B ) The immunofluorescence detected the expression of PINK in AML12 cells. ( C ) The lysosomes in AML12 cells were stained with LysoSensor™ and detected by using confocal microscopy after treatment. All data are expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).

Journal: International Journal of Molecular Sciences

Article Title: DHA Protects Hepatocytes from Oxidative Injury through GPR120/ERK-Mediated Mitophagy

doi: 10.3390/ijms22115675

Figure Lengend Snippet: The inhibition of ERK1/2 signaling blocked DHA-mediated mitophagy. Cells were pre-treated with U0126 (10 μM) for 2 h, and then treated with DHA (50 μM) for 12 h followed with H 2 O 2 (400 μM) 2h challenge. ( A ) The protein expression of Beclin1, P62/SOSTM1, LC3B, PINK, and Parkin was determined by Western-blotting. ( B ) The immunofluorescence detected the expression of PINK in AML12 cells. ( C ) The lysosomes in AML12 cells were stained with LysoSensor™ and detected by using confocal microscopy after treatment. All data are expressed as mean ± SEM of three independent experiments. Significant differences between each group are shown with different letters (e.g., a, b, and c mean a statistically significant differences between each other, p < 0.05).

Article Snippet: Therefore, we inhibited the expression of ERK1/2 with the specific inhibitor U0126 (HY-12031A, MCE, Shanghai, China).

Techniques: Inhibition, Expressing, Western Blot, Immunofluorescence, Staining, Confocal Microscopy

The schematic representation shows that DHA attenuates H 2 O 2 -induced hepatocyte injury through ERK1/2-dependent mitophagy. Oxidative stress would induce hepatocyte apoptosis by impairing mitochondrial function. DHA and TUG891 (a agonist of GPR120) supplementation activates GPR120/ERK1/2 signaling pathway which regulates PINK1/Parkin-mediated mitophagy. The up-regulation of protective mitophagy level promotes mitochondrial renewal and maintains mitochondrial homeostasis during oxidative injury. However, inhibiting the activation of ERK1/2 and autophagy by selective inhibitor U0126 or 3-MA, respectively, could block the protective effect of DHA.

Journal: International Journal of Molecular Sciences

Article Title: DHA Protects Hepatocytes from Oxidative Injury through GPR120/ERK-Mediated Mitophagy

doi: 10.3390/ijms22115675

Figure Lengend Snippet: The schematic representation shows that DHA attenuates H 2 O 2 -induced hepatocyte injury through ERK1/2-dependent mitophagy. Oxidative stress would induce hepatocyte apoptosis by impairing mitochondrial function. DHA and TUG891 (a agonist of GPR120) supplementation activates GPR120/ERK1/2 signaling pathway which regulates PINK1/Parkin-mediated mitophagy. The up-regulation of protective mitophagy level promotes mitochondrial renewal and maintains mitochondrial homeostasis during oxidative injury. However, inhibiting the activation of ERK1/2 and autophagy by selective inhibitor U0126 or 3-MA, respectively, could block the protective effect of DHA.

Article Snippet: Therefore, we inhibited the expression of ERK1/2 with the specific inhibitor U0126 (HY-12031A, MCE, Shanghai, China).

Techniques: Activation Assay, Blocking Assay