| Protein Name: | Mitogen-activated protein kinase(ERK) (P28482) |
|---|---|
| Gene Name: | MAPK1 |
| Description: | Mitogen-activated protein kinase 1 (EC 2 7 11 24) (Extracellular signal-regulated kinase 2) (ERK-2) (Mitogen-activated protein kinase 2) (MAP kinase 2) (MAPK 2) (p42-MAPK) (ERT1) |
| PDB ID: | 1PME |
| Protein Family: | |
| Protein Category: | Enzyme |
This panel provides drug-protein interaction and their ADRs along with references
| Interacting Drugs | Toxicity | Mechanism | Reference |
|---|---|---|---|
| Brain-derived neurotrophic factor (BDNF) | Apoptosis | The activation of both p38 MAPK and ERK is involved in the signaling cascade of the BDNF-accelerated@ no donor-induced apoptosis [ ADR Type 2 ] | Brain-derived neurotrophic factor accelerates nitric oxide donor-induced apoptosis of cultured cortical neurons |
| Cisplatin | Apoptosis | AP-1 complexes were activated by cisplatin including mainly c-jun/ATF-2 heterodimers suggesting that AP-1-dependent transcription partially mediated cisplatin-induced apoptosis [ ADR Type 2 ] | Lack of c-Jun activity increases survival to cisplatin |
| Dehydrated Alcohol | Alcohol Intoxication | Lockade of ERK 1/2 phosphorylation with the mitogen-activated protein kinase (MEK) 1/2 inhibitor SL327 blocked alcohol-induced c-Fos expression@showing that the Edinger-Westphal nucleus is preferentially sensitive to alcohol intoxication [ ADR Type 2 ] | Alcohol-induced c-Fos expression in the Edinger-Westphal nucleus: pharmacological and signal transduction mechanisms |
| Dehydrated Alcohol | Impair Liver Regeneration | Ethanol treatment caused phosphorylation of Erk2@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to Chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation. [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Dehydrated Alcohol | Inhibit Dna Synthesis | Ethanol treatment caused phosphorylation of Erk2@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to Chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation. [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Dehydrated Alcohol | Mute Cellular Responses To Growth Factor Stimulation | Ethanol treatment caused phosphorylation of Erk2@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to Chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation. [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Etoposide | Apoptosis | Induction of apoptotic cell death and DNA damage by treatment of U937 cells with etoposide (100 microM) was associated with a modest@ but sustained@ recruitment of the mitogen-activated protein kinases p42-extracellular signal receptor-activated kinase (ERK)1 and p44-extracellular signal receptor-activated kinase 2 [ ADR Type 2 ] | Evidence that the apoptotic actions of etoposide are independent of c-Jun/activating protein-1-mediated transregulation |
| Etoposide | Dna Damage | Induction of apoptotic cell death and DNA damage by treatment of U937 cells with etoposide (100 microM) was associated with a modest@ but sustained@ recruitment of the mitogen-activated protein kinases p42-extracellular signal receptor-activated kinase (ERK)1 and p44-extracellular signal receptor-activated kinase 2 [ ADR Type 2 ] | Evidence that the apoptotic actions of etoposide are independent of c-Jun/activating protein-1-mediated transregulation |
| Genistein | Erk Activity Was Slightly Elevated | Extracellular signal-regulated kinase (ERK) 1 activity was slightly elevated in adenosine-treated Ecs. [ ADR Type 2 ] | Adenosine induces endothelial apoptosis by activating protein tyrosine phosphatase: a possible role of p38alpha |
| Paclitaxel | Apoptosis | Bcl-2 phosphorylation is tightly associated with mitotic arrest and fail to demonstrate that it is a determinant of progression into apoptosis after mitotic arrest induced by anti-tubulin agents. [ ADR Type 2 ] | Paclitaxel-induced apoptosis is associated with expression and activation of c-Mos gene product in human ovarian carcinoma SKOV3 cells |
| Progesterone | Oocyte Maturation | The increase in Raf-1 activity was concurrent with an elevation in the activity of mitogen-activated protein (MAP) kinase@which leads to progesterone-induced oocyte maturation [ ADR Type 1 ] | Raf-1 protein kinase is important for progesterone-induced Xenopus oocyte maturation and acts downstream of mos |
| urokinase-type Plasminogen activator (uPA) | Cellular Migration | uPA-induced ERK activation and stimulation of cellular migration [ ADR Type 2 ] | Myosin light chain kinase functions downstream of Ras/ERK to promote migration of urokinase-type plasminogen activator-stimulated cells in an integrin-selective manner |
| urokinase-type Plasminogen activator (uPA) | Diabetes Mellitus | Urban minority HIV-infected patients receiving combination antiretroviral therapy including a protease inhibitor may be at increased risk for the development of hyperglycemia and diabetes mellitus Risk factors for diabetes mellitus should be identified and blood glucose monitored in all patients receiving protease inhibitors [ ADR Type 2 ] | Myosin light chain kinase functions downstream of Ras/ERK to promote migration of urokinase-type plasminogen activator-stimulated cells in an integrin-selective manner |
| urokinase-type Plasminogen activator (uPA) | Hyperglycemia | Urban minority HIV-infected patients receiving combination antiretroviral therapy including a protease inhibitor may be at increased risk for the development of hyperglycemia and diabetes mellitus Risk factors for diabetes mellitus should be identified and blood glucose monitored in all patients receiving protease inhibitors [ ADR Type 2 ] | Myosin light chain kinase functions downstream of Ras/ERK to promote migration of urokinase-type plasminogen activator-stimulated cells in an integrin-selective manner |
This panel provides information on drug category
| Toxicity | Source |
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