Pub. Date : 2006 Jun 16
PMID : 16621802
8 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Previous results with pharmacological agents implicated the extracellular signal-regulated kinases-1/2 (ERK1/2) in glutamate toxicity in HT22 cells and immature embryonic rat cortical neurons. | Glutamic Acid | mitogen-activated protein kinase 3 | Mus musculus |
| 2 | Previous results with pharmacological agents implicated the extracellular signal-regulated kinases-1/2 (ERK1/2) in glutamate toxicity in HT22 cells and immature embryonic rat cortical neurons. | Glutamic Acid | mitogen-activated protein kinase 3 | Mus musculus |
| 3 | In this report, we definitively establish a role for ERK1/2 in oxidative toxicity using dominant negative MEK1 expression in transiently transfected HT22 cells to block glutamate-induced cell death. | Glutamic Acid | mitogen-activated protein kinase 3 | Mus musculus |
| 4 | Activation of ERK1/2 in HT22 cells has a distinct kinetic profile with an initial peak occurring between 30 min and 1 h of glutamate treatment and a second peak typically emerging after 6 h. We demonstrate here that the initial phase of ERK1/2 induction is because of activation of metabotropic glutamate receptor type I (mGluRI). | Glutamic Acid | mitogen-activated protein kinase 3 | Mus musculus |
| 5 | Activation of ERK1/2 in HT22 cells has a distinct kinetic profile with an initial peak occurring between 30 min and 1 h of glutamate treatment and a second peak typically emerging after 6 h. We demonstrate here that the initial phase of ERK1/2 induction is because of activation of metabotropic glutamate receptor type I (mGluRI). | Glutamic Acid | mitogen-activated protein kinase 3 | Mus musculus |
| 6 | ERK1/2 activation by mGluRI contributes to an HT22 cell adaptive response to oxidative stress as glutamate-induced toxicity is enhanced upon pharmacological inhibition of mGluRI. | Glutamic Acid | mitogen-activated protein kinase 3 | Mus musculus |
| 7 | The protective effect of ERK1/2 activation at early times after glutamate treatment is mediated by a restoration of glutathione (GSH) levels that are reduced because of depletion of intracellular cysteine pools. | Glutamic Acid | mitogen-activated protein kinase 3 | Mus musculus |
| 8 | Thus, ERK1/2 appears to play dual roles in HT22 cells acting as part of a cellular adaptive response during the initial phases of glutamate-induced oxidative stress and contributing to toxicity during later stages of stress. | Glutamic Acid | mitogen-activated protein kinase 3 | Mus musculus |