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• W1991323513 endingPage "9263" @default.
• W1991323513 startingPage "9250" @default.
• W1991323513 abstract "The death of motor neurons in amyotrophic lateral sclerosis (ALS) is thought to result from the interaction of a variety of factors including excitotoxicity, accumulation of toxic proteins, and abnormal axonal transport. Previously, we found that the susceptibility of motor neurons to excitotoxic insults can be limited by inhibiting signals evoked by brain-derived neurotrophic factor (BDNF) activation of the receptor tyrosine kinase B (TrkB). Here we show that this can be achieved by direct kinase inhibition or by blockade of a transactivation pathway that uses adenosine A2a receptors and src-family kinases (SFKs). Downstream signaling cascades (such as mitogen-activated protein kinase and phosphatidylinositol-3 kinase) are inhibited by these blockers. In addition to protecting motor neurons from excitotoxic insult, these agents also prevent toxicity that follows from the expression of mutant proteins (G85R superoxide dismutase 1; G59S p150 glued ) that cause familial motor neuron disease. TrkB, adenosine A2a receptors, and SFKs associate into complexes in lipid raft and nonlipid raft membranes and the signaling from lipids rafts may be particularly important because their disruption by cholesterol depletion blocks the ability of BDNF to render motor neurons vulnerable to insult. The neuroprotective versatility of Trk antagonism suggests that it may have broad utility in the treatment of ALS patients." @default.
• W1991323513 created "2016-06-24" @default.
• W1991323513 creator A5000106307 @default.
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• W1991323513 creator A5036309178 @default.
• W1991323513 creator A5038956152 @default.
• W1991323513 creator A5039390883 @default.
• W1991323513 date "2006-09-06" @default.
• W1991323513 modified "2023-10-11" @default.
• W1991323513 title "Protecting Motor Neurons from Toxic Insult by Antagonism of Adenosine A2a and Trk Receptors" @default.
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