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Studies of mouse models with mutations in these genes point towards deficits at synapses that use the neurotransmitter glutamate (Auerbach et al., 2011

Notably, total IGF-I and IGFBPs were unchanged over this short-duration window, dissociating the observed bone-growth effect from sustained IGF-1 axis activation in this model

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1: effects on mortality, pathology and sensory-motor performance in aging rats

a ubiquitous protein, important for gene expression) that we will not discuss

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