Ciliary neurotrophic factor (CNTF) induces neuronal differentiation and promotes the survival of various neuronal cell types by binding to a receptor complex formed by CNTF receptor α (CNTFRα), gp130, and the leukemia inhibitory factor (LIF) receptor (LIFR).
Taken together, our data indicate that Mef2 activates miRNA expression in response to neuronal activity by binding to a site located 20 kb upstream of the miRNA cluster.
We now report that p53 protein is transcriptionally activated in NGF-mediated neuronal differentiation and describe its binding to a number of novel and previously unreported genomic regions as well as the transcriptional outcome of this binding.
Calsenilin, a neuronal calcium binding protein that has been shown to have multiple functions in the cell, interacts with presenilin 1 (PS1) and presenilin 2 (PS2), represses gene transcription and binds to A-type voltage-gated potassium channels.
Additionally, rabies virus infects neurons potentially through binding to the neuronal cell adhesion molecule (NCAM) or other neuronal receptors irrespective of neurotransmitter phenotype, size, or morphology, enabling an unbiased assessment of presynaptic populations (Thoulouze et al., 1998; Ugolini, 2010).
In contrast to other antiepileptic drugs, levetiracetam (Keppra®, UCB Pharma Ltd., Slough, Berkshire, UK) has a unique mechanism of action, binding to the neuronal synaptic vesicle protein 2A (SV2A) in the brain [1].
Furthermore, others have reported that NSE has a neurotrophic and neuroprotective effect on neurons in the CNS mediated by specific binding to the neuronal surface [ 24].
Studies in neuronal cultures demonstrated that BoNT/A ad cannot cleave synaptosomal-associated protein 25 (SNAP25), the substrate of wt BoNT/A, and that it effectively competes with wt BoNT/A for binding to endogenous neuronal receptors.
In a recent report, Simakova and Arispe [38] have shown that Aβ proteins elicit their toxicity by binding to the neuronal cell membrane.
