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doi: 10.1038/12153
pmid: 10461216
We have identified a calcium-dependent pathway in neurons that regulates expression levels of the alpha1B subunit and N channel current. When neurons are depolarized and voltage-gated calcium channels activated, the half-life of cellular N channel alpha1B mRNA is prolonged. This stabilizing effect of depolarization is mediated through the 3' untranslated region of a long form of the alpha1B mRNA and may represent a form of modulation of N-channel levels that does not require changes in gene transcription. Increases in N channel expression would affect several key neuronal functions controlled by calcium, including transmitter release and neurite outgrowth.
Neurons, Calcium Channels, L-Type, Transcription, Genetic, Action Potentials, Superior Cervical Ganglion, Calcium Channel Blockers, Membrane Potentials, Rats, Gene Expression Regulation, omega-Conotoxin GVIA, Animals, Nimodipine, Calcium Channels, Nerve Growth Factors, RNA, Messenger, Peptides, 3' Untranslated Regions, Cells, Cultured
Neurons, Calcium Channels, L-Type, Transcription, Genetic, Action Potentials, Superior Cervical Ganglion, Calcium Channel Blockers, Membrane Potentials, Rats, Gene Expression Regulation, omega-Conotoxin GVIA, Animals, Nimodipine, Calcium Channels, Nerve Growth Factors, RNA, Messenger, Peptides, 3' Untranslated Regions, Cells, Cultured
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 28 | |
popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Average | |
influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 10% |