Regulating K+-channel genes constitutes a novel mechanism for producing intricate long-term changes in cellular excitability.
Answers are grounded in this paper and cite their sources.
May guide excitability research in cardiovascular and neural disease; leaves open whether transcriptional K+ channel targeting alters clinical outcomes.
Recent studies have determined that K+ channel gene expression is dynamically controlled in endocrine, cardiac, and neuronal cells. This regulation is induced by physiological stimuli (e.g., hormones, transmitters, depolarization), drugs (e.g., opiates) and with pathophysiological conditions (e.g., seizures, hypertension). In many cases, alterations in subunit expression are driven by transcriptional changes. Furthermore, resultant changes in excitability can be produced within hours because of the rapid turnover of Kv-channel proteins. Finally, the consequences of altering K+-channel subunit are complex because a single gene product can participate in forming functionally distinct homomeric and heteromeric channels in the same cell. Thus, regulating K+-channel genes constitutes a novel mechanism for producing intricate long-term changes in excitability.
No takes yet. Share an insight, caveat, or question.
Levitan et al. (1998) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: