Pathways modulating neural KCNQ/M (Kv7) potassium channels

By P. Delmas, D. Brown. Nature Reviews Neuroscience, 2005

675 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/7c54b1e286669aa5d815cb2b938eb52b510a2089

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cardiology and Cardiovascular Medicine

1. D. Hilgemann

In Cellular and Molecular Neuroscience

1. B. Suh
2. Bertil Hille
3. D. Hilgemann

In Molecular Biology

1. B. Suh
2. Bertil Hille
3. D. Hilgemann
4. C. Dart

Citations in the corpus

• SYMPOSIUM REVIEW: Phosphoinositides: lipid regulators of membrane proteins (2010, neutral): “Figure 2A shows PLC being activated via M1 muscarinic receptors and Gq.”
• Acetylcholine as a neuromodulator: cholinergic signaling shapes nervous system function and behavior (2012, background): “The slow depolarization is mediated by M1 mAChRmediated closure of M-type (KCNQ) potassium channels in pyramidal neurons (Delmas and Brown, 2005), enhancing their”
• Local PIP2 signals: when, where, and how? (2007, background): “Ion channel and transporter regulation The “M-current” of sympathetic neurons is the best established ion channel model in which receptor activation of PIP2 hydrolysis appears to physiologically regulate a channel activity [17, 82, 88].”
• PIP2 is a necessary cofactor for ion channel function: how and why? (2008, background): “Their current is suppressed by activation of Gq/11-coupled receptors through the activation of PLC and depletion of PIP2 (11, 80).”