B
Byung-Chang Suh
Researcher at Daegu Gyeongbuk Institute of Science and Technology
Publications - 81
Citations - 4369
Byung-Chang Suh is an academic researcher from Daegu Gyeongbuk Institute of Science and Technology. The author has contributed to research in topics: Phospholipase C & Phosphatidylinositol. The author has an hindex of 26, co-authored 73 publications receiving 3965 citations. Previous affiliations of Byung-Chang Suh include University of Washington & Pohang University of Science and Technology.
Papers
More filters
Journal ArticleDOI
PIP2 is a necessary cofactor for ion channel function: how and why?
Byung-Chang Suh,Bertil Hille +1 more
TL;DR: This review discusses the dependence of ion channels on phosphoinositides and considers possible mechanisms by which PIP2 and analogues regulate ion channel activity.
Journal ArticleDOI
Rapid chemically induced changes of PtdIns(4,5)P2 gate KCNQ ion channels.
TL;DR: To resolve the controversy about messengers regulating KCNQ ion channels during phospholipase C–mediated suppression of current, translocatable enzymes that quickly alter the phosphoinositide composition of the plasma membrane after application of a chemical cue are designed.
Journal ArticleDOI
Recovery from muscarinic modulation of M current channels requires phosphatidylinositol 4,5-bisphosphate synthesis.
Byung-Chang Suh,Bertil Hille +1 more
TL;DR: It is demonstrated here that intracellular ATP is required for recovery of KCNQ2/KCNQ3 current from muscarinic suppression, with an EC(50) of approximately 0.5 mM.
Journal ArticleDOI
Regulation of ion channels by phosphatidylinositol 4,5-bisphosphate.
Byung-Chang Suh,Bertil Hille +1 more
TL;DR: Recent work has characterized the regulation of a wide range of ion channels by phosphatidylinositol 4,5-bisphosphate, helping to redefine the role of this lipid in cells and in neurobiology.
Journal ArticleDOI
Phospholipase C in Living Cells: Activation, Inhibition, Ca2+ Requirement, and Regulation of M Current
Lisa F. Horowitz,Wiebke Hirdes,Wiebke Hirdes,Byung-Chang Suh,Donald W. Hilgemann,Ken Mackie,Bertil Hille +6 more
TL;DR: The M1 receptor–mediated activation of PLC and suppression of KCNQ current were stopped by lowering intracellular calcium well below resting levels and were slowed by not allowing intrace cellular calcium to rise in response to PLC activation.