Fitting KV potassium channels into the PIP2 puzzle: Hille group connects dots between illustrious HH groups

Cell Cycle-dependent Changes in Localization and Phosphorylation of the Plasma Membrane Kv2.1 K+ Channel Impact Endoplasmic Reticulum Membrane Contact Sites in COS-1 Cells

“…While a comprehensive analysis of Kv2.1 regulation by PIP 2 and its molecular determinants has not been performed, PIP 2 does prevent the rundown of Kv2.1 seen during excised patch clamp recordings (81), although depletion of PIP 2 in intact cells does not affect Kv2.1 function (82); see Ref. 83 for a discussion of conflicting reports. In certain cell types Kv2.1 is associated with noncaveolar lipid rafts, and this association impacts Kv2.1 function (84 -87).…”

The G Protein–Coupled Receptor–Transient Receptor Potential Channel Axis: Molecular Insights for Targeting Disorders of Sensation and Inflammation

“…Although ion channels appear to nonselectively bind PIP 2 over other PI species, its precise regulatory role continues to be debated (Chuang et al, 2001;Prescott and Julius, 2003;Hilgemann, 2012;Cao et al, 2013a). PIP 2 interactions with TRP channels regulate their function through PLC-mediated breakdown of PIP 2 , which relieves TRP channel inhibition, leading to heat/ capsaicin-induced pain.…”

Phosphoinositide regulation of TRPV1 revisited

“…On several voltage gated K + channels for example, excised patch data suggested various effects of PI(4,5)P 2 , which could not be confirmed by subsequent experiments in intact cells using inducible lipid phosphatases [52], for detailed discussion see reference [39]. Chemically inducible and voltage-sensitive phosphoinositide phosphatases dephosphorylate PI(4,5)P 2 and in some cases PI(4)P, and thus decrease phosphoinositide levels without generating second messengers, offering a “cleaner” way than PLC activation to reduce PI(4,5)P 2 levels [74, 111, 125].…”