Research Highlights

SeMet-containing sodium channels

SeMet Incorporation

Hemin inhibits cadiac NaV channels

Fluorescent Sensor for Methionine Oxidation

Genetically Encoded Voltage Indicator

Photoactivation of Dendra2 by NIR radiation of UCNPs

CORM-S1 releases CO and Fe2+, both of which activate BK channels

N-terminal sequence of Kv1.4 (top); current traces of Kv1.4 before and after polysulfide application (left); MALDI spectra showing sulfhydration of C13 in the N-terminal inactivation peptide.

Dual effects of tricarbonyldichlororuthenium(II) dimer (CORM-2) on voltage-dependent potassium channels. Channel modification may result from binding of either carbon monoxide (blue) and/or of Ru(CO)2 fragments (red). The latter involves adduction to target histidines and, thus, can be quenched by excess free histidine or histidine-containing proteins such as human serum albumin.

Pulse protocol (top) and current recordings of roNaV2 channels in HEK293 cells (bottom). The blue bar marks illumination of the cell with blue light via a 63x objective. The red curve is a mono-exponential fit to describe the time course of inactivation loss upon illumination.

Blocking effects of 10 µM µ-SIIIA (blue) and µ-PIIIA (red) on ion currents of the indicated voltage-gated ion channels.

Stimulated action potentials of DRG neurons before (black) and after 150 s illumination with blue light (blue) from wild-type (left) and NaV1.8-deficient mice (right).

Score pattern for potential calmodulin binding to the N terminus of Kvβ1.1 (top) and current recordings of Kv1.1+Kvβ1.1 channels with and without Ca(2+)/CaM for wild-type Kvβ1.1 (left) and after replacement of three asparagine residues for arginine (right).

Representative current traces measured in the whole-cell mode in response to depolarizations ranging from -127 to 3 mV of HEK 293T cells expressing human NaV1.9 (left) or chimera NaV1.9-C4 (right).

Response of roGFP2 (top) and the ratiometric roNaV signal (bottom) to blue light. At -50 mV roNaV is inactivated and, thus, protected from ROS attack.

Kv1 4 current traces without (black) and with hemin (red). Part of the N-terminal ball domain with a docked hemin moiety.

A mutation in SCN11A causes a gain-of-function of the voltage-gated sodium channel NaV1.9 and leads to suppression of the electrical signaling in nociceptive neurons.