Voltage-activated ion channels are essential for electrical signaling, yet the mechanism of voltage sensing remains under intense investigation. The voltage-sensor paddle is a crucial structural motif in voltage-activated potassium (Kv) channels that has been proposed to move at the protein–lipid interface in response to changes in membrane voltage. Here we explore whether tarantula toxins like hanatoxin and SGTx1 inhibit Kv channels by interacting with paddle motifs within the membrane. We find that these toxins can partition into membranes under physiologically relevant conditions, but that the toxin–membrane interaction is not sufficient to inhibit Kv channels. From mutagenesis studies we identify regions of the toxin involved in binding to the paddle motif, and those important for interacting with membranes. Modification of membranes with sphingomyelinase D dramatically alters the stability of the toxin–channel complex, suggesting that tarantula toxins interact with paddle motifs within the membrane and that they are sensitive detectors of lipid–channel interactions.
Radiation damage produced in 4H-SiC n-epilayers by electrons of different energies is presented. Junction barrier Schottky power SiC diodes are irradiated with 1.05, 2.1, 5, and 10 MeV electrons with doses up to 600 kGy. Radiation defects are characterized by capacitance deep-level transient spectroscopy and capacitance-to-voltage (C-V) measurement. Results, which are compared with previous data obtained on 4.5 MeV electrons, show that the damage structure is very similar for all irradiation energies. Dominating is the generation of simple, thermally unstable defects evidenced by the presence of acceptor levels located at 0.25, 0.38, 0.60, and 0.72 eV below the 4H-SiC conduction band edge. With increasing energy of electrons, the number of simple defects saturates, and the production of more complex, cluster-related defects grow. Majority of introduced defects are acceptor centers, which compensate n-type (nitrogen) doping of the epilayer. The carrier removal rate increases with electron energy and follows well the classical nonionization energy loss (NIEL) scaling for electrons in silicon. The stability of introduced defects and their effect on carrier lifetime reduction are discussed, as well.
The ON-state characteristics of a 1.7-kV 4H-SiC junction barrier Schottky diode were studied after 4.5-MeV electron irradiation. Irradiation doses were chosen to cause a light, strong, and full doping compensation of an epitaxial layer. The diodes were characterized using Deep Level Transient Spectroscopy, C-V (T), and I-V measurements without postirradiation annealing. The calibration of model parameters of a device simulator, which reflects the unique defect structure caused by the electron irradiation, was verified up to 2000 kGy. The quantitative agreement between simulation and measurement requires: 1) the Shockley-Read-Hall model with at least two deep levels on the contrary to ion irradiation and 2) a new model for enhanced mobility degradation due to radiation defects. The diode performance at high electron fluences is shown to be limited by the doping compensation at the epitaxial layer.
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