MTSET chloride

MTSET chloride (1 mM; 5 min) significantly inhibits Na⁺ currents in tsA201 cells expressing Nav1.5 D4S6 cysteine mutants F1760C, V1763C, Y1767C, S1759C, V1764C and M1766C, with the strongest inhibitory effect on Y1767C (a 42.1% decrease)^[1].
MTSET chloride (1 mM; 15 min) inhibits ATP-evoked currents in Xenopus oocytes expressing concatenated tetrameric rat P2X2 receptors in a position-dependent manner: the inhibitory effect is stronger when the mutated subunit is located near the amino terminus, and weaker when located near the carboxyl terminus; the maximum inhibition rate of single-mutant constructs reaches up to 50.2%, while the minimum inhibition rate of single-wild-type constructs is only 24.2%^[2].
MTSET chloride (1 mM; 15 min) inhibits ATP-evoked currents in Xenopus oocytes expressing tandem hexameric rat P2X2 receptors in a position-dependent manner; the inhibition is significant (34.2%) only when the mutant subunit is located at the amino terminus, whereas the inhibition is attenuated (58.1%) only when the wild-type subunit is located at the amino terminus^[2].
MTSET chloride (100 μM; 10-40 sec) exerts a state-dependent modification effect on the I248C mutant Ci-HV channel expressed in Xenopus oocytes, modifying the channel only when it is in the open (depolarized) state, with a second-order rate constant of 5620 M^-1s^-1[3].
MTSET chloride exhibits state-dependent accessibility to the V252C mutant Ci-HV channel expressed in Xenopus oocytes, and only modifies the channel when it is in the open (depolarized) state^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.