Key result
Insertion of the SLEN tetrapeptide in the S3-S4 linker of D4 in HEK293 cells resulted in repriming twice as fast as wild type at -100 mV, without affecting activation or inactivation kinetics.
The SLEN tetrapeptide contributes to the rapid repriming of TTX-resistant Na currents by accelerating recovery from inactivation.
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Identifies SLEN motif as key for fast TTX-resistant Na channel recovery; extends structural insights but leaves open physiological relevance.
Na channel subunits alphaSNS (PN3) and alpha mu1(SkM1) produce slowly inactivating/TTX-resistant and rapidly inactivating/TTX-sensitive currents, respectively. AlphaSNS (PN3) current recovers from inactivation (reprimes) rapidly. Sequence alignment identified the tetrapeptide SLEN, in the S3-S4 linker of D4, as alphaSNS-specific. To determine whether SLEN endows Na channels with slow kinetics and/or rapid repriming, we analyzed the transient Na current produced by a chimera mu1SLEN in HEK293 cells. Neither kinetics nor voltage dependence of activation and inactivation was affected. However, repriming was twice as fast as in the wild type at -100 mV. This suggests that SLEN may contribute to the rapid repriming of TTX-resistant Na current.
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Dib‐Hajj et al. (1997) studied this question. Insertion of SLEN tetrapeptide (chimera mu1SLEN) vs. Wild type was evaluated on Transient Na current kinetics, voltage dependence, and repriming. Insertion of the SLEN tetrapeptide in the S3-S4 linker of D4 in HEK293 cells resulted in repriming twice as fast as wild type at -100 mV, without affecting activation or inactivation kinetics.
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