Key result
Replacing the III-IV linker of alpha1G with that of alpha1C decreased the rate of inactivation at -20 mV from 15.8 to 8.5 ms and shifted the potential for half-maximal inactivation.
Population
HEK 293 cells transfected with different alpha1G chimeras
Design
Preclinical
Authors
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No immediate clinical implications; leaves open targeted T-type channel modulation in cardiovascular models.
Absolute Event Rate: 8.5% vs 15.8%
Identifies a specific 23-amino acid region in the C-terminus of the T-type calcium channel alpha1G that is critical for its fast inactivation.
Staes et al. (2001) studied this question. alpha1G chimeras vs. wild-type alpha1G was evaluated on rate of inactivation at -20 mV. Replacing the III-IV linker of alpha1G with that of alpha1C decreased the rate of inactivation at -20 mV from 15.8 to 8.5 ms and shifted the potential for half-maximal inactivation.
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