Stephen P. Brazier

TL;DR: The generation and characterization of 14 induced pluripotent stem cell (iPSC) lines from HD patients and controls reveal CAG-repeat-expansion-associated gene expression patterns that distinguish patient lines from controls, and early onset versus late onset HD.

TL;DR: Data show that BK(Ca) is a K(+) channel target of H(2)S, and suggest a mechanism to explain the H( 2)S-dependent component of O(2)'s sensing in the carotid body.

TL;DR: It is shown that H(2)S and CO have opposing effects on BK(Ca)channels, suggesting that these gases have separate modes of action and that they modulate carotid body activity by binding at different motifs in the BK (Ca)alphasubunit.

TL;DR: Findings show that a motif in the S9–S10 part of the C-terminal is essential for CO activation and suggest that this gas transmitter activates the BKCa channel by redox-independent changes in gating, and “super-stimulated” BK Ca activity even in saturating [Ca2+]i.

TL;DR: The rapid reversibility of CO and cyanide binding, coupled to information garnered from other CO-binding proteins, suggests that C911 may be involved in formation of a transition metal cluster which can bind and, thereafter, activate BKCa.