Ezana M. Azene

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Although ample evidence suggests the presence of an intracellular activation gate in HCN (pacemaker) channels, mutations in the outer pore can alter gating properties. Here we investigated the role of the outer pore residue A354 in HCN1 gating by systematically converting it to the equivalent residues (T, Y, and F) found in K(+)-channels. A354T negatively(More)
OBJECTIVE I(f), encoded by the hyperpolarization-activated, cyclic nucleotide-modulated (HCN) channel gene family, modulates cardiac pacing. During cardiac pacing, changes in membrane potential are rapid, preventing the very slow HCN channels from reaching equilibrium. Here, we examined the properties of HCN channels under non-equilibrium conditions to shed(More)
Hyperpolarization-activated cyclic-nucleotide-gated (HCN) channels modulate the firing rates of neuronal and cardiac pacemaker cells. HCN channels resemble voltage-gated K+ channels structurally, but much less is known about their structure-function correlation. Although modulation of K+ channel gating by external K+ is a well-known phenomenon, such a link(More)
The hyperpolarization-activated cyclic nucleotide-modulated channel gene family (HCN1-4) encodes the membrane depolarizing current that underlies pacemaking. Although the topology of HCN resembles K(v) channels, much less is known about their structure-function correlation. Previously, we identified several pore residues in the S5-P linker and P-loop that(More)
lies in the presence of hematologic precursors within the PMGCT stroma and vessels within the yolk sac tumor component of these tumors. 11 It can be further speculated that expression of hema-topoietic growth and differentiation factors in some PMGCT could drive the differentiation of primordial germ cells into hematopoietic progeny. The differentiation(More)
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