Christopher A Ahern
University of Iowa, IA·Biophysics
Every heartbeat, muscle twitch and thought depends on ion channels. These proteins open and close in response to voltage to let sodium, potassium or calcium ions cross cell membranes.
- Fields
Biophysics
Pharmacology
Physiology
- Topics
ion channels
voltage-gated sodium channels
voltage-gated calcium channels
- Grants
- 2 known grants, through Jan 2028
What they work on
- Develop light-activated photochemical 'stapling' to lock voltage-gated sodium, calcium and potassium channels into key shapes in live cell membranes before purification for structural determination.
- Introduce modified chemistries into the protein backbone of voltage-sensor and gate segments to reveal how voltage-gated channels move and open.
- Use light-controlled, site-specific phosphorylation to dissect step by step how fight-or-flight signals make CaV1.2 calcium channels in the heart open faster and longer.
- Measure energetic contributions of aromatic phenylalanine and tyrosine residues in drug-binding pockets of CaV and hERG potassium channels, using a high-resolution method in mammalian cells.
- Compare acute NaV1.5 silencing in CRISPR-engineered NaV1.5-GX mice treated with acylsulfonamide (GX) drugs to chronic loss in Scn5a+/- mice, measuring calcium handling, fibrosis, cardiac function and arrhythmias.
- Test how sodium channel blockade affects heart remodeling and arrhythmia risk after transverse aortic constriction, and build in vivo and ex vivo platforms to study patient SCN5A mutations.
More about the research
Scientists can now picture these channels at high resolution, but it remains hard to connect their shapes to how they work in living cells. Many common drugs also act on these channels, sometimes in harmful ways. Using chemical tools, the lab studies how voltage-gated channels move and how drugs bind to them. It also builds a mouse in which the heart's main sodium channel can be switched off on demand to learn how its defects cause heart disease.
Why it matters
Calcium channel drugs treat pain, epilepsy, arrhythmia, high blood pressure and heart failure, while accidental hERG blockade by otherwise useful drugs can cause deadly arrhythmias. Mapping how drugs bind these channels could help design safer medicines. A switchable NaV1.5 mouse could also clarify how SCN5A mutations cause inherited arrhythmias and cardiomyopathy.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Robert Piper
University of Iowa, IA·Physiology
Produce stably expressing human HEK cell lines that pair individual β subunits (Scn2b, Scn3b, Scn4b) with specific pore-forming NaV α subunits.
Gucan Dai
Saint Louis University, MO·Biophysics
Determine how the voltage-sensing domain of hyperpolarization-activated HCN pacemaker channels moves during activation, including its intermediate conformations, using patch-clamp fluorometry on channels expressed in human cell lines.
Manu Ben Johny
Columbia University, NY·Biophysics
Determine whether CaV2.1 and CaV2.2 calcium channels are S-palmitoylated, carrying an attached lipid group, in central and peripheral neurons, and how this modification alters channel activity.
The school
University of Iowa: 32 labs on PI Pages, $703M a year on research, 418 research doctorates a year.
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