Research in Dr. Abbott’s lab is focused on elucidating the molecular basis for ion channel and transporter physiology and pathophysiology. We are fortunate to have received funding for this work from the US National Institutes of Health (NHLBI, NIGMS and NIDDK), American Heart Association, and also UC Irvine UROP and E-SURP programs. One of the main directions of the lab has been to define the roles of the KCNE gene family of ion channel subunits, using a combination of techniques including mouse and human genetics, electrophysiology, pharmacology, and state-of-the-art imaging modalities. Other interests include discovery of novel ion channel subunits and small molecules to modulate ion channel function, and investigation of ion channel trafficking. More recently, we discovered several novel macromolecular complexes comprising KCNQ family Kv alpha subunits and sodium-coupled solute transporters, and we are currently studying their roles in physiology and molecular mechanisms of action. Abnormal functioning of ion channels causes many different disorders, including cardiac arrhythmia, diabetes, epilepsy, myotonia and periodic paralysis. Dr. Abbott's lab uses a multidisciplinary approach aimed at understanding the molecular bases for these “channelopathies” and also how these proteins function normally to enable the
complex signaling and cellular processes required by living organisms.
3.10.2017 - Congratulations to recent graduate Dr. Dan Neverisky, whose work in the Abbott lab discovering novel chansporter complexes is published in FASEB J.
3.29.2017 - Congratulations to Liz King,
whose work in the Abbott lab demonstrating that Kcne3 deletion causes skeletal muscle dysfunction in mice, is published in FASEB J. This work was a collaboration with Noah Weisleder (now at Ohio State) and supports our earlier paper published in Cell showing that human KCNE3 gene sequence variants associated with periodic paralysis.
4.26.2017 - An article from the lab of alumnus Dr. Zhaoyang Hu in collaboration with the Abbott lab, demonstrating differential arrhythmogenesis and preconditioning cardioprotection in diabetes is published in Cardiovascular Diabetology.
8.8.2017 - Congratulations to Drs. Rian Manville and Dan Neverisky, whose work demonstrating physical interaction between solute transporters and the KCNQ potassium channel pore is published in Biophysical Journal and highlighted in a "new and notable" editorial.
5.10.2018 - Congratulations to Drs. Rian Manville and Maria Papanikolaou, whose work in the Abbott lab discovering a novel mode of neurotransmitter signaling has been published in Nature Communications.
7.20.2018 - Congratulations to birthday boy Dr. Rian Manville, whose work in the Abbott lab discovering a novel target for the gabapentin has been published in Molecular Pharmacology.
Join us at the international Kv7 channels symposium in Naples, 2019.
5.29.2018 - A collaboration between the Hu and Abbott labs showing how Kcne4 deletion sex-specifically predisposes to cardiac arrhythmias in aged mice is published in Scientific Reports.
5.16.2018 - A collaboration between the Hu and Abbott labs showing how remote ischemic preconditioning protects against lung damage is published in PLoS One.
5.10.2018 - Congratulations to Dr. Rian Manville , whose work in the Abbott lab discovering a molecular mechanism for the anticonvulsant action of a
traditional herbal medicine has been published in Nature Communications.
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OUR LATEST RESEARCH
Following up on GWAS that associated polymorphisms in or near the human KCNE2 gene with predisposition to early-onset myocardial infarction and atherosclerosis, we recently discovered that Kcne2 deletion in mice promotes atherosclerosis. This is the only the third single-gene knockout to cause atherosclerosis in Mus musculus, a species resistant to plaque formation. View our 2015 JMCC paper to learn more.
We recently found that despite a number of cardioavscular and other disorders arising from Kcne2 disruption, mice with germline Kcne2 deletion are better equipped to handle an imposed myocardial infarction. This is because cardioprotective pathways are chronically upregulated in Kcne2-/- mice. This work, a collaboration between the Abbott lab and Zhaoyang Hu's lab, was published in 2016 in Cardiovascular Research, and featured on the front cover and as an Editor's Choice article.