Mike T. Lin, Ph.D.
Assistant Professor
Department of Physiology,
University of South Alabama
College of Medicine

Email: mlin@southalabama.edu
Mailing address:

Mailing address:
Department of Physiology
5851 USA Dr. N., MSB 3074
University of South Alabama
Mobile, Alabama 36688


B.S., Biochemistry, University of British Columbia
Ph.D., Physiology, Loma Linda University
Postdoc, Oregon Health and Science University

Research Interests:
My laboratory currently focuses on trafficking of calcium-activated potassium channels (eg. BK, IK, and SK channels) in two main areas: neuroscience and vascular biology.

Neuroscience: Long-term synaptic plasticity (LTP) is widely thought to be the cellular substrate for learning and memory, thus mechanisms by which this plasticity is induced and maintained are potential therapeutic targets for the wide range of disorders that affect these processes. My recent work has found an unexpected role for SK2 channels in the expression of long-term plasticity, and my new findings suggest a novel mechanism for dual regulation of SK2 channel and glutamate receptor levels within dendritic spines that is orchestrated by previously unappreciated synaptic proteins.

Vascular biology: Post-menopause, aging, and hypertension are all major risk factors for cardiovascular disease morbidity and mortality: the leading cause of death in the United States. Hypertension, the so-called ‘silent killer’, usually does not present clinical symptoms until complications emerge. Physiological changes including menopause and aging induce irreversible changes in the cardiovascular system that frequently result in diminished endothelium-dependent regulation of vascular tone and can lead to hypertension. Ca2+ signaling in vascular endothelium is a key regulator for many of the endothelium-derived vasoactive factors, including endothelins, prostaglandins, nitric oxide, and endothelium-derived hyperpolarizing factor (EDHF).  EDHF remains the least understood, because despite its central and potent role first described 25 years ago, EDHF has not been molecularly identified. Recent advances have demonstrated unequivocally that SK3 and IK1 (or SK4) channels play crucial roles in EDHF-mediated vasorelaxation, due in large part to their characteristic biophysical properties and sub-cellular localizations.

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