Current and ongoing beta cell research is presented in this weekly seminar by faculty, postdoctoral fellows and students. If you are interested in attending the Beta Cell Interest Group (BIG) seminars and joining the BIG community, please contact David Jacobson.


Keywords: beta cell BIG

Record History
Added on January 9, 2015 at 2:44 PM by Brown, Deborah
Modified on August 28, 2015 at 10:18 AM by Brown, Deborah
Shared with (contributions)
BIG: Beta Cell Interest Group (BIG) Seminar Master

Meeting Details

Start Date / Time September 2, 2015 at 9:00 AM
End Date / Time September 2, 2015 at 9:55 AM
Duration 55 minutes
Location 512 Light Hall
Presenter Name Matthew Dickerson, PhD (Jacobson's lab)
Presentation Title "Uncovering Regulatory Mechanisms of the Diabetes Associated Potassium Channel, TALK-1"
Status This meeting has already occurred

Meeting Agenda/Notes

Glucose stimulated insulin secretion (GSIS) is critical for the maintenance of glucose homeostasis. GSIS depends on calcium influx into pancreatic beta cells, which is controlled by ion channels. Recently, a nonsynonymous polymorphism in the most highly expressed islet-specific potassium channel, TALK-1, has been associated with an increased risk of developing type-2 diabetes. Thus, we investigated the physiological regulation of TALK-1 channels to increase our understanding of mechanisms that modulate GSIS. Utilizing a membrane specific yeast two-hybrid assay we found that osteopontin interacts with TALK-1 and increases potassium flux through the channel in a phosphorylation dependent manner. We also determined that N-terminal palmitoylation of TALK-1 serves to limit its potassium flux, whereas lysophospholipase-1 (Lypla1) cleavage of palmitate from the channel increases potassium flux. These findings suggest that osteopontin binding as well as N-terminal palmitoylation of TALK-1 channels may serve to regulate beta cell calcium entry and GSIS.