Date of Award

8-1-2013

Document Type

Masters Thesis

Degree Name

M.S.

Organizational Unit

College of Natual Science and Mathematics

First Advisor

Joseph K. Angleson, Ph.D.

Second Advisor

David Patterson

Third Advisor

Nancy Lorenzon

Fourth Advisor

Robert Amme

Keywords

Ca2+ /calmodulin-dependent protein kinase II (CaMKII), GABAA-receptors, α-cells

Abstract

Calcium/calmodulin-dependent protein kinase II (CaMKII) has been identified as an important modulator in controlling electrical activity in neurons and the heart; however, a role for CaMKII in pancreatic alpha cell signaling has not been previously reported. Upon activation by calcium/calmodulin, CaMKII phosphorylates proteins involved in intracellular calcium homeostasis by inducing downstream effects such as an increase in AMPA-receptor single channel conductance, potentiation of L-type voltage dependent calcium channels, and enhanced surface expression of inhibitory GABAA-receptors. In the pancreas, an increase in intracellular calcium drives secretion of glucagon from alpha cells within the Islets of Langerhans. α-cells contain many of the known targets of CaMKII described in neurons, including AMPA/GluR1 receptors, L-type VGCC and GABAA-receptors. CaMKII may also regulate other aspects of glucagon secretion, aside from calcium homeostasis, such as vesicle trafficking, exocytosis, and cytoskeleton dynamics. Based on the expression of CaMKII targets and the requirement of calcium influx for hormone secretion, we explored which CaMKII genes, if any, are found in α-cells, and are involved in the regulation of α-cell signaling and glucagon release.

Publication Statement

Copyright is held by the author. User is responsible for all copyright compliance.

Rights Holder

Brooke A. Buckland

Provenance

Received from ProQuest

File Format

application/pdf

Language

en

File Size

76 p.

Discipline

Cellular biology

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