Grant: $100,335 - National Institutes of Health - Sep. 29, 2009
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Award Description: The main objectives of the administrative supplement are to further establish the mechanisms by which colonic inflammation results in down-regulation of smooth muscle calcium channels. Part of the long-term goals of the parent grant are to define the cellular mechanisms resulting in altered motility, a hallmark feature of colonic inflammation. The L-type calcium channels play a critical role in calcium influx that importantly controls muscle contraction, intracellular signaling and gene expression. We have recently defined a working model in which inflammation induced nitration of the tyrosine residues within the c-terminue region of the calcium currents and hence down-regulation of calcium influx. The two specific aims of this administrative supplement are to define the mechanism by which src kinase alters the gating behavior of the calcium channel and to establish protein-protein interaction between src and the calcium channel in live cells using flourescence resonance energy transfer (FRET). Using standard single hannel and whole cell voltage clamp protocols, we will examine the modal gating behavior and shifts induced by tyrosine, phosphorylation, nitration and depolarization. We will examine the voltage-dependence of inactivation in whole cell and compare the shifts in gating bewtween control and inflamed cells.
Project Description: Not Started
Jobs Summary: Not Started (Total jobs reported: 0)
Project Status: Not Started
This award's data was last updated on Sep. 29, 2009. Help expand these official descriptions using the wiki below.