The purpose of this project was to determine the effects of phosphorylation on K-CI cotransport in human red blood cells. The effects of a number of molecules on the propranolol activated K-CI cotransport system were investigated. Test molecules included the Ca calmodulin kinase II inhibitor KN-62, the antioxidant Vitamin E, as well as Genistein and PMA. The necessary experiments were intended to elucidate further information on the mechanism of regulatory volume decrease in human red blood cells. Experiments were completed using a cell suspension system and measurements were taken by a special computer system using potassium ion selective electrodes. Genistein was found to be a potent inhibitor of the propranolol-induced system and KN-62 was found to activate the system beyond normal levels. Data indicate the presence of a protein tyrosine kinase in the mechanism of K-CI cotransport. As well, Protein Kinase C was generally found to have no place in the mechanism, while Ca calmodulin kinase II likely plays a role.

• This report represents the work of one or more WPI undergraduate students submitted to the faculty as evidence of completion of a degree requirement. WPI routinely publishes these reports on its website without editorial or peer review.

Creator

• Jasinski, Christopher Frank
• Staples, Gregory Owen

Publisher

• Worcester Polytechnic Institute

Identifier

• 04D115M

Advisor

• Hobey, William D.

Year

• 2004

Date created

• 2004-01-01

Resource type

• Major Qualifying Project

Major

• Biochemistry

Rights statement

• In Copyright