Affiliation: University of Nebraska Medical Center
Bidasee K, Nallani K, Besch H, Dincer U. Streptozotocin-induced diabetes increases disulfide bond formation on cardiac ryanodine receptor (RyR2). J Pharmacol Exp Ther. 2003;305:989-98 pubmed
..These data suggest that the dysfunction of RyR2 induced by diabetes may be due in part to formation of disulfide bonds between adjacent sulfhydryl groups and that these changes were attenuated with insulin treatment. ..
Bidasee K, Zheng H, Shao C, Parbhu S, Rozanski G, Patel K. Exercise training initiated after the onset of diabetes preserves myocardial function: effects on expression of beta-adrenoceptors. J Appl Physiol (1985). 2008;105:907-14 pubmed publisher
..These findings demonstrate for the first time that ExT initiated after the onset of diabetes blunts primarily beta(1)-adrenoceptor expression loss, providing mechanistic insights for exercise-induced improvements in cardiac function. ..
Bidasee K, Nallani K, Yu Y, Cocklin R, Zhang Y, Wang M, et al
. Chronic diabetes increases advanced glycation end products on cardiac ryanodine receptors/calcium-release channels. Diabetes. 2003;52:1825-36 pubmed
..Because AGE complexes are known to compromise protein activity, these data suggest a potential mechanism for diabetes-induced RyR2 dysfunction. ..
Bidasee K, Zhang Y, Shao C, Wang M, Patel K, Dincer U, et al
. Diabetes increases formation of advanced glycation end products on Sarco(endo)plasmic reticulum Ca2+-ATPase. Diabetes. 2004;53:463-73 pubmed
..These data demonstrate for the first time that AGEs are formed on SERCA2a during diabetes, suggesting a novel mechanism by which cardiac relaxation can be slowed during diabetes. ..