AI Article Synopsis
- Current electrophoretic methods lack effectiveness in separating different forms of tropomyosin in cardiac samples.
- A new method using a modified 2-D PAGE/2-D DIGE protocol successfully distinguishes between native, mutant (E54K), and phosphorylated versions of tropomyosin.
- The study finds a notable decrease in tropomyosin phosphorylation in transgenic mouse hearts, suggesting that changes in phosphorylation could be linked to the E54K mutation and its association with dilated cardiomyopathy.
Article Abstract
Current electrophoretic methods have not been optimized to fully separate post-translationally modified mutant forms of tropomyosin (Tm) from wild-type cardiac samples. We describe here a method employing a modified 2-D PAGE/2-D DIGE protocol, to fully separate native, mutant (E54K), and phosphorylated forms of Tm. Our data demonstrate the first evidence of a significant (approximately 40%) decrease in Tm phosphorylation in transgenic compared to non-transgenic mouse hearts, and indicate that altered phosphorylation may be a significant factor in the linkage of the E54K mutation to dilated cardiomyopathy.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2586826 | PMC |
| http://dx.doi.org/10.1002/pmic.200700772 | DOI Listing |
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