Abstract:
:Although the role of tropomyosin is well-defined in striated muscle, the precise mechanism of how tropomyosin functions is still unclear. It has been shown that extension of either N- or C-terminal ends of sarcomeric tropomyosin do not affect cardiac myofibrillogenesis, but it is not known whether simultaneous extension of both ends affects the process. For studying structural/functional relationships of sarcomeric tropomyosin, we have chosen the Ambystoma mexicanum because cardiac mutant hearts are deficient in sarcomeric tropomyosin. In this study, we have made an expression construct, pEGFP.TPM4alpha.E-L-FLAG, that, on transfection into normal and mutant axolotl hearts in organ culture, expresses GFP.TPM4alpha.E-L-FLAG fusion protein in which both the N- and C-termini of TPM4alpha are being extended. TPM4alpha is one of the three tropomyosins expressed in normal axolotl hearts. Both confocal and electron microscopic analyses show that this modified sarcomeric tropomyosin can form organized myofibrils in axolotl hearts.
journal_name
Cardiovasc Toxicoljournal_title
Cardiovascular toxicologyauthors
Narshi A,Denz CR,Nakatsugawa M,Zajdel RW,Dube S,Poiesz BJ,Dube DKdoi
10.1385/ct:5:1:001keywords:
subject
Has Abstractpub_date
2005-01-01 00:00:00pages
1-8issue
1eissn
1530-7905issn
1559-0259pii
CT:5:1:001journal_volume
5pub_type
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