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- W4377233071 abstract "Abstract Cardiac troponin I (cTnI) contains a N-terminal extension harboring protein kinase A targets (Ser 23/24 ), which are phosphorylated during ß-adrenergic stimulation to increase cardiomyocyte relaxation rate. Here, we show that exon 3 of TNNI3 , encoding most of the cTnI N-terminal extension including Ser 23/24 , was pseudoexonized multiple times in shrews and moles to mimic Ser 23/24 phosphorylation without adrenergic stimulation, thus facilitating the evolution of exceptionally high resting heart rates (>1100 beats/minute). Cardiac transcriptomes further reveal alternative splicing of TNNI3 exon 3 in two distantly related bat families, thereby representing an intermediate state preceding the genomic assimilation of exon 3 skipping. As human TNNI3 may similarly be amenable to exon 3 alternative splicing, our results offer a new approach to restore diastolic function in chronic heart failure patients. One-Sentence Summary Shrews and moles independently evolved a truncated cardiac troponin I to facilitate rapid heart rates without chronic adrenergic stimulation." @default.
- W4377233071 created "2023-05-23" @default.
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- W4377233071 date "2023-05-22" @default.
- W4377233071 modified "2023-09-26" @default.
- W4377233071 title "Parallel genetic excisions of the cardiac troponin I N-terminal extension in tachycardic mammals" @default.
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- W4377233071 doi "https://doi.org/10.1101/2023.05.19.541292" @default.
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