Article
The prevalent I686T human variant and loss-of-function mutations in the cardiomyocyte-specific kinase gene TNNI3K cause adverse contractility and concentric remodeling in mice.
Human molecular genetics - 6 Jan 2021
Gan Peiheng, Baicu Catalin, Watanabe Hirofumi, Wang Kristy, Tao Ge, Judge Daniel P, Zile Michael R, Makita Takako, Mukherjee Rupak, Sucov Henry M
Abstract excerpt
TNNI3K expression worsens disease progression in several mouse heart pathology models. TNNI3K expression also reduces the number of diploid cardiomyocytes, which may be detrimental to adult heart regeneration. However, the gene is evolutionarily conserved, suggesting a beneficial function that has remained obscure. Here, we show that C57BL/6J-inbred Tnni3k mutant mice develop concentric remodeling, characterized...
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