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

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 r...

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Veröffentlicht in:Hum Mol Genet
Hauptverfasser: Gan, Peiheng, Baicu, Catalin, Watanabe, Hirofumi, Wang, Kristy, Tao, Ge, Judge, Daniel P, Zile, Michael R, Makita, Takako, Mukherjee, Rupak, Sucov, Henry M
Format: Artigo
Sprache:Inglês
Veröffentlicht: Oxford University Press 2020
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General Article
Online Zugang:https://ncbi.nlm.nih.gov/pmc/articles/PMC7788294/
https://ncbi.nlm.nih.gov/pubmed/33084860
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1093/hmg/ddaa234
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