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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Détails bibliographiques
Publié dans:Hum Mol Genet
Auteurs principaux: 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
Langue:Inglês
Publié: Oxford University Press 2020
Sujets:
General Article
Accès en ligne: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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