NaV1.5 knockout in iPSCs: a novel approach to study NaV1.5 variants in a human cardiomyocyte environment
Abstract Cardiomyocytes derived from patient-specific induced pluripotent stem cells (iPSC-CMs) successfully reproduce the mechanisms of several channelopathies. However, this approach involve cell reprogramming from somatic tissue biopsies or genomic editing in healthy iPSCs for every mutation foun...
Guardado en:
Autores principales: | Marion Pierre, Mohammed Djemai, Hugo Poulin, Mohamed Chahine |
---|---|
Formato: | article |
Lenguaje: | EN |
Publicado: |
Nature Portfolio
2021
|
Materias: | |
Acceso en línea: | https://doaj.org/article/4bf1dac3ef8f4d93b3a3c3419f760e38 |
Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
Ejemplares similares
-
Ca2+-dependent regulation of sodium channels NaV1.4 and NaV1.5 is controlled by the post-IQ motif
por: Jesse B. Yoder, et al.
Publicado: (2019) -
Phosphorylation of Lamin A/C at serine 22 modulates Nav1.5 function
por: Michael A. Olaopa, et al.
Publicado: (2021) -
Spider venom-derived peptide induces hyperalgesia in Nav1.7 knockout mice by activating Nav1.9 channels
por: Xi Zhou, et al.
Publicado: (2020) -
Identification of Navβ1 residues involved in the modulation of the sodium channel Nav1.4.
por: Angel A Islas, et al.
Publicado: (2013) -
Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure
por: Philipp Bengel, et al.
Publicado: (2021)