Kcnh2 deletion is associated with rat embryonic development defects via destruction of KCNH2‑integrin β1 complex.

ABSTRACT: The Kv11.1 potassium channel encoded by the Kcnh2 gene is crucial in conducting the rapid delayed rectifier K⁺ current in cardiomyocytes. Homozygous mutation in Kcnh2 is embryonically lethal in humans and mice. However, the molecular signaling pathway of intrauterine fetal loss is unclear. The present study generated a Kcnh2 knockout rat based on edited rat embryonic stem cells (rESCs). Kcnh2 knockout was embryonic lethal on day 11.5 of development due to a heart configuration defect. Experiments with human embryonic heart single cells (6.5‑7 weeks post‑conception) suggested that potassium voltage‑gated channel subfamily H member 2 (KCNH2) plays a crucial role in the development of compact cardiomyocytes. By contrast, apoptosis was found to be trigger

SUBMITTER: Hu S 

PROVIDER: S-EPMC10760793 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature