CFTR-β-catenin interaction regulates mouse embryonic stem cell differentiation and embryonic development.

ABSTRACT: Cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-regulated anion channel capable of conducting both Cl^- and HCO₃^-, mutations of which cause cystic fibrosis (CF), a common autosomal recessive disease. Although CF patients are known to have varied degree of developmental problems, the biological role of CFTR in embryonic development remains elusive. Here, we show that CFTR is functionally expressed in mouse ESCs. CFTR^-/- mESCs exhibit dramatic defect in mesendoderm differentiation. In addition, CFTR physically interacts with β-catenin, defect of which leads to premature degradation of β-catenin and suppressed activation of β-catenin signaling. Furthermore, knockdown of CFTR retards the early development of Xenopus laevis with im

SUBMITTER: Liu Z 

PROVIDER: S-EPMC5260497 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature