Embryonic Expression of Nras^{G 12 D} Leads to Embryonic Lethality and Cardiac Defects.

ABSTRACT: Ras proteins control a complex intracellular signaling network. Gain-of-function mutations in RAS genes lead to RASopathy disorders in humans, including Noonan syndrome (NS). NS is the second most common syndromic cause of congenital heart disease. Although conditional expression of the Nras^{G12D/ +} mutation in adult hematopoietic system is leukemogenic, its effects on embryonic development remain unclear. Here, we report that pan-embryonic expression of endogenous Nras^{G12D/ +} by Mox2-Cre in mice caused embryonic lethality from embryonic day (E) 15.5 and developmental defects predominantly in the heart. At E13.5, Nras^{G12D/ +} ; Mox2^{Cre/ +} embryos displayed a moderate exp

SUBMITTER: You X 

PROVIDER: S-EPMC7928391 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature