Manganese transporter Slc39a14 deficiency revealed its key role in maintaining manganese homeostasis in mice.

ABSTRACT: SLC39A14 (also known as ZIP14), a member of the SLC39A transmembrane metal transporter family, has been reported to mediate the cellular uptake of iron and zinc. Recently, however, mutations in the SLC39A14 gene have been linked to manganese (Mn) accumulation in the brain and childhood-onset parkinsonism dystonia. It has therefore been suggested that SLC39A14 deficiency impairs hepatic Mn uptake and biliary excretion, resulting in the accumulation of Mn in the circulation and brain. To test this hypothesis, we generated and characterized global Slc39a14-knockout (Slc39a14^-/- ) mice and hepatocyte-specific Slc39a14-knockout (Slc39a14^fl/fl;Alb-Cre⁺ ) mice. Slc39a14^-/-

SUBMITTER: Xin Y 

PROVIDER: S-EPMC5519003 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature