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

@inproceedings{Xin2017ManganeseTS,
  title={Manganese transporter Slc39a14 deficiency revealed its key role in maintaining manganese homeostasis in mice},
  author={Yongjuan Xin and Hong Gao and Jia Wang and Yuzhen Qiang and Mustapha Umar Imam and Yang Li and Jianyao Wang and Ruochen Zhang and Hui-Zhen Zhang and Yingying Yu and Hao Wang and Haiyang Luo and Chang-he Shi and Yuming Xu and Shintaro Hojyo and Toshiyuki Fukada and Junxia Min and Fudi Wang},
  booktitle={Cell Discovery},
  year={2017}
}
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… CONTINUE READING
Related Discussions
This paper has been referenced on Twitter 1 time. VIEW TWEETS

From This Paper

Topics from this paper.

Citations

Publications citing this paper.
Showing 1-4 of 4 extracted citations

Correction for “ SLC 39 A 14 deficiency alters manganese homeostasis and excretion resulting in brain manganese accumulation and motor deficits in mice

Adenike Akinyodea, Elizabeth Paulusa, +8 authors Mitchell D. Knutsona
2018
View 4 Excerpts
Highly Influenced

Metal transporter Slc39a10 regulates susceptibility to inflammatory stimuli by controlling macrophage survival

Proceedings of the National Academy of Sciences of the United States of America • 2017