A dominant negative heterozygous G87R mutation in the zinc transporter, ZnT-2 (SLC30A2), results in transient neonatal zinc deficiency.

@article{Lasry2012ADN,
  title={A dominant negative heterozygous G87R mutation in the zinc transporter, ZnT-2 (SLC30A2), results in transient neonatal zinc deficiency.},
  author={Inbal Lasry and Young Ah Seo and Hadas Ityel and Nechama Shalva and Ben Pode-Shakked and Fabian Glaser and Bluma Berman and Igor N. Berezovsky and Alexander Goncearenco and Aharon Klar and Jacob Y. Levy and Yair Anikster and Shannon L. Kelleher and Yehuda G Assaraf},
  journal={The Journal of biological chemistry},
  year={2012},
  volume={287 35},
  pages={29348-61}
}
Zinc is an essential mineral, and infants are particularly vulnerable to zinc deficiency as they require large amounts of zinc for their normal growth and development. We have recently described the first loss-of-function mutation (H54R) in the zinc transporter ZnT-2 (SLC30A2) in mothers with infants harboring transient neonatal zinc deficiency (TNZD). Here we identified and characterized a novel heterozygous G87R ZnT-2 mutation in two unrelated Ashkenazi Jewish mothers with infants displaying… CONTINUE READING
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