{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T11:49:57Z","timestamp":1791978597800,"version":"4.4.0"},"reference-count":38,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2004,9,10]],"date-time":"2004-09-10T00:00:00Z","timestamp":1094774400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genesis"],"published-print":{"date-parts":[[2004,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The SLC30 family of cation diffusion transporters includes at least nine members in mammals, most of which have been documented to play a role in zinc transport. The founding member of this family, Znt1, was discovered by virtue of its ability to efflux zinc from cells and to protect them from zinc toxicity. However, its physiological functions remain unknown. To address this issue, mice with targeted knockout of the <jats:italic>Znt1<\/jats:italic> gene were generated by homologous recombination in embryonic stem cells. Heterozygous <jats:italic>Znt1<\/jats:italic> mice were viable. In contrast, homozygous <jats:italic>Znt1<\/jats:italic> mice died in utero soon after implantation due to a catastrophic failure of embryonic development. Although extraembryonic membranes formed around these embryos, the embryo proper failed to undergo morphogenesis past the egg cylinder stage and was amorphous by d9 of pregnancy. Expression of the <jats:italic>Znt1<\/jats:italic> gene was detected predominantly in trophoblasts and in the maternal deciduum during the postimplantation period (d5 to d8). The failure of homozygous <jats:italic>Znt1<\/jats:italic> embryos to develop could not be rescued by manipulating maternal dietary zinc (either excess or deficiency) during pregnancy. However, embryos in <jats:italic>Znt1<\/jats:italic> heterozygous females were \u223c3 times more likely to develop abnormally when exposed to maternal dietary zinc deficiency during later pregnancy than were those in wildtype females. These studies suggest that Znt1 serves an essential function of transporting maternal zinc into the embryonic environment during the egg cylinder stage of development, and further suggest that Znt1 plays a role in zinc homeostasis in adult mice. genesis 40:74\u201381, 2004. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/gene.20067","type":"journal-article","created":{"date-parts":[[2004,9,14]],"date-time":"2004-09-14T09:47:23Z","timestamp":1095155243000},"page":"74-81","source":"Crossref","is-referenced-by-count":133,"title":["Mouse <i>zinc transporter 1<\/i> gene provides an essential function during early embryonic development"],"prefix":"10.1002","volume":"40","author":[{"given":"Glen K.","family":"Andrews","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haibin","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.K.","family":"Dey","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard 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