{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T08:43:20Z","timestamp":1790066600697,"version":"4.0.1"},"reference-count":34,"publisher":"Bioscientifica","issue":"4","content-domain":{"domain":["jme.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,9,5]]},"abstract":"<jats:p>\n                    Wnt\/\u03b2-catenin signaling is essential for adrenocortical development. Zinc and ring finger 3 (ZNRF3), an E3 ubiquitin ligase that attenuates Wnt\/\u03b2-catenin signaling, is negatively regulated by R-spondin via an extracellular domain that is partially encoded by exon 2 of\n                    <jats:italic>ZNRF3<\/jats:italic>\n                    . We recently identified\n                    <jats:italic>ZNRF3<\/jats:italic>\n                    exon 2 deletions in three individuals with congenital adrenal hypoplasia.\n                    <jats:italic>ZNRF3<\/jats:italic>\n                    exon 2 deletion impairs R-spondin binding, thereby attenuating \u03b2-catenin expression and eventually leading to the development of congenital adrenal hypoplasia. To elucidate the influence of\n                    <jats:italic>ZNRF3\/Znrf3<\/jats:italic>\n                    exon 2 deletion on adrenocortical development, we generated homozygous\n                    <jats:italic>Znrf3<\/jats:italic>\n                    exon 2 deletion (\n                    <jats:italic>Znrf3<\/jats:italic>\n                    <jats:sup>\u03942\/\u03942<\/jats:sup>\n                    ) mice. Whereas the adrenal glands of\n                    <jats:italic>Znrf3<\/jats:italic>\n                    <jats:sup>\u03942\/\u03942<\/jats:sup>\n                    mice did not show gross morphological changes at birth, moderate hyperplasia of the zona fasciculata (ZF), dispersed medulla arrangement, and a radially spreading zone with macrophage infiltration between the ZF and medulla were observed at 6 weeks of age. 20\u03b1-hydroxysteroid dehydrogenase, a marker of the adrenal X-zone, was hardly detected by immunostaining, and gene expression was significantly downregulated. The number of activated \u03b2-catenin-positive cells decreased in the zona glomerulosa, consistent with the results of\n                    <jats:italic>in situ<\/jats:italic>\n                    hybridization for\n                    <jats:italic>Axin2,<\/jats:italic>\n                    a Wnt\/\u03b2-catenin target gene. Plasma ACTH and serum corticosterone levels in\n                    <jats:italic>Znrf3<\/jats:italic>\n                    <jats:sup>\u03942\/\u03942<\/jats:sup>\n                    mice did not differ significantly from those in wild-type mice. These results show a species-specific difference in the effects of\n                    <jats:italic>ZNRF3\/Znrf3<\/jats:italic>\n                    exon 2 deletions in humans and mice;\n                    <jats:italic>Znrf3<\/jats:italic>\n                    <jats:sup>\u03942\/\u03942<\/jats:sup>\n                    mice do not develop congenital adrenal hypoplasia but instead exhibit moderate ZF hyperplasia, dispersed medulla arrangement, X-zone dysplasia, and macrophage infiltration occurred in the inner cortex.\n                  <\/jats:p>","DOI":"10.1530\/jme-24-0015","type":"journal-article","created":{"date-parts":[[2024,9,5]],"date-time":"2024-09-05T09:54:19Z","timestamp":1725530059000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-6","source":"Crossref","is-referenced-by-count":1,"title":["Znrf3 exon 2 deletion mice do not recapitulate congenital adrenal hypoplasia"],"prefix":"10.1530","volume":"73","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3817-6285","authenticated-orcid":true,"given":"Noboru","family":"Uchida","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Keio University School of Medicine, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7360-2465","authenticated-orcid":true,"given":"Tomohiro","family":"Ishii","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Keio University School of Medicine, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0457-6173","authenticated-orcid":true,"given":"Naoko","family":"Amano","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Keio University School of Medicine, Tokyo, Japan"},{"name":"Department of Pediatrics, Saitama City Hospital, Saitama, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9406-4683","authenticated-orcid":true,"given":"Shuji","family":"Takada","sequence":"additional","affiliation":[{"name":"Department of Systems BioMedicine, National Research Institute for Child Health and Development, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kyoko","family":"Kobayashi","sequence":"additional","affiliation":[{"name":"Laboratory of Veterinary Toxicology, Tokyo University of Agriculture and Technology, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5706-7842","authenticated-orcid":true,"given":"Tomoaki","family":"Murakami","sequence":"additional","affiliation":[{"name":"Laboratory of Veterinary Toxicology, Tokyo University of Agriculture and Technology, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0940-4517","authenticated-orcid":true,"given":"Satoshi","family":"Narumi","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Keio University School of Medicine, Tokyo, Japan"},{"name":"Department of Molecular Endocrinology, National Research Institute for Child Health and Development, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0143-3989","authenticated-orcid":true,"given":"Tomonobu","family":"Hasegawa","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Keio University School of Medicine, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"bib1","series-title":"Journal of Clinical Endocrinology and Metabolism","first-page":"641","article-title":"Single-exon deletions of ZNRF3 exon 2 cause congenital adrenal hypoplasia","volume":"20","author":"Amano","year":"2024","unstructured":"Amano NNarumi SAizu KMiyazawa MOkamura KOhashi HKatsumata NTomohiro I & Hasegawa T2024Single-exon deletions of ZNRF3 exon 2 cause congenital adrenal hypoplasia. 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