{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T00:03:55Z","timestamp":1761523435228,"version":"build-2065373602"},"reference-count":52,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2002,4,3]],"date-time":"2002-04-03T00:00:00Z","timestamp":1017792000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Developmental Dynamics"],"published-print":{"date-parts":[[2002,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Gene\u2010targeted disruption of <jats:italic>Grg5<\/jats:italic>, a mouse homologue of Drosophila groucho (<jats:italic>gro<\/jats:italic>), results in postnatal growth retardation in mice. The growth defect, most striking in approximately half of the <jats:italic>Grg5<\/jats:italic> null mice, occurs during the first 4\u20135 weeks of age, but most mice recover retarded growth later. We used the nonlinear mixed\u2010effects model to fit the growth data of wild\u2010type, heterozygous, and <jats:italic>Grg5<\/jats:italic> null mice. On the basis of preliminary evidence suggesting an interaction between <jats:italic>Grg5<\/jats:italic> and the transcription factor <jats:italic>Cbfa1\/Runx2<\/jats:italic>, critical for skeletal development, we further investigated the skeleton in the mice. A long bone growth plate defect was identified, which included shorter zones of proliferative and hypertrophic chondrocytes and decreased trabecular bone formation. This decreased trabecular bone formation is likely caused by a reduced recruitment of osteoblasts into the growth plate region of <jats:italic>Grg5<\/jats:italic> null mice. Like the growth defect, the growth plate and trabecular bone abnormality improved as the mice grew older. The growth plate defect was associated with reduced <jats:italic>Indian hedgehog<\/jats:italic> expression and signaling. We suggest that <jats:italic>Grg5<\/jats:italic>, a transcriptional coregulator, modulates the activities of transcription factors, such as <jats:italic>Cbfa1\/Runx2<\/jats:italic> in vivo to affect <jats:italic>Ihh<\/jats:italic> expression and the function of long bone growth plates. \u00a9 2002 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/dvdy.10089","type":"journal-article","created":{"date-parts":[[2002,8,25]],"date-time":"2002-08-25T19:24:15Z","timestamp":1030303455000},"page":"79-89","source":"Crossref","is-referenced-by-count":26,"title":["Growth defect in <i>Grg5<\/i> null mice is associated with reduced Ihh signaling in growth plates"],"prefix":"10.1002","volume":"224","author":[{"given":"Wen\u2010Fang","family":"Wang","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"You\u2010Gan","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anthony 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