{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T21:32:23Z","timestamp":1788298343106,"version":"build-2803163510"},"reference-count":35,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2025,10,3]],"date-time":"2025-10-03T00:00:00Z","timestamp":1759449600000},"content-version":"vor","delay-in-days":2,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2025,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    GPR39, a zinc\u2010sensing receptor, is essential for bone homeostasis in male mice through regulation of osteoblast function and matrix composition. This study examined the effects of GPR39 deficiency in female mice using both global and osteoblast lineage\u2010specific GPR39 knockout models (\n                    <jats:italic>Gpr39<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>Ob<\/jats:italic>\n                      \u2212\n                      <jats:italic>\/Ob<\/jats:italic>\n                      \u2212\n                    <\/jats:sup>\n                    ). In vivo, GPR39\u2010deficient female mice exhibited reduced bone mass, increased mineralization rates, and significantly lower and more variable serum levels of pro\u2010collagen type I N\u2010propeptide (PINP), indicating impaired collagen synthesis and matrix remodeling. OVX models further demonstrated that GPR39 deficiency exacerbates estrogen\u2010deficiency\u2010induced bone loss, highlighting its protective role in postmenopausal\u2010like states. Osteoblast lineage\u2010specific GPR39 deletion replicated the skeletal abnormalities observed in global knockouts, revealing that GPR39 activity in the osteoblast lineage is indispensable for proper collagen deposition and mineralization. Western blot analysis of\n                    <jats:italic>Gpr39<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>Ob<\/jats:italic>\n                      \u2212\n                      <jats:italic>\/Ob<\/jats:italic>\n                      \u2212\n                    <\/jats:sup>\n                    osteoblasts confirmed reduced extracellular collagen levels, while quantitative mRNA analysis of Col1a2 revealed zinc signaling through GPR39 as a key regulator of collagen production. Zinc\u2010induced Col1a2 expression, dependent on GPR39 and mediated via G\u03b1\n                    <jats:sub>q<\/jats:sub>\n                    signaling, was abolished in GPR39\u2010deficient osteoblasts. These findings provide insights into how zinc signaling via GPR39 regulates osteoblast function and collagen synthesis, emphasizing its role in maintaining matrix composition. Targeting GPR39 may offer novel therapeutic strategies for osteoporosis and other bone disorders characterized by impaired matrix remodeling.\n                  <\/jats:p>","DOI":"10.1002\/jcp.70095","type":"journal-article","created":{"date-parts":[[2025,10,3]],"date-time":"2025-10-03T11:59:26Z","timestamp":1759492766000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["The Role of GPR39 in Regulating Osteoblast Function, Bone Matrix Quality, and Gender\u2010Specific Bone Homeostasis"],"prefix":"10.1002","volume":"240","author":[{"given":"Biplab","family":"Chaterjee","sequence":"first","affiliation":[{"name":"Department of Physiology and Cell Biology Ben\u2010Gurion University of the Negev Beer\u2010Sheva Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gal","family":"Gozlan","sequence":"additional","affiliation":[{"name":"Department of Physiology and Cell Biology Ben\u2010Gurion University of the Negev Beer\u2010Sheva Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chen","family":"Abramovitch\u2010Dahan","sequence":"additional","affiliation":[{"name":"Department of Physiology and Cell Biology Ben\u2010Gurion University of the Negev Beer\u2010Sheva Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anton","family":"Davydok","sequence":"additional","affiliation":[{"name":"Institute of Material Physics, Hereon Outstation at DESY Helmholtz Zentrum Hereon Hamburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anat","family":"Reiner\u2010Benaim","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Biostatistics and Community Health Sciences Ben\u2010Gurion University of the Negev Beer\u2010Sheva Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes","family":"Krug","sequence":"additional","affiliation":[{"name":"Department of Osteology and Biomechanics University Medical Center Hamburg\u2010Eppendorf Hamburg Germany"},{"name":"Interdisciplinary Competence Center for Interface Research Hamburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katharina","family":"J\u00e4hn\u2010Rickert","sequence":"additional","affiliation":[{"name":"Department of Osteology and Biomechanics University Medical Center Hamburg\u2010Eppendorf Hamburg Germany"},{"name":"Interdisciplinary Competence Center for Interface Research Hamburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bj\u00f6rn","family":"Busse","sequence":"additional","affiliation":[{"name":"Department of Osteology and Biomechanics University Medical Center Hamburg\u2010Eppendorf Hamburg Germany"},{"name":"Interdisciplinary Competence Center for Interface Research Hamburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7747-3883","authenticated-orcid":false,"given":"Noam","family":"Levaot","sequence":"additional","affiliation":[{"name":"Department of Physiology and Cell Biology Ben\u2010Gurion University of the Negev Beer\u2010Sheva Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2025,10,3]]},"reference":[{"issue":"1","key":"e_1_2_9_2_1","first-page":"231","article-title":"The Role of Zinc in the Endocrine System","volume":"32","author":"Baltaci A. 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