{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T16:32:13Z","timestamp":1789662733596,"version":"4.0.1"},"reference-count":60,"publisher":"Bioscientifica","issue":"1","content-domain":{"domain":["jme.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,8]]},"abstract":"<jats:p>\n                    Insulin-like 3 (INSL3), a hormone produced by Leydig cells, regulates testicular descent during foetal life and bone metabolism in adults. Despite its importance, little is known about the molecular mechanisms controlling\n                    <jats:italic>INSL3<\/jats:italic>\n                    expression. Reduced\n                    <jats:italic>Insl3<\/jats:italic>\n                    mRNA levels were reported in the testis of mice deficient for chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII), an orphan nuclear receptor known to play critical roles in cell differentiation and lineage determination in several tissues. Although COUP-TFII-deficient mice had Leydig cell dysfunction and impaired fertility, it remained unknown whether\n                    <jats:italic>Insl3<\/jats:italic>\n                    expression was directly regulated by COUP-TFII. In this study, we observed a significant decrease in\n                    <jats:italic>Insl3<\/jats:italic>\n                    mRNA levels in MA-10 Leydig cells depleted of COUP-TFII. Furthermore, a \u22121087\u200abp mouse\n                    <jats:italic>Insl3<\/jats:italic>\n                    promoter was activated fourfold by COUP-TFII in MA-10 Leydig cells. Using 5\u2032 progressive deletions, the COUP-TFII-responsive element was located between \u2212186 and \u221279\u200abp, a region containing previously uncharacterised direct repeat 0-like (DR0-like) and DR3 elements. The recruitment and direct binding of COUP-TFII to the DR0-like element were confirmed by chromatin immunoprecipitation and DNA precipitation assay respectively. Mutation of the DR0-like element, which prevented COUP-TFII binding, significantly decreased COUP-TFII-mediated activation of the \u22121087\u200abp\n                    <jats:italic>Insl3<\/jats:italic>\n                    reporter in CV-1 fibroblast cells but not in MA-10 Leydig cells. Finally, we found that COUP-TFII cooperates with the nuclear receptor steroidogenic factor 1 (SF1) to further enhance\n                    <jats:italic>Insl3<\/jats:italic>\n                    promoter activity. Our results identify\n                    <jats:italic>Insl3<\/jats:italic>\n                    as a target for COUP-TFII in Leydig cells and revealed that COUP-TFII acts through protein\u2013protein interactions with other DNA-bound transcription factors, including SF1, to activate\n                    <jats:italic>Insl3<\/jats:italic>\n                    transcription in these cells.\n                  <\/jats:p>","DOI":"10.1530\/jme-13-0290","type":"journal-article","created":{"date-parts":[[2014,4,29]],"date-time":"2014-04-29T22:38:35Z","timestamp":1398811115000},"page":"43-55","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":45,"title":["The INSL3 gene is a direct target for the orphan nuclear receptor, COUP-TFII, in Leydig cells"],"prefix":"10.1530","volume":"53","author":[{"given":"Raifish 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