{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T22:08:48Z","timestamp":1787004528502,"version":"build-2736575974"},"reference-count":26,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2001,12,20]],"date-time":"2001-12-20T00:00:00Z","timestamp":1008806400000},"content-version":"vor","delay-in-days":141,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes to Cells"],"published-print":{"date-parts":[[2001,8]]},"abstract":"<jats:p>\n                    <jats:bold>Background<\/jats:bold>\n                    Sp4 is a zinc finger transcription factor which is closely related to Sp1 and Sp3. All three proteins recognize the same DNA elements and can act as transcriptional activators through glutamine\u2010rich activation domains. Unlike Sp1 and Sp3, which are ubiquitous proteins, Sp4 is highly abundant in the central nervous system, but also detectable in many other tissues.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results<\/jats:bold>\n                    We have disrupted the mouse\n                    <jats:italic>Sp4<\/jats:italic>\n                    gene by a targeted deletion of the exons encoding the N\u2010terminal activation domains.\n                    <jats:italic>Sp4<\/jats:italic>\n                    knockout mice show a complete absence of\n                    <jats:italic>Sp4<\/jats:italic>\n                    expression. They develop until birth without obvious abnormalities. After birth, two\u2010thirds die within 4 weeks. Surviving mice are growth retarded. Male\n                    <jats:italic>Sp4<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>null<\/jats:italic>\n                    <\/jats:sup>\n                    mice do not breed. The cause for the breeding defect remains obscure since they show complete spermatogenesis. In addition, pheromone receptor genes in the vomeronasal organ appear unaffected. Female\n                    <jats:italic>Sp4<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>null<\/jats:italic>\n                    <\/jats:sup>\n                    mice have a smaller thymus, spleen and uterus. In addition, they exhibit a pronounced delay in sexual maturation.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusions<\/jats:bold>\n                    The phenotype of the\n                    <jats:italic>Sp4<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>null<\/jats:italic>\n                    <\/jats:sup>\n                    mice differs significantly from those described for\n                    <jats:italic>Sp1<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2013\/\u2013<\/jats:italic>\n                    <\/jats:sup>\n                    and\n                    <jats:italic>Sp3<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2013\/\u2013<\/jats:italic>\n                    <\/jats:sup>\n                    mice. Thus, the structural similarities, the common recognition motif and the overlapping expression pattern of these three transcription factors do not reflect similar physiological functions.\n                  <\/jats:p>","DOI":"10.1046\/j.1365-2443.2001.00455.x","type":"journal-article","created":{"date-parts":[[2003,3,11]],"date-time":"2003-03-11T17:48:28Z","timestamp":1047404908000},"page":"689-697","source":"Crossref","is-referenced-by-count":50,"title":["Complex phenotype of mice homozygous for a null mutation in the\n                    <i>Sp4<\/i>\n                    transcription factor 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