{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T17:17:33Z","timestamp":1793812653366,"version":"4.6.1"},"reference-count":75,"publisher":"American Society of Hematology","issue":"1","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2002,1,1]]},"abstract":"<jats:p>The effects of colony-stimulating factor 1 (CSF-1), the primary regulator of mononuclear phagocyte production, are thought to be mediated by the CSF-1 receptor (CSF-1R), encoded by the c-fms proto-oncogene. To investigate the in vivo specificity of CSF-1 for the CSF-1R, the mouse Csf1r gene was inactivated. The phenotype ofCsf1\u2212\/Csf1r\u2212 mice closely resembled the phenotype of CSF-1-nullizygous(Csf1op\/Csf1op) mice, including the osteopetrotic, hematopoietic, tissue macrophage, and reproductive phenotypes. Compared with their wild-type littermates, splenic erythroid burst-forming unit and high-proliferative potential colony-forming cell levels in bothCsf1op\/Csf1op andCsf1\u2212\/Csf1r\u2212 mice were significantly elevated, consistent with a negative regulatory role of CSF-1 in erythropoiesis and the maintenance of primitive hematopoietic progenitor cells. The circulating CSF-1 concentration inCsf1r\u2212\/Csf1r\u2212 mice was elevated 20-fold, in agreement with the previously reported clearance of circulating CSF-1 by CSF-1R\u2013mediated endocytosis and intracellular destruction. Despite their overall similarity, several phenotypic characteristics of theCsf1r\u2212\/Csf1r\u2212 mice were more severe than those of theCsf1op\/Csf1op mice. The results indicate that all of the effects of CSF-1 are mediated via the CSF-1R, but that subtle effects of the CSF-1R could result from its CSF-1\u2013independent activation.<\/jats:p>","DOI":"10.1182\/blood.v99.1.111","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T08:47:58Z","timestamp":1027759678000},"page":"111-120","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":1077,"title":["Targeted disruption of the mouse colony-stimulating factor 1 receptor gene results in osteopetrosis, mononuclear phagocyte deficiency, increased primitive progenitor cell frequencies, and reproductive defects"],"prefix":"10.1182","volume":"99","author":[{"given":"Xu-Ming","family":"Dai","sequence":"first","affiliation":[{"name":"From the Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory R.","family":"Ryan","sequence":"additional","affiliation":[{"name":"From the Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew J.","family":"Hapel","sequence":"additional","affiliation":[{"name":"From the Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melissa G.","family":"Dominguez","sequence":"additional","affiliation":[{"name":"From the Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert G.","family":"Russell","sequence":"additional","affiliation":[{"name":"From the Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sara","family":"Kapp","sequence":"additional","affiliation":[{"name":"From the Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vonetta","family":"Sylvestre","sequence":"additional","affiliation":[{"name":"From the Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E. 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