| First Author | Li J | Year | 2006 |
| Journal | Genesis | Volume | 44 |
| Issue | 7 | Pages | 328-35 |
| PubMed ID | 16823860 | Mgi Jnum | J:110981 |
| Mgi Id | MGI:3652474 | Doi | 10.1002/dvg.20219 |
| Citation | Li J, et al. (2006) Conditional deletion of the colony stimulating factor-1 receptor (c-fms proto-oncogene) in mice. Genesis 44(7):328-35 |
| abstractText | Colony stimulating factor-1 (CSF-1) is the primary regulator of the mononuclear phagocytic lineage acting through its transmembrane tyrosine kinase receptor, CSF-1R, that is the product of the c-fms proto-oncogene. Null mutations in either the ligand or the receptor genes result in a severe osteopetrosis as well as a number of other phenotypes, including reproductive defects and perturbations in organ development. The CSF-1R is also expressed in oocytes, myoblast progenitors, decidual, and trophoblastic cells. To distinguish cell type specific phenotypes, we have created a conditional allele of the Csf1r by placing LoxP sites around Exon 5 of the Csf1r gene in mice. Excision of this floxed sequence results in a null allele that in the homozygous state gives a phenotype indistinguishable of the complete Csf1r null mutant mouse. This conditional allele will prove extremely valuable to study the spatial and temporal roles of CSF-1R. genesis 44:328-335, 2006. (c) 2006 Wiley-Liss, Inc. |
