First Author | Harrington M | Year | 1997 |
Journal | Mol Reprod Dev | Volume | 46 |
Issue | 1 | Pages | 39-44; discussion 44-5 |
PubMed ID | 8981362 | Mgi Jnum | J:37431 |
Mgi Id | MGI:84824 | Doi | 10.1002/(SICI)1098-2795(199701)46:1<39::AID-MRD7>3.0.CO;2-S |
Citation | Harrington M, et al. (1997) Transcriptional regulation of the mouse CSF-1 gene. Mol Reprod Dev 46(1):39-44 |
abstractText | Research in our laboratory is aimed at understanding the cellular and molecular mechanisms that govern colony stimulating factor-1 (CSF-1) gene expression. Our hypothesis is that a basal set of trans-acting factors is bound to the CSF-1 gene during fibroblast proliferation, resulting in constitutive CSF-1 gene expression. Modulation of CSF-1 gene transcription by growth-arrest (decrease) or stimulation of growth-arrested fibroblasts (re-initiate) is mediated by changes in the basal set of factors bound and/or by the addition of stimulus-specific factors. We have extended our hypothesis to include other cell types (monocytes) to determine if mechanisms used to control CSF-1 gene expression in fibroblasts are unique or represent common nontissue-specific regulatory mechanisms. Analysis of CSF-1-CAT reporter constructs in transiently transfected fibroblasts and monocytes was used to identify CSF-1 genomic sequences that affect transcriptional activity. DNase I protection, electrophoretic mobility shift, and methylation interference assays were used to identify the putative cis-acting elements. Results of our study suggest multiple trans-acting factors may regulate CSF-1 gene expression; some may be tissue specific, while others, such as AP1, CTF/NF1, Sp1, and Sp3, are shared in common. |