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Publication : Transcriptional regulation of the mouse CSF-1 gene.

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.
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