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Mad upregulation and Id2 repression accompany transforming growth factor (TGF)-beta-mediated epithelial cell growth suppression.

Author	Peter M Siegel, Weiping Shu, Joan Massagué
Citation Information	The Journal of biological chemistry, 278:35444-50 (2003)
Keywords	Animals, Base Sequence, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Cell Division, Chromatin, DNA Primers, DNA-Binding Proteins, Dimerization, Epithelial Cells, Gene Expression Regulation, Genes, myc, Helix-Loop-Helix Motifs, Humans, Inhibitor of Differentiation Protein 2, Keratinocytes, Mice, Recombinant Proteins, Repressor Proteins, Transcription Factors, Transfection, Transforming Growth Factor beta
Applications	Chromatin Immunoprecipitation
Related Products	12-370, 12-371
Pub Med ID	12824180

The growth inhibitory cytokine TGF-beta enforces homeostasis of epithelia by activating processes such as cell cycle arrest and apoptosis. Id2 expression is often highest in proliferating epithelial cells and declines during differentiation. Recently, Id2 expression has been found to depend on Myc-Max transcriptional complexes. We observed that TGF-beta signaling inhibits Id2 expression in human and mouse epithelial cell lines from different tissue origins. Furthermore, the observed Id2 down-regulation by TGF-beta in mouse mammary epithelial cells occurs without a concurrent drop in c-Myc levels. However, sustained Id2 repression in these cells and in human keratinocytes coincides with induction of the Myc antagonistic repressors Mad2 and Mad4, decreased formation of Myc-Max heterodimers and the replacement of Myc-Max complexes with Mad-Max complexes on the Id2 promoter. These results argue that induction of Mad expression and Id2 down-regulation are important events during the TGF-beta cytostatic program in epithelial cells.