A kinase-inactive type II TGFbeta receptor impairs BMP signaling in human breast cancer cells.

Dumont N, Arteaga CL
Biochem Biophys Res Commun. 2003 301 (1): 108-12

PMID: 12535648 · DOI:10.1016/s0006-291x(02)02977-7

Dominant negative receptor mutants are often utilized in order to abrogate signaling induced by growth factors. We have previously shown that expression of a dominant negative type II TGFbeta receptor (dnTbetaRII) in MDA-MB-231 breast cancer cells effectively abrogates TGFbeta signaling. In this letter, we report that expression of dnTbetaRII also impairs BMP2-mediated Smad1 phosphorylation as well as BMP2-mediated Smad-dependent transcriptional responses, resulting in an attenuation of BMP-mediated anti-proliferative effects. The fact that dnTbetaRII not only abrogates TGFbeta signaling but BMP signaling as well has important implications for the interpretation of data in which dominant negative mutants are utilized.

MeSH Terms (22)

Bone Morphogenetic Protein 2 Bone Morphogenetic Proteins Breast Neoplasms DNA-Binding Proteins Female Genes, Reporter Green Fluorescent Proteins Humans Luminescent Proteins Phosphorylation Protein-Serine-Threonine Kinases Receptor, Transforming Growth Factor-beta Type II Receptors, Transforming Growth Factor beta Recombinant Fusion Proteins Recombinant Proteins Signal Transduction Smad1 Protein Smad Proteins Trans-Activators Transcription, Genetic Transforming Growth Factor beta Tumor Cells, Cultured

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