Abstract
Yoshida et al. generated knockout mice lacking the Tob protein, a member of a family of proteins implicated in inhibition of cell proliferation. The Tob knockout animals showed increased bone mass that apparently resulted from increased abundance of osteoblasts. Bone formation in response to bone morphogenetic protein 2 (BMP2) was increased in the knockout animals. In transiently transfected cells, the authors could show that BMP-mediated transcriptional regulation mediated by Smad proteins was inhibited by overexpression of Tob. Immunoprecipitation of protein complexes from cells overexpressing Tob and Smads showed that Tob interacted with Smads 1, 4, 5, and 8 and that BMP signaling could enhance the interaction. Overexpression of Tob also caused localization of Smads to nuclear bodies. The authors suggest that Tob functions as an inhibitor of BMP-Smad signaling through direct interaction with Smads. Yoshida, Y., Tanaka, S., Umemori, H., Minowa, O., Usui, M., Ikematsu, N., Hosoda, E., Imamura, T., Kuno, J., Yamashita, T., Miyazono, K., Noda, M., Noda, T., and Yamamoto, T. (2000) Negative regulation of BMP/Smad signaling by Tob in osteoblasts. Cell 103 : 1085-1097. [Online Journal]
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