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    J Biol Chem. 2004 Jan 23;279(4):2666-72. Epub 2003 Nov 11.

    A novel E1A-like inhibitor of differentiation (EID) family member, EID-2, suppresses transforming growth factor (TGF)-beta signaling by blocking TGF-beta-induced formation of Smad3-Smad4 complexes.

    Lee HJ, Lee JK, Miyake S, Kim SJ.

    Source

    Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892-5055, USA.

    Abstract

    Smad proteins play key roles in intracellular signaling of the transforming growth factor-beta (TGF-beta) superfamily. E1A, an adenoviral oncoprotein, is known to inhibit TGF-beta-induced transactivation through binding to Smad proteins. Recently, an EID-1 (E1A-like inhibitor of differentiation-1) and EID-2 (EID-1-like inhibitor of differentiation-2) were identified. In this study, we examined the effect of EID-2 on Smad-mediated TGF-beta signaling. Here, we show that EID-2 inhibits TGF-beta/Smad transcriptional responses. EID-2 interacts constitutively with Smad proteins, and most strongly with Smad3. Stable expression of EID-2 in the TGF-beta1-responsive cell line inhibits endogenous Smad3-Smad4 complex formation and TGF-beta1-induced expression of p21 and p15. These results suggest that EID-2 may function as an endogenous suppressor of TGF-beta signaling.

    PMID:
    14612439
    [PubMed - indexed for MEDLINE]
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