Smad7 binds to Smurf2 to form an E3 ubiquitin ligase that targets the TGF beta receptor for degradation.

[1]  H. Lodish,et al.  The types II and III transforming growth factor-beta receptors form homo-oligomers , 1994, The Journal of cell biology.

[2]  M. Sudol,et al.  The WW domain of Yes-associated protein binds a proline-rich ligand that differs from the consensus established for Src homology 3-binding modules. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[3]  B. André,et al.  NPI1, an essential yeast gene involved in induced degradation of Gap1 and Fur4 permeases, encodes the Rsp5 ubiquitin—protein ligase , 1995, Molecular microbiology.

[4]  P. Hoodless,et al.  MADR2 Is a Substrate of the TGFβ Receptor and Its Phosphorylation Is Required for Nuclear Accumulation and Signaling , 1996, Cell.

[5]  M. Centrella,et al.  Rapid Flux in Transforming Growth Factor-β Receptors on Bone Cells* , 1996, The Journal of Biological Chemistry.

[6]  C. Arteaga,et al.  Processing of the transforming growth factor beta type I and II receptors. Biosynthesis and ligand-induced regulation. , 1997, The Journal of biological chemistry.

[7]  O. Staub,et al.  Regulation of stability and function of the epithelial Na+ channel (ENaC) by ubiquitination , 1997, The EMBO journal.

[8]  J. Wrana,et al.  The MAD-Related Protein Smad7 Associates with the TGFβ Receptor and Functions as an Antagonist of TGFβ Signaling , 1997, Cell.

[9]  C. Heldin,et al.  Identification of Smad7, a TGFβ-inducible antagonist of TGF-β signalling , 1997, Nature.

[10]  K. Miyazono,et al.  Smad6 inhibits signalling by the TGF-β superfamily , 1997, Nature.

[11]  H. Lodish,et al.  Biosynthesis of the type I and type II TGF-beta receptors. Implications for complex formation. , 1997, The Journal of biological chemistry.

[12]  J. Bonifacino,et al.  Ubiquitin and the control of protein fate in the secretory and endocytic pathways. , 1998, Annual review of cell and developmental biology.

[13]  C. Heldin,et al.  Induction of inhibitory Smad6 and Smad7 mRNA by TGF-beta family members. , 1998, Biochemical and biophysical research communications.

[14]  A. Ciechanover,et al.  The ubiquitin system. , 1998, Annual review of biochemistry.

[15]  J. Massagué,et al.  Smad6 inhibits BMP/Smad1 signaling by specifically competing with the Smad4 tumor suppressor. , 1998, Genes & development.

[16]  J. Doré,et al.  Differential Requirement for Type I and Type II Transforming Growth Factor β Receptor Kinase Activity in Ligand-mediated Receptor Endocytosis* , 1998, The Journal of Biological Chemistry.

[17]  Liliana Attisano,et al.  SARA, a FYVE Domain Protein that Recruits Smad2 to the TGFβ Receptor , 1998, Cell.

[18]  C. Heldin,et al.  Transforming Growth Factor β1 Induces Nuclear Export of Inhibitory Smad7* , 1998, The Journal of Biological Chemistry.

[19]  B. André,et al.  Nitrogen-regulated ubiquitination of the Gap1 permease of Saccharomyces cerevisiae. , 1998, Molecular biology of the cell.

[20]  R. Derynck,et al.  Transcriptional Activators of TGF-β Responses: Smads , 1998, Cell.

[21]  A Ciechanover,et al.  Ubiquitin ligase activity and tyrosine phosphorylation underlie suppression of growth factor signaling by c-Cbl/Sli-1. , 1999, Molecular cell.

[22]  R. Baron,et al.  Ligand-induced Ubiquitination of the Epidermal Growth Factor Receptor Involves the Interaction of the c-Cbl RING Finger and UbcH7* , 1999, The Journal of Biological Chemistry.

[23]  L. Hicke.  Gettin' down with ubiquitin: turning off cell-surface receptors, transporters and channels. , 1999, Trends in cell biology.

[24]  T. Hunter,et al.  The tyrosine kinase negative regulator c-Cbl as a RING-type, E2-dependent ubiquitin-protein ligase. , 1999, Science.

[25]  J. Massagué,et al.  Ubiquitin-dependent degradation of TGF-β-activated Smad2 , 1999, Nature Cell Biology.

[26]  Jeffrey L. Wrana,et al.  A SMAD ubiquitin ligase targets the BMP pathway and affects embryonic pattern formation , 1999, Nature.

[27]  K. Luo,et al.  Negative Feedback Regulation of TGF-β Signaling by the SnoN Oncoprotein , 1999 .

[28]  J. Massagué,et al.  Inhibition of transforming growth factor-β/SMAD signalling by the interferon-γ/STAT pathway , 1999, Nature.

[29]  R. Weinberg,et al.  SnoN and Ski protooncoproteins are rapidly degraded in response to transforming growth factor beta signaling. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[30]  M. O’Connor-McCourt,et al.  Down-regulation of transforming growth factor-beta receptors: cooperativity between the types I, II, and III receptors and modulation at the cell surface. , 1999, Experimental cell research.

[31]  E. Bottinger,et al.  A mechanism of suppression of TGF–β/SMAD signaling by NF-κB/RelA , 2000, Genes & Development.

[32]  J. Massagué,et al.  Controlling TGF-β signaling , 2000, Genes & Development.

[33]  J. Wrana.  Regulation of Smad Activity , 2000, Cell.

[34]  Z. Ronai,et al.  SUMO-1 Modification of Mdm2 Prevents Its Self-Ubiquitination and Increases Mdm2 Ability to Ubiquitinate p53 , 2000, Cell.

[35]  P. van Kerkhof,et al.  Endocytosis and Degradation of the Growth Hormone Receptor Are Proteasome-dependent* , 2000, The Journal of Biological Chemistry.