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Gene Review

smad7  -  SMAD family member 7

Xenopus laevis

Synonyms: Smad10, madh7, smad8, xsmad7
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Disease relevance of madh7

  • Smad7 inhibits additional TGF-beta related pathways, and causes spina bifida when misexpressed dorsally [1].

High impact information on madh7

  • In contrast, memory is abolished by increasing the targeting of receptors to the lysosome through expression of the Smad7/Smurf2 ubiquitin ligase [2].
  • Other cell-autonomous inhibitors of the BMP pathway are more widely expressed, such as the inhibitory Smads, Smad6 and Smad7 [3].
  • In order to address this issue and to identify downstream targets after BMP inhibition, we have monitored the transcriptional changes in ectodermal explants neuralized by Smad7 using a Xenopus laevis 5000-clone gastrula-stage cDNA microarray [4].
  • The mutation results in enhanced association of Smad10 with the nuclear transcription corepressor Ski and leads to its neural inducing activity through inhibition of bone morphogenetic protein (BMP) signaling [5].
  • We report that Smad10 is a mutant form of Smad4beta that harbors a missense mutation of a conserved arginine to histidine in the MH1 domain [5].

Anatomical context of madh7

  • Thus, Smad7 acts as a potent inhibitor of mesoderm formation and also activates the default neural induction pathway [6].
  • Smad7 is present at fairly constant levels throughout early development and at blastula stages enriched in the ventral side of the animal hemisphere [6].
  • Smad7 is able to directly activate neural markers in explants in the absence of mesoderm or endoderm [6].

Other interactions of madh7

  • In addition, Smurf1 associates with transforming growth factor-beta type I receptor through the inhibitory Smad (I-Smad) Smad7 and induces their degradation [7].

Analytical, diagnostic and therapeutic context of madh7

  • In this report, we show that Smad10, a member of the Smad family of intracellular transducers of TGFbeta signaling, is required for formation of the nervous system [8].


  1. Dissection of inhibitory Smad proteins: both N- and C-terminal domains are necessary for full activities of Xenopus Smad6 and Smad7. Nakayama, T., Berg, L.K., Christian, J.L. Mech. Dev. (2001) [Pubmed]
  2. Morphogen gradient interpretation by a regulated trafficking step during ligand-receptor transduction. Jullien, J., Gurdon, J. Genes Dev. (2005) [Pubmed]
  3. Cell fate specification and competence by Coco, a maternal BMP, TGFbeta and Wnt inhibitor. Bell, E., Muñoz-Sanjuán, I., Altmann, C.R., Vonica, A., Brivanlou, A.H. Development (2003) [Pubmed]
  4. Gene profiling during neural induction in Xenopus laevis: regulation of BMP signaling by post-transcriptional mechanisms and TAB3, a novel TAK1-binding protein. Muñoz-Sanjuán, I., Bell, E., Altmann, C.R., Vonica, A., Brivanlou, A.H. Development (2002) [Pubmed]
  5. Function of the two Xenopus smad4s in early frog development. Chang, C., Brivanlou, A.H., Harland, R.M. J. Biol. Chem. (2006) [Pubmed]
  6. Smad7 inhibits mesoderm formation and promotes neural cell fate in Xenopus embryos. Bhushan, A., Chen, Y., Vale, W. Dev. Biol. (1998) [Pubmed]
  7. Cooperative inhibition of bone morphogenetic protein signaling by Smurf1 and inhibitory Smads. Murakami, G., Watabe, T., Takaoka, K., Miyazono, K., Imamura, T. Mol. Biol. Cell (2003) [Pubmed]
  8. Smad10 is required for formation of the frog nervous system. LeSueur, J.A., Fortuno, E.S., McKay, R.M., Graff, J.M. Dev. Cell (2002) [Pubmed]
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