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].

References