High impact information on SMAD2

• We also provide evidence that Gdf11 induces Smad2 phosphorylation and activated Smad2 is able to induce caudal Hox gene expression [1].
• Interestingly, the effect is specific for Smad2, since expression of the structurally and functionally closely related Smad3 remains entirely unaffected [2].
• The cytosolic signal transducer Smad2 is most highly expressed in chicken granulosa cells (cGC) of preovulatory follicles [2].
• In the absence of activin A, strong PKA activators such as follicle-stimulating hormone (FSH) and 8-bromo-cyclic AMP fail to elicit Smad2 induction [2].
• However, FSH and 8-bromo-cyclic AMP boost activin A-dependent Smad2 up-regulation, giving rise to Smad2 levels similar to expression in vivo levels [2].

Biological context of SMAD2

• Moreover, TGFbeta1-evoked increases in phosphorylation of SMAD2 were reduced by manumycin-A, suggesting that Ras-dependent transduction cascades activated by TGFbeta1 feed back onto SMAD signaling [3].

Associations of SMAD2 with chemical compounds

• Smad2 RNA injection leads to ectopic expression of XFD-4'. Since activation is also observed in activin A treated animal cap explants in the presence of cycloheximide, XFD-4/4' genes represent direct targets of activin signaling [4].

Other interactions of SMAD2

• Aza-treated ACs displayed less Smad2 and 3 and increased Smad1, 5, and Smurf2 protein and showed a loss of TGF-beta signaling on the P3TP-luciferase reporter [5].
• Suggesting that Aza-induction of Smurf2 may be responsible for the loss of Smad2 and 3 protein via this pathway, immunoprecipitation and metabolic labeling experiments confirmed that Aza accelerated the ubiquitination and degradation of these targets [5].

References