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SMAD3  -  SMAD family member 3

Gallus gallus

 
 
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Disease relevance of SMAD3

  • Furthermore, infection with a Smad 3-expressing retrovirus mimicked the effects of exogenously added TGF-beta, and induced PTHrP mRNA expression in the infected chondrocyte culture [1].
 

Psychiatry related information on SMAD3

 

High impact information on SMAD3

  • The TGF{beta} intracellular effector Smad3 regulates neuronal differentiation and cell fate specification in the developing spinal cord [2].
  • Within the intermediate and ventral domains, Smad3 promotes differentiation of ventral interneurons at the expense of motoneuron generation [2].
  • Interestingly, the effect is specific for Smad2, since expression of the structurally and functionally closely related Smad3 remains entirely unaffected [3].
  • In contrast, a dominant negative Smad 3 completely inhibited PTHrP promoter stimulation by TGF-beta, but only partially blocked the effect of TGF-beta on PTHrP mRNA synthesis [1].
 

Anatomical context of SMAD3

References

  1. PTHrP expression in chick sternal chondrocytes is regulated by TGF-beta through Smad-mediated signaling. Pateder, D.B., Ferguson, C.M., Ionescu, A.M., Schwarz, E.M., Rosier, R.N., Puzas, J.E., O'Keefe, R.J. J. Cell. Physiol. (2001) [Pubmed]
  2. The TGF{beta} intracellular effector Smad3 regulates neuronal differentiation and cell fate specification in the developing spinal cord. Garc??a-Campmany, L., Mart??, E. Development (2007) [Pubmed]
  3. Activin a signaling induces Smad2, but not Smad3, requiring protein kinase a activity in granulosa cells from the avian ovary. Schmierer, B., Schuster, M.K., Shkumatava, A., Kuchler, K. J. Biol. Chem. (2003) [Pubmed]
 
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