| First Author | Ueberham U | Year | 2009 |
| Journal | Int J Dev Neurosci | Volume | 27 |
| Issue | 5 | Pages | 501-10 |
| PubMed ID | 19375497 | Mgi Jnum | J:157285 |
| Mgi Id | MGI:4430473 | Doi | 10.1016/j.ijdevneu.2009.04.001 |
| Citation | Ueberham U, et al. (2009) Smad2 isoforms are differentially expressed during mouse brain development and aging. Int J Dev Neurosci 27(5):501-10 |
| abstractText | Smad2 and Smad3 are central molecules of the TGFbeta and activin receptor complex mediated intracellular signaling pathway. They function as important transcription factors playing essential roles in brain development. Interestingly they are also known to be involved in the pathogenesis of various neurological disorders (including Alzheimer's disease). Due to structural differences in the N-terminal Mad homology domain 1, Smad2 and Smad3 differ in their ability to bind DNA directly. A splice form of Smad2 lacking exon3, Smad2(Deltaexon3), assumes features of Smad3, in that it can directly bind to DNA resulting in a functional hybrid of Smad2 and Smad3 properties. There is very little information available on the expression of Smad2 isoforms in the brain. We report here that Smad2(Deltaexon3) is the most abundant of the two Smad2 isoforms in mouse brain and that Smad expression pattern alters during development and aging. Neuronal expression of Smad2(Deltaexon3) was confirmed by a single-cell PCR approach. Moreover, Smad2(Deltaexon3) predominates in the nuclear fraction of neurons, suggesting special function during brain differentiation. Our data indicate that there may be a specific role for Smad2(Deltaexon3) in neurons. |
