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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Kjellman, C. et al.

Kjellman, Honeth, Järnum, Lindvall, Darabi, Nilsson, Edvardsen, Salford, Widegren,

Identification and characterization of a human smad3 splicing variant lacking part of the linker region.

Smad3 is one of the signal transducers that are activated in response to transforming growth factor-beta (TGF-beta). We have identified and characterized a splicing variant of smad3. The splicing variant (smad3-Delta3) lacks exon 3 resulting in a truncated linker region. We could detect mRNA expression of smad3-Delta3 in all investigated human tissues. Real-time PCR analyses demonstrated that the fraction of smad3-Delta3 mRNA compared to normal smad3 varies between tissues. The amount of spliced mRNA was estimated to represent 0.5-5% of the normal smad3 mRNA. When smad3-Delta3 is overexpressed in a fibrosarcoma cell line, the Smad3-Delta3 is translocated to the nucleus upon TGF-beta stimulation and binds the Smad responsive element. Using a CAGA luciferase reporter system, we demonstrate that Smad3-Delta3 has transcriptional activity and we conclude that Smad3-Delta3 possesses functional transactivating properties.[1]

References

Identification and characterization of a human smad3 splicing variant lacking part of the linker region. Kjellman, C., Honeth, G., Järnum, S., Lindvall, M., Darabi, A., Nilsson, I., Edvardsen, K., Salford, L.G., Widegren, B. Gene (2004) [Pubmed]

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