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Gene. 2004 Mar 3;327(2):141-52.

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

Author information

1
Section of Tumor Immunology, Department of Cell and Molecular Biology, Lund University, BMC I12, 221 84, Lund, Sweden. Christian.Kjellman@wblab.lu.se

Abstract

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.

PMID:
14980711
DOI:
10.1016/j.gene.2003.11.026
[Indexed for MEDLINE]

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