MiniSOX9, a dominant-negative variant in XXXX cells.

@entity1 @entity19 @entity5 @entity1373 @entity430 @entity694 @entity1935
Inherited and acquired changes in pre-mRNA processing have significant roles in @entity1 diseases, especially @entity5 . Characterization of aberrantly spliced mRNAs may thus contribute to understand malignant transformation. We recently reported an anti-oncogenic potential for the @entity1935 transcription factor in the colon. For instance, the @entity430 gene knock out in the @entity19 intestine results in an excess of proliferation with appearance of @entity1373 . @entity1935 is expressed in @entity694 cells but its endogenous activity is weak. We looked for @entity1935 variants that may impair @entity1935 activity in @entity694 cells and we discovered MiniSOX9, a truncated version of @entity1935 devoid of transactivation domain as a result of retention of the second intron. A significant overexpression of MiniSOX9 mRNA in @entity1 @entity5 samples compared with their matched normal tissues was observed by real-time reverse transcriptase-PCR. Immunohistochemistry revealed that MiniSOX9 is expressed at high levels in @entity1 @entity694 samples whereas it is undetectable in the surrounding healthy tissues. Finally, we discovered that MiniSOX9 behaves as a @entity1935 inhibitor, inhibits protein kinase Ca promoter activity and stimulates the canonical Wnt pathway. This potential oncogenic activity of the @entity1935 locus gives new insights on its role in @entity694 .
