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

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Repression of the antiapoptotic molecule galectin-3 by homeodomain-interacting protein kinase 2- activated p53 is required for p53-induced apoptosis.

Galectin 3 (Gal-3), a member of the beta-galactoside binding lectin family, exhibits antiapoptotic functions, and its aberrant expression is involved in various aspects of tumor progression. Here we show that p53-induced apoptosis is associated with transcriptional repression of Gal-3. Previously, it has been reported that phosphorylation of p53 at Ser46 is important for transcription of proapoptotic genes and induction of apoptosis and that homeodomain-interacting protein kinase 2 ( HIPK2) is specifically involved in these functions. We show that HIPK2 cooperates with p53 in Gal-3 repression and that this cooperation requires HIPK2 kinase activity. Gene-specific RNA interference demonstrates that HIPK2 is essential for repression of Gal-3 upon induction of p53-dependent apoptosis. Furthermore, expression of a nonrepressible Gal-3 prevents HIPK2- and p53-induced apoptosis. These results reveal a new apoptotic pathway induced by HIPK2- activated p53 and requiring repression of the antiapoptotic factor Gal-3.[1]

References

  1. Repression of the antiapoptotic molecule galectin-3 by homeodomain-interacting protein kinase 2-activated p53 is required for p53-induced apoptosis. Cecchinelli, B., Lavra, L., Rinaldo, C., Iacovelli, S., Gurtner, A., Gasbarri, A., Ulivieri, A., Del Prete, F., Trovato, M., Piaggio, G., Bartolazzi, A., Soddu, S., Sciacchitano, S. Mol. Cell. Biol. (2006) [Pubmed]
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