Cell type-specific regulation of calmodulin 2 expression by mutant p53

FEBS Letters
K X Knaup, K Roemer

Abstract

To identify genes that are stimulated by oncogenic forms of mutant p53, we studied, by microarray analysis and PCR-select subtractive hybridization, gene expression changes in human wild-type (wt) p53-negative immortal 041 fibroblasts infected to stably express p53 mutant 175H. In contrast to the wt p53 transactivator, 175H induced only few and weak, gene expression changes. We report here the stimulation of calmodulin 2 (CaM 2), but not CaM 1 or 3, gene expression specifically in 041 cells. The stimulation of the CaM 2 promoter required the 5' untranslated sequences as well as the integrity of the transactivation domain of 175H. However, direct binding of 175H to the 5'UT in vitro could not be demonstrated.

References

May 1, 1988·Molecular and Cellular Biology·J PohlV Schirrmacher
May 1, 1993·Nature Genetics·D DittmerA J Levine
Mar 1, 1996·Journal of Neuroscience Research·F B Berry, I R Brown
Nov 21, 1997·Nature·B InbalA Kimchi
Jun 6, 1998·Proceedings of the National Academy of Sciences of the United States of America·A GualbertoT D Tlsty
Jun 25, 1998·Molecular and Cellular Biology·M W FrazierG P Zambetti
Nov 13, 1998·Proceedings of the National Academy of Sciences of the United States of America·K WillW Deppert
Apr 28, 1999·The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society·A PalfiK Gulya
Aug 3, 2001·The Journal of Biological Chemistry·J SampathJ D Schuetz
Aug 3, 2002·Nature Reviews. Cancer·Karen H Vousden, Xin Lu
Aug 5, 2003·Biochemistry and Cell Biology = Biochimie Et Biologie Cellulaire·Ella Kim, Wolfgang Deppert

❮ Previous
Next ❯

Citations

Apr 3, 2007·Oncogene·L WeiszV Rotter
Feb 26, 2010·Cold Spring Harbor Perspectives in Biology·Moshe Oren, Varda Rotter
Dec 2, 2006·Journal of Proteome Research·Kim A WoodrowJames R Swartz

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis