Effects of Ser2 and Tyr6 mutants of BAF53 on cell growth and p53-dependent transcription.
BAF53 is an actin-related protein that shuttles between nucleus and cytoplasm. In the nucleus, it constitutes an integral component of many chromatin-modifying complexes such as the SWI/SNF, TIP60, TRRAP, and TIP48/49 complexes. BAF53 is essential for growth, but its function remains elusive. BAF53 homologues from yeast to humans have a conserved N-terminal motif, MS_(G/A)(G/A)_(V/L)YGG, which is unique to these proteins. Previously we showed that over-expression of an N-terminal deletion mutant of BAF53 (BAF53_deltaN) reduced the viability of HEK293 and HeLa cells. When we replaced the serine 2 and tyrosine 6 of this N-terminal motif with alanine, over-expression of the alanine-replaced BAF53 strongly impaired the growth of HEK293 cells whereas replacement with aspartate/glutamate had no effect. The alanine-replaced BAF53 mutants also stimulated p53-dependent transcription, in which the SWI/SNF and TRRAP complexes are involved. Our results demonstrate that serine 2 and tyrosine 6 play important roles in BAF53 activity.[1]References
- Effects of Ser2 and Tyr6 mutants of BAF53 on cell growth and p53-dependent transcription. Lee, J.H., Lee, J.Y., Chang, S.H., Kang, M.J., Kwon, H. Mol. Cells (2005) [Pubmed]
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