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Background
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DAXX is proposed to mediate activation of the JNK pathway and apoptosis via MAP3K5 in response to signaling from TNFRSF6 and TGFBR2. Interaction with HSPB1/HSP27 may prevent interaction with TNFRSF6 and MAP3K5 and block DAXX-mediated apoptosis. In contrast, in lymphoid cells JNC activation and TNFRSF6-mediated apoptosis may not involve DAXX. DAXX seems to regulate transcription in PML/POD/ND10 nuclear bodies together with PML and may influence TNFRSF6-dependent apoptosis thereby. This protein down-regulates basal and activated transcription, and it also seems to act as a transcriptional co-repressor and inhibits PAX3 and ETS1 through direct protein-protein interaction. DAXX modulates PAX5 activity. Its transcription repressor activity is modulated by recruiting it to subnuclear compartments like the nucleolus or PML/POD/ND10 nuclear bodies through interactions with MCSR1 and PML, respectively.
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Background
References
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- Cantrell, S.R., et al., J. Virol. 79(12):7792-7802 (2005).
- Greger, J.G., et al., J. Virol. 79(8):4610-4618 (2005).
- Chang, C.C., et al., J. Biol. Chem. 280(11):10164-10173 (2005).
- Beausoleil, S.A., et al., Proc. Natl. Acad. Sci. U.S.A. 101(33):12130-12135 (2004).
- Gostissa, M., et al., J. Biol. Chem. 279(46):48013-48023 (2004).
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