Daxx Recombinant Rabbit Monoclonal Antibody [SC54-06]

Function

Activation of the cell surface receptor FAS by FAS ligand leads to the initiation of apoptosis, a process necessary for the regulation of the immune system and tissue homeostasis. FAS-mediated apoptosis appears to involve a number of divergent and overlapping pathways. Daxx appears to be a central component of a FAS-mediated apoptotic pathway involving the activation of Jun N-terminal kinase (JNK). Although Daxx itself does not contain a death domain, it specifically binds to the death domain of FAS. Overexpression of Daxx activates the JNK pathway and enhances FAS-mediated apoptosis. The Daxx apoptotic pathway acts cooperatively with but is distinct from the FAS-mediated pathway that involves interactions between the death domain-containing protein FADD and the cysteine protease FLICE. Unlike the FAS-FADD-FLICE pathway, the Daxx pathway is sensitive to the apoptotic inhibitor protein Bcl-2.

Background References

1. Full F et al. Herpesvirus saimiri antagonizes nuclear domain 10-instituted intrinsic immunity via an ORF3-mediated selective degradation of cellular protein Sp100. J Virol 86:3541-53 (2012).

2. Jiang M et al. Functional reorganization of promyelocytic leukemia nuclear bodies during BK virus infection. MBio 2:e00281-10 (2011).

Sequence Similarity

Belongs to the DAXX family.

Tissue Specificity

Ubiquitous.

Post-translational Modification

Sumoylated with SUMO1 on multiple lysine residues.; Phosphorylated by HIPK1 upon glucose deprivation.; Polyubiquitinated; which is promoted by CUL3 and SPOP and results in proteasomal degradation. Ubiquitinated by MDM2; inducing its degradation. Deubiquitinated by USP7; leading to stabilize it.

Subcellular Location

Cytoplasm, Nucleus, Chromosome.

UNIPROT

SwissProt: Q9UER7 Human

Synonyms