Description
Product Characteristics:
The death domain (DD) containing protein PIDD is a p53 target gene in an erythroleukemia cell line that undergoes G1 phase arrest and subsequent apoptosis after p53 expression. Independently, PIDD was also described as a DD-containing protein with unknown function. The N-terminal region of PIDD contains seven leucine-rich repeats (LRRs), a protein interaction motif found in various proteins with diverse functions, followed by two ZU-5 domains and a C-terminal DD. PIDD forms a complex with caspase-2 and the adaptor protein RAIDD. Increased PIDD expression results in spontaneous activation of caspase-2 and sensitization to apoptosis by genotoxic stimuli, via interaction with caspase-2 and CRADD/RAIDD. PIDD also promotes apoptosis downstream of p53 as component of the DNA damage/stress response pathway that connects p53/TP53 to apoptosis. PIDD has also been shown to interact with NEMO/IKBKG and RIP1 and enhance sumoylation and ubiquitination of NEMO/IKBKG, an important component for activation of the transcription factor NF-kappa-B.
Subcellular location: Cytoplasm, Nucleus
Synonyms: Leucine rich repeats and death domain containing, Leucine-rich repeats and death domain containing, MGC16925, p53-induced protein with a death domain, PIDD, DKFZp434D229, PIDD_HUMAN.
Target Information: The protein encoded by this gene contains a leucine-rich repeat and a death domain. This protein has been shown to interact with other death domain proteins, such as Fas (TNFRSF6)-associated via death domain (FADD) and MAP-kinase activating death domain-containing protein (MADD), and thus may function as an adaptor protein in cell death-related signaling processes. The expression of the mouse counterpart of this gene has been found to be positively regulated by the tumor suppressor p53 and to induce cell apoptosis in response to DNA damage, which suggests a role for this gene as an effector of p53-dependent apoptosis. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Aug 2010]