|Calculated MW||22745 Da|
|Other Names||Death domain-containing protein CRADD, Caspase and RIP adapter with death domain, RIP-associated protein with a death domain, CRADD, RAIDD|
|Target/Specificity||A synthetic peptide corresponding to residues in human RAIDD was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||RAIDD Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Apoptotic adaptor molecule specific for caspase-2 and FASL/TNF receptor-interacting protein RIP. In the presence of RIP and TRADD, CRADD recruits caspase-2 to the TNFR-1 signalling complex.|
|Cellular Location||Cytoplasm. Nucleus|
|Tissue Location||Constitutively expressed in most tissues, with particularly high expression in adult heart, testis, liver, skeletal muscle, fetal liver and kidney|
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Provided below are standard protocols that you may find useful for product applications.
RAIDD (RIP-associated ICH-1/CED-3-homologous protein with a death domain), is a dual-domain adaptor protein that is constitutively expressed in many tissues (1, 2). RAIDD has an N-terminal caspase recruitment domain (CARD) that interacts with the CARD of caspase-2, and a C-terminal death domain (DD) that interacts with the DD in PIDD (p53-induced protein with a death domain) (3). RAIDD has been shown to mediate the recruitment of CASPASE-2 to tumour necrosis factor receptor-1 (TNF-R1) signalling complex through RIP kinase. Apart from its established role in apoptosis, RAIDD may have an additional function in cell differentiation, supported by its expression in developing organs derived from the ectoderm, like heart and kidney. In developing heart and kidney RAIDD expression patterns are reported to overlap with known zones of cell death suggesting RAIDD may be involved in apoptosis-mediated remodeling (1).
1. Motaln H, et al. Transgenic Research, 14(1):27-40(14),2005
2. Ahmad M, et al. Cancer Res 57(4):615-9, 1997
3. Park HH, et al. J Mol Biol. 357(2):358-64, 2006
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