|Positive WB detected in||K-562 cells, HEK-293 cells, HeLa cells, MCF-7 cells, mouse heart tissue, mouse kidney tissue, mouse liver tissue, mouse skeletal muscle tissue, mouse testis tissue, Raji cells|
|Positive IP detected in||mouse kidney tissue|
|Positive IHC detected in||human colon cancer tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Western Blot (WB)||WB : 1:500-1:2000|
|Immunoprecipitation (IP)||IP : 0.5-4.0 ug for IP and 1:500-1:2000 for WB|
|Immunohistochemistry (IHC)||IHC : 1:20-1:200|
|Sample-dependent, check data in validation data gallery|
10401-1-AP targets RAIDD in WB, IP, IHC,ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||RAIDD fusion protein Ag0630|
|Full Name||CASP2 and RIPK1 domain containing adaptor with death domain|
|Calculated molecular weight||23 kDa|
|Observed molecular weight||23 kDa|
|GenBank accession number||BC017042|
|Gene ID (NCBI)||8738|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
RAIDD, also named as CRADD, is an 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. CRADD interacts with BCL10 through its caspase recruitment domain and suppresses interactions between BCL10 and CARMA1. It is a negative regulator of the CARMA1 signalosome and suppressor of Th1-and Th17-mediated inflammatory responses.
J Biol Chem
The Adaptor CRADD/RAIDD Controls Activation of Endothelial Cells by Proinflammatory Stimuli.
Cutting edge: the "death" adaptor CRADD/RAIDD targets BCL10 and suppresses agonist-induced cytokine expression in T lymphocytes.
PIDDosome-induced p53-dependent ploidy restriction facilitates hepatocarcinogenesis.
E2F-Family Members Engage the PIDDosome to Limit Hepatocyte Ploidy in Liver Development and Regeneration.