High impact information on Cradd

• Furthermore, cells lacking the adapter molecule RAIDD failed to activate caspase-2 after heat shock treatment and showed resistance to apoptosis in this setting [1].
• Our results also show that caspase-2(-/-), in contrast to RAIDD(-/-), mouse embryonic fibroblasts, are only partially resistant to PIDD [2].
• Apoptosis caused by p53-induced protein with death domain (PIDD) depends on the death adapter protein RAIDD [2].
• A 500-kb YAC and BAC contig encompassing the high-growth deletion in mouse chromosome 10 and identification of the murine Raidd/Cradd gene in the candidate region [3].
• The human RAIDD/CRADD was mapped using radiation hybrid mapping to human chromosome 12, 2.9 cR distal to marker AFMB311WC5 [3].

Biological context of Cradd

• In situ analysis of Raidd-beta-galactosidase fusion gene expression in transgenic mouse midgestation embryos [4].
• In developing heart and kidney Raidd expression patterns overlapped with known zones of cell death suggesting Raidd may be involved in apoptosis-mediated remodelling [4].
• Thus, to elucidate the role of Raidd during mouse embryogenesis when the processes of organogenesis are most dynamic, we studied the Raidd expression pattern in midgestation mouse embryos [4].
• We generated Raidd+/- transgenic mice with a reporter transgene encoding the bacterial Beta-galactosidase (beta-gal) under the control of Raidd promoter [4].
• However, Raidd overexpression studies suggest that apart from the established role in apoptosis, Raidd may have an additional function in cell differentiation [4].

Anatomical context of Cradd

• In addition, Raidd expression was found in developing mesenchyme organs like heart and kidney and in the endothelial lining of the midgut at the time when profound morphological changes take place in these organs [4].
• During the midgestation period (E8.5-E12.5), Raidd is expressed in developing organs derived from the ectoderm such as lens, structures of the inner ear and the fourth brain ventricle in regions where differentiation takes place implicating Raidd role in this process [4].
• To study the possibility of a novel system of cell ablation mediated by RAIDD, a preadipocyte cell line (3T3L1) was stably transfected with a plasmid containing the murine Raidd cDNA under the control of the adipocyte specific promoter aP2 [5].

Associations of Cradd with chemical compounds

• RAIDD (RIP-associated ICH-1 homologous protein with a death domain) is an adaptor molecule that mediates the action of cysteine proteases involved in apoptosis [5].

Other interactions of Cradd

• In this study, we could not generate Raidd null adult mice suggesting that lack of function of Raidd might be embryonic lethal [4].

References