DGKζ, a lipid kinase, phosphorylates the
second messenger DAG, terminating DAG - mediated activation of RasGRP1 and PKC - θ, whereas Cbl - b, an E3 ubiquitin ligase, facilitates ubiquitination and subsequent degradation of the p85 subunit of PI (3) K. Previous studies have evaluated numerous aspects of T cell biology in the two
models (16 — 18, 25, 38), but the signaling and functional effects of DKGζ deficiency and Cbl - b deficiency in T cells had not been directly compared.