Intracellular C3 protects β-cells from IL-1β-driven cytotoxicity via interaction with Fyn-related kinase.

In our hands, extracellular addition of C3a did not make statistically significant changes in cell survival, although there was a nonsignificant trend toward improved survival of C3 −/− clones ( Fig. 3 B ) up to 100 nM C3a, levels which are unlikely to be achieved in vivo, where C3a is rapidly inactivated by serum carboxypeptidase N ( 44 ).

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