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To elucidate the specific role of each putative binding site, we generated constructs with mutations in the P65 binding motif 1 (MutA), motif 2 (MutB), or both (MutAB) (Fig

Taken together, these results confirm the involvement of CD38 in cancer cell proliferation, chemotaxis and survival, and highlight its potential as a target for therapy in CLL [33]