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Both antibodies induce cADPR consumption to increase ADPR production, consistent with a shift toward CD38 hydrolase activity and a 2–3‑fold rise in the ADPR/cADPR ratio
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IL-1α and IL-8, HSPA1A and FOSL1 were significantly upregulated following 24-h treatment with CuCl 2 and Cu(OAc) 2 at 58 and 580 μM without concomitant inhibition in cell viability
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