Duncan M R, Rankin P R, King R L, Jacobson M K, Dell'Orco R T
Samuel Roberts Noble Foundation, Inc., Ardmore, Oklahoma 73402.
J Cell Physiol. 1988 Jan;134(1):161-5. doi: 10.1002/jcp.1041340121.
Lowering extracellular calcium in cultures of human diploid fibroblast-like cells caused a rapid depletion of NAD pools. This loss of NAD was reversed by restoring extracellular Ca2+ and was inhibited by 3-aminobenzamide, an inhibitor of ADP-ribosyl transfer reactions. The concentrations of 3-aminobenzamide needed to inhibit the loss of NAD were consistent with those required to inhibit cellular mono(ADP-ribosyl) rather than poly(ADP-ribosyl) reactions. Calcium depletion did not inhibit the biosynthesis of NAD. These results suggest that mono(ADP-ribosyl)ation is involved in the regulation of cellular Ca2+ levels.
降低人二倍体成纤维样细胞培养物中的细胞外钙会导致NAD池迅速耗尽。通过恢复细胞外Ca2+可逆转这种NAD的损失，并且该过程受到3-氨基苯甲酰胺（一种ADP-核糖基转移反应抑制剂）的抑制。抑制NAD损失所需的3-氨基苯甲酰胺浓度与抑制细胞单（ADP-核糖基）反应而非多（ADP-核糖基）反应所需的浓度一致。钙耗竭并不抑制NAD的生物合成。这些结果表明，单（ADP-核糖基）化参与细胞Ca2+水平的调节。
