2.4.99.20 malfunction generation of CD38(-/-) knockout mice of determine the role of this enzyme 724210 2.4.99.20 physiological function calcium signaling messengers nicotinate-adenine dinucleotide phosphate and 2'-phospho-cyclic ADP-ribose are not produced when lymphokine-activated killer cells prepared from CD38 knock-out mice are treated with interleukin IL-8. Application of 2'-phospho-cyclic ADP-ribose to lymphikine-activated killer cells induces nicotinate-adenine dinucleotide phosphate production, whereas nicotinate-adenine dinucleotide phosphate fails to increase intracellular 2'-phospho-cyclic ADP-ribose levels. IL-8-induced nicotinate-adenine dinucleotide phosphate production is mediated by CD38 activation through the actions of cAMP/Epac/protein kinaseA/Rap1 in lymphokine-activated killer cells and nicotinate-adenine dinucleotide phosphate plays a key role in Ca2+ signaling of IL-8-induced lymphokine-activated killer cell migration. 727868 2.4.99.20 physiological function gene silencing of CD38 does not inhibit NAADP synthesis in intact Jurkat T cells. In vitro, both NAADP formation by base-exchange and degradation to 2-phospho adenosine diphosphoribose are efficiently decreased. Thus in vivo CD38 appears to be a NAADP degrading rather than a NAADP forming enzyme 727515 2.4.99.20 physiological function gene silencing of CD38 does not inhibit NAADP synthesis in thymus or spleen obtained from CD38 knock out mice 727515 2.4.99.20 physiological function L-thyroxine modifies nephrotoxicity by regulating the apoptotic pathway. Possible role of CD38/ADP-ribosyl cyclase mediated calcium mobilization 760029 2.4.99.20 physiological function the enzyme is involved in synthesis of nicotinic acid-adenine dinucleotide phosphate, a calcium messenger that can mobilize intracellular Ca2+ stores and activate Ca2+ influx to regulate a wide range of physiological processes 724210