Titlebook: Cyclic ADP-Ribose and NAADP; Structures, Metaboli Hon Cheung Lee Book 2002 Springer Science+Business Media New York 2002 Calcium.Nucleotide

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A Yeast Expression System of High Efficiency for Producing Recombinant Enzymes,entified and they are the . ADP-ribosyl cyclase and the mammalian antigens, CD38 and CD157 (formerly called BST-1) [1–4]. The sequence homology among these three enzymes is shown in Figure 1. All three enzymes are widespread in occurrence and are localized in a variety of tissues [1, 5–8]. The novel

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Novel Cycling Assays for cADPR and NAADP,pecific and sensitive assays for cADPR and NAADP be widely available for monitoring their endogenous levels under a variety of physiological conditions. The first assay for cADPR was a bioassay based on its Ca. releasing activity in sea urchin egg homogenates [1, 2]. Using this assay, it was demonst

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Pharmacology of Cyclic ADP-Ribose and NAADP,that inositol trisphosphate mobilizes Ca. stores in the endoplasmic reticulum [1]. Also present in the organelle is another Ca. release channel, the ryanodine receptor. The discovery of two other Ca. signaling molecules, cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NA

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Separate but Interacting Calcium Stores,nd internal. One of the most dramatic examples occurs during fertilization. Immediately after sperm-egg fusion, a highly localized Ca. elevation is initiated right at the fusion site. This spark of Ca. then grows into a wave propagating across the entire egg. Intriguingly, the initiation of apoptoti

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,The CD38-Cyclic ADP-Ribose Signal System in Pancreatic ?-Cells,of insulin, and proposed a unifying model for the action of the diabetogenic agents alloxan and streptozotocin on pancreatic β-cells (Figure 1) [1–10]. Central to the model are breaks in the nuclear DNA of β-cells, resulting from either an accumulation of free radicals or from the alkylation of DNA.

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The Role of cADPR and NAADP in T Cell Calcium Signaling and Activation,years ago many researchers believed that Ca. release in T cells is exclusively operated by D-.-inositol 1,4,5-trisphosphate (InsP3; reviewed in ref. 4) while the capacitative mechanism of Ca. entry proposed by Putney [5] was thought to play a central role in the influx process.