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New aspects of nuclear calcium signalling Gerasimenko O; Gerasimenko JJ Cell Sci 2004[Jul]; 117 (Pt 15): 3087-94Nuclear calcium signalling has been a controversial battlefield for many years and the question of how permeable the nuclear pore complexes (NPCs) are to Ca2+ has been the subject of a particularly hot dispute. Recent data from isolated nuclei suggest that the NPCs are open even after depletion of the Ca2+ store in the nuclear envelope. Other research has suggested that a new Ca2+ -releasing messenger, nicotinic acid adenine dinucleotide phosphate (NAADP), can liberate Ca2+ only from acidic organelles, probably lysosomes, rather than from the traditional Ca2+ store in the endoplasmic reticulum (ER). Recent work indicates that NAADP can release Ca2+ from the nuclear envelope (NE), which has a thapsigargin-sensitive, ER-type Ca2+ store. NAADP acts in a manner similar to inositol (1,4,5)-trisphosphate [Ins(1,4,5)P3] or cyclic ADP-ribose (cADPR): all three messengers are equally able to reduce the Ca2+ concentration inside the NE and this is associated with a transient rise in the nucleoplasmic Ca2+ concentration. The NE contains ryanodine receptors (RyRs) and Ins(1,4,5)P3 receptors [Ins(1,4,5)P3Rs], and these can be activated separately and independently: the RyRs by either NAADP or cADPR, and the Ins(1,4,5)P3Rs by Ins(1,4,5)P3.|*Signal Transduction[MESH]|Animals[MESH]|Calcium/*metabolism[MESH]|Cell Nucleus/*metabolism[MESH]|Cyclic ADP-Ribose/metabolism[MESH]|Endoplasmic Reticulum/metabolism[MESH]|Humans[MESH]|Inositol 1,4,5-Trisphosphate/metabolism[MESH]|Lysosomes/metabolism[MESH]|Models, Biological[MESH]|NADP/*analogs & derivatives/pharmacology[MESH]|Pancreas/metabolism[MESH]|Ryanodine Receptor Calcium Release Channel/metabolism[MESH]|Thapsigargin/pharmacology[MESH] |
