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NAADP mobilizes Ca2+ from a thapsigargin-sensitive store in the nuclear envelope by activating ryanodine receptors

Gerasimenko, Julia Vladimirovna ORCID: https://orcid.org/0000-0002-2262-2543, Maruyama, Yoshio, Yano, Kojiro, Dolman, Nick J., Tepikin, Alexei V., Petersen, Ole Holger ORCID: https://orcid.org/0000-0002-6998-0380 and Gerasimenko, Oleg Vsevolodovich ORCID: https://orcid.org/0000-0003-2573-8258 2003. NAADP mobilizes Ca2+ from a thapsigargin-sensitive store in the nuclear envelope by activating ryanodine receptors. Journal of Cell Biology 163 (2) , pp. 271-282. 10.1083/jcb.200306134

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Abstract

Ca2+ release from the envelope of isolated pancreatic acinar nuclei could be activated by nicotinic acid adenine dinucleotide phosphate (NAADP) as well as by inositol 1,4,5-trisphosphate (IP3) and cyclic ADP-ribose (cADPR). Each of these agents reduced the Ca2+ concentration inside the nuclear envelope, and this was associated with a transient rise in the nucleoplasmic Ca2+ concentration. NAADP released Ca2+ from the same thapsigargin-sensitive pool as IP3. The NAADP action was specific because, for example, nicotineamide adenine dinucleotide phosphate was ineffective. The Ca2+ release was unaffected by procedures interfering with acidic organelles (bafilomycin, brefeldin, and nigericin). Ryanodine blocked the Ca2+-releasing effects of NAADP, cADPR, and caffeine, but not IP3. Ruthenium red also blocked the NAADP-elicited Ca2+ release. IP3 receptor blockade did not inhibit the Ca2+ release elicited by NAADP or cADPR. The nuclear envelope contains ryanodine and IP3 receptors that can be activated separately and independently; the ryanodine receptors by either NAADP or cADPR, and the IP3 receptors by IP3.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
Systems Immunity Research Institute (SIURI)
Publisher: Rockefeller University Press,
ISSN: 0021-9525
Last Modified: 27 Oct 2022 08:42
URI: https://orca.cardiff.ac.uk/id/eprint/63140

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