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Cited by 441

The DOI matches its Crossref record; 25 of the 25 references it cites were found in a registry or an index.

Cyclic ADP-Ribose in Insulin Secretion from Pancreatic βCells

Takasawa, Shin, Nata, Koji, Yonekura, Hideto, Okamoto, Hiroshi·1993·Science

Abstract

Inositol 1,4,5-trisphosphate (IP 3 ) is thought to be a second messenger for intracellular calcium mobilization. However, in a cell-free system of islet microsomes, cyclic adenosine diphosphate-ribose (cADP-ribose), a nicotinamide adenine dinucleotide (NAD + ) metabolite, but not IP 3 , induced calcium release. In digitonin-permeabilized islets, cADP-ribose and calcium, but not IP 3 , induced insulin secretion. Islet microsomes released calcium when combined with the extract from intact islets that had been incubated with high concentrations of glucose. Sequential additions of cADP-ribose inhibited the calcium release response to extracts from islets treated with high concentrations of glucose. Conversely, repeated additions of the islet extract inhibited the calcium release response to a subsequent addition of cADP-ribose. These results suggest that cADP-ribose is a mediator of calcium release from islet microsomes and may be generated in islets by glucose stimulation, serving as a second messenger for calcium mobilization in the endoplasmic reticulum.

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Metadata

Authors
Takasawa, S., Nata, K., Yonekura, H., & Okamoto, H.
Venue
Science
Published
1993-01-15
Volume
259
Issue
5093
Pages
370-373
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2040593177
Cited by
441
References
25
FWCI
18.76
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Cyclic ADP-Ribose in Insulin Secretion from Pancreatic βCells. https://app.cochat.ai/papers/10.1126/science.8420005
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Takasawa, S., Nata, K., Yonekura, H., & Okamoto, H. (1993). Cyclic ADP-Ribose in Insulin Secretion from Pancreatic βCells. Science. https://doi.org/10.1126/science.8420005

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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