| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10926501 | Cell Calcium | 2007 | 13 Pages |
Abstract
Despite the strong IP3R3-gradient, in saponin-permeabilized colonic crypts exogenously administered IP3 or adenophostin A evoked a similar depletion of mag-fura-2-loaded intracellular Ca2+ stores in crypt and surface cells suggesting a contribution of the nuclear IP3R2 to the Ca2+ release. This conclusion was confirmed by experiments with isolated nuclei from colonic epithelium, at which IP3 was able to induce changes in the Ca2+ concentration, which were inhibited by 2-aminoethoxy-diphenylborate (2-APB), a blocker of IP3 receptors. These results demonstrate that the colonic epithelial cells undergo changes in IP3R subtype expression during differentiation.
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Authors
Anne Siefjediers, Martin Hardt, Gundula Prinz, Martin Diener,