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Diabetes, Vol 46, Issue 9 1440-1444, Copyright © 1997 by American Diabetes Association
Localization of the ATP-sensitive K+ channel subunit Kir6.2 in mouse pancreas
M Suzuki, K Fujikura, N Inagaki, S Seino and K Takata
Laboratory of Molecular and Cellular Morphology, Institute for Molecular and Cellular Regulation, Gunma University, Japan. msuzuki@sb.gunma-u.ac.jp
Kir6.2, a member of the inward rectifier K+ channel family, is a component
of the ATP-sensitive K+ (K[ATP]) channel considered to play a key role in
glucose-induced insulin secretion. We studied the distribution of Kir6.2 in
mouse pancreas at the cellular level. The sites of Kir6.2 mRNA expression
were determined by in situ hybridization histochemistry with a digoxigenin
(DIG)-labeled antisense cRNA probe. The hybridization signal was unevenly
present throughout the islets of Langerhans, while no distinct signal was
detected in exocrine acinar cells. This distribution was confirmed by
another cRNA probe complementary to a different region of Kir6.2 mRNA. In
situ hybridization and immunofluorescence staining of serial sections with
the anti-insulin, the anti-glucagon, and the anti-somatostatin antibodies
showed Kir6.2 mRNA to be present in alpha-, beta-, and delta-cells.
Furthermore, immunofluorescence staining with antibody raised against
Kir6.2 revealed that Kir6.2 protein is localized within the pancreatic
islets and is not found in exocrine pancreas. Kir6.2 was further shown to
be located together with insulin, glucagon, or somatostatin. The positive
staining of Kir6.2 appeared concentrated along the contour of each islet
cell, suggesting that Kir6.2 is at the plasma membrane of islet cells.
These results suggest that Kir6.2, as a component of K(ATP) channels, is an
important molecule in the regulation of all the release of insulin,
glucagon, and somatostatin.

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Copyright © 1997 by the American Diabetes Association.
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