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Meeting Abstracts

Establishment of a tet-on gene expression system in glucose-responsive and -unresponsive MIN6 cells.

Y Kashima, T Miki, K Minami, S Seino
Journal: Diabetes
Diabetes 2001;50(suppl_1):S133
https://doi.org/10.2337/diabetes.50.2007.S133
Published: 01 February 2001
View article titled, Establishment of a tet-on gene expression system in glucose-responsive and -unresponsive MIN6 cells.
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Meeting Abstracts

Roles of ATP-sensitive K+ channels in cell survival and differentiation in the endocrine pancreas.

T Miki, T Iwanaga, K Nagashima, Y Ihara, S Seino
Journal: Diabetes
Diabetes 2001;50(suppl_1):S48
https://doi.org/10.2337/diabetes.50.2007.S48
Published: 01 February 2001
View article titled, Roles of ATP-sensitive K+ channels in cell survival and differentiation in the endocrine pancreas.
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Meeting Abstracts

Synaptotagmin III isoform is compartmentalized in pancreatic beta-cells and has a functional role in exocytosis.

H Brown, B Meister, J Deeney, B E Corkey, S N Yang, O Larsson, C J Rhodes, S Seino, P O Berggren, G Fried
Journal: Diabetes
Diabetes 2000;49(3):383–391
https://doi.org/10.2337/diabetes.49.3.383
Published: 01 March 2000
View article titled, Synaptotagmin III isoform is compartmentalized in pancreatic beta-cells and has a functional role in exocytosis.
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Meeting Abstracts

Diverse roles of K(ATP) channels learned from Kir6.2 genetically engineered mice.

S Seino, T Iwanaga, K Nagashima, T Miki
Journal: Diabetes
Diabetes 2000;49(3):311–318
https://doi.org/10.2337/diabetes.49.3.311
Published: 01 March 2000
View article titled, Diverse roles of K(ATP) channels learned from Kir6.2 genetically engineered mice.
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Meeting Abstracts

Unresponsiveness to glibenclamide during chronic treatment induced by reduction of ATP-sensitive K+ channel activity.

J Kawaki, K Nagashima, J Tanaka, T Miki, M Miyazaki, T Gonoi, N Mitsuhashi, N Nakajima, T Iwanaga, H Yano, S Seino
Journal: Diabetes
Diabetes 1999;48(10):2001–2006
https://doi.org/10.2337/diabetes.48.10.2001
Published: 01 October 1999
View article titled, Unresponsiveness to glibenclamide during chronic treatment induced by reduction of ATP-sensitive K+ channel activity.
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Meeting Abstracts

Tissue specificity of sulfonylureas: studies on cloned cardiac and beta-cell K(ATP) channels.

F M Gribble, S J Tucker, S Seino, F M Ashcroft
Journal: Diabetes
Diabetes 1998;47(9):1412–1418
https://doi.org/10.2337/diabetes.47.9.1412
Published: 01 September 1998
View article titled, Tissue specificity of sulfonylureas: studies on cloned cardiac and beta-cell K(ATP) channels.
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