KATP channels as molecular sensors of cellular metabolism

被引：678

作者：

Nichols, CG ^{[1
]}

机构：

[1] Washington Univ, Sch Med, Dept Cell Biol & Physiol, St Louis, MO 63110 USA

来源：

NATURE | 2006年 / 440卷 / 7083期

关键词：

D O I：

10.1038/nature04711

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

In responding to cytoplasmic nucleotide levels, ATP-sensitive potassium (K-ATP) channel activity provides a unique link between cellular energetics and electrical excitability. Over the past ten years, a steady drumbeat of crystallographic and electrophysiological studies has led to detailed structural and kinetic models that define the molecular basis of channel activity. In parallel, the uncovering of disease-causing mutations of K-ATP has led to an explanation of the molecular basis of disease and, in turn, to a better understanding of the structural basis of channel function.

引用

页码：470 / 476

页数：7

共 92 条

[81] ATP binding to the motor domain from an ABC transporter drives formation of a nucleotide sandwich dimer [J].

Smith, PC ;

Karpowich, N ;

Millen, L ;

Moody, JE ;

Rosen, J ;

Thomas, PJ ;

Hunt, JF .

MOLECULAR CELL, 2002, 10 (01) :139-149

[82] Functional roles of cardiac and vascular ATP-sensitive potassium channels clarified by Kir6.2-knockout mice [J].

Suzuki, M ;

Li, RA ;

Miki, T ;

Uemura, H ;

Sakamoto, N ;

Ohmoto-Sekine, Y ;

Tamagawa, M ;

Ogura, T ;

Seino, S ;

Marbán, E ;

Nakaya, H .

CIRCULATION RESEARCH, 2001, 88 (06) :570-577

[83] Hyperinsulinism of infancy:: Novel ABCC8 and KCNJ11 mutations and evidence for additional locus heterogeneity [J].

Tornovsky, S ;

Crane, A ;

Cosgrove, KE ;

Hussain, K ;

Lavie, J ;

Heyman, M ;

Nesher, Y ;

Kuchinski, N ;

Ben-Shushan, E ;

Shatz, O ;

Nahari, E ;

Potikha, T ;

Zangen, D ;

Tenenbaum-Rakover, Y ;

De Vries, L ;

Argente, J ;

Gracia, R ;

Landau, H ;

Eliakim, A ;

Lindley, K ;

Dunne, MJ ;

Aguilar-Bryan, L ;

Glaser, B .

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2004, 89 (12) :6224-6234

[84] Molecular determinants of KATP channel inhibition by ATP [J].

Tucker, SJ ;

Gribble, FM ;

Proks, P ;

Trapp, S ;

Ryder, TJ ;

Haug, T ;

Reimann, F ;

Ashcroft, FM .

EMBO JOURNAL, 1998, 17 (12) :3290-3296

[85] Truncation of Kir6.2 produces ATP-sensitive K+ channels in the absence of the sulphonylurea receptor [J].

Tucker, SJ ;

Gribble, FM ;

Zhao, C ;

Trapp, S ;

Ashcroft, FM .

NATURE, 1997, 387 (6629) :179-183

[86] Cooperative binding of ATP and MgADP in the sulfonylurea receptor is modulated by glibenclamide [J].

Ueda, K ;

Komine, J ;

Matsuo, M ;

Seino, S ;

Amachi, T .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (04) :1268-1272

[87] Sulphonylurea receptor 2B and Kir6.1 form a sulphonylurea-sensitive but ATP-insensitive K+ channel [J].

Yamada, M ;

Isomoto, S ;

Matsumoto, S ;

Kondo, C ;

Shindo, T ;

Horio, Y ;

Kurachi, Y .

JOURNAL OF PHYSIOLOGY-LONDON, 1997, 499 (03) :715-720

[88] Sulfonylureas correct trafficking defects of ATP-sensitive potassium channels caused by mutations in the sulfonylurea receptor [J].

Yan, FF ;

Lin, CW ;

Weisiger, E ;

Cartier, EA ;

Taschenberger, G ;

Shyng, SL .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (12) :11096-11105

[89] The C42R mutation in the Kir6.2 (KCNJ11) gene as a cause of transient neonatal diabetes, childhood diabetes, or later-onset, apparently type 2 diabetes mellitus [J].

Yorifuji, T ;

Nagashima, K ;

Kurokawa, K ;

Kawai, M ;

Oishi, M ;

Akazawa, Y ;

Hosokawa, M ;

Yamada, Y ;

Inagaki, N ;

Nakahata, T .

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2005, 90 (06) :3174-3178

[90] Tandem function of nucleotide binding domains confers competence to sulfonylurea receptor in gating ATP-sensitive K+ channels [J].

Zingman, LV ;

Hodgson, DM ;

Bienengraeber, M ;

Karger, AB ;

Kathmann, EC ;

Alekseev, AE ;

Terzic, A .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (16) :14206-14210

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