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Cited by 513

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

PIP 2 and PIP as Determinants for ATP Inhibition of K ATP Channels

Baukrowitz, Thomas, Schulte, Uwe, Oliver, Dominik, Herlitze, Stefan, Krauter, Tobias, Tucker, Stephen J., Ruppersberg, J. Peter, Fakler, Bernd·1998·Science

Abstract

Adenosine triphosphate (ATP)–sensitive potassium (K ATP ) channels couple electrical activity to cellular metabolism through their inhibition by intracellular ATP. ATP inhibition of K ATP channels varies among tissues and is affected by the metabolic and regulatory state of individual cells, suggesting involvement of endogenous factors. It is reported here that phosphatidylinositol-4,5-bisphosphate (PIP 2 ) and phosphatidylinositol-4-phosphate (PIP) controlled ATP inhibition of cloned K ATP channels (K ir 6.2 and SUR1). These phospholipids acted on the K ir 6.2 subunit and shifted ATP sensitivity by several orders of magnitude. Receptor-mediated activation of phospholipase C resulted in inhibition of K ATP -mediated currents. These results represent a mechanism for control of excitability through phospholipids.

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Metadata

Authors
Baukrowitz, T., Schulte, U., Oliver, D., Herlitze, S., Krauter, T., Tucker, S. J., Ruppersberg, J. P., & Fakler, B.
Venue
Science
Published
1998-11-06
Volume
282
Issue
5391
Pages
1141-1144
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2082648108
Cited by
513
References
1
FWCI
13.96
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: PIP 2 and PIP as Determinants for ATP Inhibition of K ATP Channels. https://app.cochat.ai/papers/10.1126/science.282.5391.1141
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Baukrowitz, T., Schulte, U., Oliver, D., Herlitze, S., Krauter, T., Tucker, S. J., Ruppersberg, J. P., & Fakler, B. (1998). PIP 2 and PIP as Determinants for ATP Inhibition of K ATP Channels. Science. https://doi.org/10.1126/science.282.5391.1141

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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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