Concerted trafficking regulation of Kv2.1 and KATP channels by leptin in pancreatic β-cells

Yi Wu, Show Ling Shyng, Pei-chun Chen

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Background: Leptin recruits KATP channels to the pancreatic β-cell membrane. Results: Leptin causes a parallel increase in Kv2.1 channel density that is dependent on AMPK, PKA, and actin depolymerization. Conclusion: Leptin signaling leads to simultaneous increases in KATP and Kv2.1 channel densities. Significance: Concerted KATP and Kv2.1 channel trafficking regulation by leptin may result in coordinated inhibition of β-cell excitability.

Original languageEnglish
Pages (from-to)29676-29690
Number of pages15
JournalJournal of Biological Chemistry
Volume290
Issue number50
DOIs
Publication statusPublished - 2015 Dec 11

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KATP Channels
Leptin
Depolymerization
AMP-Activated Protein Kinases
Cell membranes
Actins
Cell Membrane

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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abstract = "Background: Leptin recruits KATP channels to the pancreatic β-cell membrane. Results: Leptin causes a parallel increase in Kv2.1 channel density that is dependent on AMPK, PKA, and actin depolymerization. Conclusion: Leptin signaling leads to simultaneous increases in KATP and Kv2.1 channel densities. Significance: Concerted KATP and Kv2.1 channel trafficking regulation by leptin may result in coordinated inhibition of β-cell excitability.",
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Concerted trafficking regulation of Kv2.1 and KATP channels by leptin in pancreatic β-cells. / Wu, Yi; Shyng, Show Ling; Chen, Pei-chun.

In: Journal of Biological Chemistry, Vol. 290, No. 50, 11.12.2015, p. 29676-29690.

Research output: Contribution to journalArticle

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AB - Background: Leptin recruits KATP channels to the pancreatic β-cell membrane. Results: Leptin causes a parallel increase in Kv2.1 channel density that is dependent on AMPK, PKA, and actin depolymerization. Conclusion: Leptin signaling leads to simultaneous increases in KATP and Kv2.1 channel densities. Significance: Concerted KATP and Kv2.1 channel trafficking regulation by leptin may result in coordinated inhibition of β-cell excitability.

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