Calcium release-activated calcium (CRAC) channels mediate the β2-adrenergic regulation of Na,K-ATPase

Michael J. Keller, Emilia Lecuona*, Murali Prakriya, Yuan Cheng, Saul Soberanes, G. R.Scott Budinger, Jacob I. Sznajder

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


β2-Adrenergic agonists have been shown to regulate Na,K-ATPase in the alveolar epithelium by recruiting Na,K-ATPase-containing vesicles to the plasma membrane of alveolar epithelial cells (AEC). Here, we provide evidence that β2-agonists induce store-operated calcium entry (SOCE) in AECs. This calcium entry is necessary for β2-agonist-induced recruitment of Na,K-ATPase to the plasma membrane of AECs. Specifically, we show that β2-agonists induce SOCE via stromal interaction molecule 1 (STIM1)-associated calcium release-activated calcium (CRAC) channels. We also demonstrate that the magnitude of SOCE affects the abundance of Na,K-ATPase at the plasma membrane of AECs.

Original languageEnglish (US)
Pages (from-to)4686-4693
Number of pages8
JournalFEBS Letters
Issue number24
StatePublished - Dec 20 2014


  • Calcium channel
  • Calcium signaling
  • Epithelial cell
  • Na,K-ATPase
  • Store-operated calcium entry

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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