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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Levitan, Irena Toth, Peter T. Kowalsky, Gregory Dopico, Alex M. Oh, Myung J. Rosenhouse-dantsker, Avia Baki, Lia Bukiya, Anna N. Kuntamallappanavar, Guruprasad Osborn, Catherine V. |
| Description | Author Affiliation: Bukiya AN ( Department of Pharmacology, The University of Tennessee Health Science Center, Memphis, TN 38163, United States.); Osborn CV ( Department of Medicine, Pulmonary Section, University of Illinois at Chicago, Chicago, IL 60612, United States.); Kuntamallappanavar G ( Department of Pharmacology, The University of Tennessee Health Science Center, Memphis, TN 38163, United States.); Toth PT ( Research Resources Center, University of Illinois at Chicago, Chicago, IL 60612, United States.); Baki L ( Department of Physiology and Biophysics, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, United States.); Kowalsky G ( Department of Medicine, Pulmonary Section, University of Illinois at Chicago, Chicago, IL 60612, United States.); Oh MJ ( Department of Medicine, Pulmonary Section, University of Illinois at Chicago, Chicago, IL 60612, United States.); Dopico AM ( Department of Pharmacology, The University of Tennessee Health Science Center, Memphis, TN 38163, United States.); Levitan I ( Department of Medicine, Pulmonary Section, University of Illinois at Chicago, Chicago, IL 60612, United States.); Rosenhouse-Dantsker A ( Department of Medicine, Pulmonary Section, University of Illinois at Chicago, Chicago, IL 60612, United States) |
| Abstract | Cholesterol is one of the major lipid components of membranes in mammalian cells. In recent years, cholesterol has emerged as a major regulator of ion channel function. The most common effect of cholesterol on ion channels in general and on inwardly rectifying potassium (Kir) channels in particular is a decrease in activity. In contrast, we have recently shown that native G-protein gated Kir (GIRK or Kir3) channels that underlie atrial $K_{ACh}$ currents are up-regulated by cholesterol. Here we unveil the biophysical basis of cholesterol-induced increase in $K_{ACh}$ activity. Using planar lipid bilayers we show that cholesterol significantly enhances the channel open frequency of the Kir3.1/Kir3.4 channels, which underlie $K_{ACh}$ currents. In contrast, our data indicate that cholesterol does not affect their unitary conductance. Furthermore, using fluorescent and TIRF microscopy as well as surface protein biotinylation, we also show that cholesterol enrichment in vitro has no effect on surface expression of GFP-tagged channels expressed in Xenopus oocytes or transfected into HEK293 cells. Together, these data demonstrate for the first time that cholesterol enhances Kir3-mediated current by increasing the channel open probability. |
| ISSN | 00063002 |
| Journal | Biochimica et Biophysica Acta (BBA) - Reviews on Cancer |
| Part | Pt A |
| Issue Number | 10 |
| Volume Number | 1848 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2015-10-01 |
| Publisher Place | Netherlands |
| Access Restriction | Open |
| Subject Keyword | Cholesterol Metabolism G Protein-Coupled Inwardly-Rectifying Potassium Channels Physiology Ion Channel Gating Models, Biological Models, Statistical Potassium Animals Computer Simulation Chemistry HEK293 Cells Models, Chemical Oocytes Xenopus Laevis Research Support, Non-U.S. Gov't Biochemistry |
| Content Type | Text |
| Resource Type | Article |
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