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Disruption of palmitate-mediated localization; a shared pathway of force and anesthetic activation of TREK-1 channels

Petersen, E. Nicholas, Pavel, Mahmud Arif, Wang, Hao, Hansen, Scott B.·2020·Biochimica et Biophysica Acta (BBA) - Biomembranes
DOI 10.1016/j.bbamem.2019.183091PMC PMC6907892
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  • Cholesterol loading with apoE caused the potassium channel TREK-1 to traffic to lipid clusters similar to APP, an effect reversed by mechanical force.

    “In separate studies, we saw that cholesterol loading with apoE caused the potassium channel TREK-1 to traffic to lipid clusters similar to APP (73, 74)—an effect that was reversed by mechanical force (75).”

    From Regulation of beta-amyloid production in neurons by astrocyte-derived cholesterol (2021) · cites this paper as [74]

    Citation (75) is attached to the mechanical-force reversal. In “Lipid domains and cholesterol-induced palmitoyl de-clustering” (page unavailable), the paper says shear force moves PLD2 out of GM1 lipid domains and links that movement to TREK-1 activation. It does not say force reverses apoE-induced trafficking of TREK-1 itself; the apoE-loading claim is attached to citations (73, 74), not this one. (LLM, conf=0.85)

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Metadata

Authors
Petersen, E. N., Pavel, M. A., Wang, H., & Hansen, S. B.
Venue
Biochimica et Biophysica Acta (BBA) - Biomembranes
Publisher
Elsevier BV
Published
2020-01
Volume
1862
Issue
1
Pages
183091
ISSN
0005-2736
DOI
10.1016/j.bbamem.2019.183091
PMC
PMC6907892
Cited by
36
References
6
Language
en
Licence
Funders
  • National Institutes of Health (W81XWH1810782)
  • U.S. Department of Defense

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