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. 2021 Feb 15;9:630654. doi: 10.3389/fcell.2021.630654

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Copyright © 2021 Gu, Zhang, Wu and Gu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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PI(4,5)P₂ rescues CFTR related defective GLUT4 translocation. (A) The membrane localization of GLUT4 in Hela cells after overexpression of Rab8 and Rab13 was detected by confocal microscopy. Glut4 (green), Scale bar, 10 μm. (B) C2C12 myotubes were treated with insulin, CFTR inh172, PIP₂ depletion agents, or PI(4,5)P₂. PIP₂ depletion agents are consist of PI₃K inhibitor (1 μM wortmanin) and PLC agonist (50 μM m-3M3FBS). GLUT4 translocation to the plasma membrane was detected by confocal microscopy. Glut4-GFP (green), Glut4-myc (red). Scale bar, 10 μm.