Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Dec 1;31(25):2816–2825. doi: 10.1091/mbc.E20-03-0173

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2020 Li et al. “ASCB®,” “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society for Cell Biology.

This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License.

PMC Copyright notice

FIGURE 2: — Recruitment of Grp1 to the recycling endosome requires PI4KΙΙΙα. Quantitative results are shown as mean with standard error from three independent experiments: *, p < 0.05, NS p > 0.05, Student’s t test. (A) PI4P level at the recycling endosome was assessed through the colocalization of PI4P with different markers of the recycling endosome followed by quantitation; n = 10 cells per experiment. (B) PIP3 level at the recycling endosome was assessed through the colocalization of PIP3 with different markers of the recycling endosome followed by quantitation; n = 10 cells per experiment. (C) Wortmannin reduces the localization of Grp1-T280D at the recycling endosome. Adipocytes were treated with wortmannin at doses as indicated, and then the colocalization of Grp1-T280D with internal glut4 (marker for the recycling endosome in adipocytes) was quantified; n = 10 cells per experiment. (D) PAO, but not PIK93 or adenosine (Ade), significantly reduces the localization of Grp1-T280D at the recycling endosome. Adipocytes were treated with pharmacologic agents as indicated, and then the colocalization of Grp1-T280D with internal glut4 (marker for the recycling endosome in adipocytes) was quantified; n = 10 cells per experiment. (E) Knocking down PI4KΙΙΙα reduces the colocalization of PI4P with markers of the recycling endosome. Adipocytes were treated as indicated, and then the colocalization of PI4P with different markers of the recycling endosome (Rab11, cellubrevin, or internal glut4) was quantified; n = 10 cells per experiment. (F) Knocking down PI4KΙΙΙα reduces the colocalization of Grp1-T280D with markers of the recycling endosome. Adipocytes were treated as indicated, and then the colocalization of Grp1-T280D different markers of the recycling endosome (Rab11, cellubrevin, or internal glut4) was quantified; n = 10 cells per experiment. (G) Knocking down PI4KΙΙΙα reduces the ability of insulin to stimulate glut4 recycling. Adipocytes were treated as indicated (SC, scrambled siRNA), and then glut4 recycling was quantified; n = 10 cells per experiment.