Antibodies used in the study were: sheep polyclonal anti-LRP1 (made in-house, IF 1:250; IP 1:200 [33 (link)]), rabbit monoclonal anti-LRP1 (abgent, AJ1448a; WB 1:10000), rabbit polyclonal anti-PID1 (Sigma-Aldrich, HPA36103; WB 1:200), rabbit polyclonal anti-GLUT4 (kindly provided by A. Schürmann, DIfE, Potsdam-Rehbrücke, Germany; WB 1:1000, IF 1:500), rabbit monoclonal anti-IRAP (Cell Signaling 6918, IF 1:250), mouse monoclonal anti-GLUT1 (Abcam, ab40084, IF 1:100), rabbit polyclonal anti-AS160 (Millipore 07–741, WB 1:500), mouse monoclonal anti-GST (Santa Cruz sc-138, WB 1:500), rabbit polyclonal anti-AKT (Cell Signaling, 9272, WB 1:1000) and rabbit polyclonal anti-p-AKT (Ser473) (Cell Signaling, 9271, WB 1:1000).
All following secondary antibodies were purchased from Jackson Immuno Research: goat anti-rabbit HRP (#111-035-144, WB 1:5000); goat anti-mouse HRP (#115-035-003, WB 1:5000); Cy2-donkey-anti-sheep (#713-225-147, IF 1:250), Cy2-donkey-anti-sheep (#713-166-147, IF 1:500), Cy2-donkey-anti-rabbit (#711-225-152, IF 1:250), Cy3-donkey-anti-rabbit (#711-165-152; IF 1:500), Alexa488-donkey-anti-mouse (#715-486-150, IF 1:250).
Fischer A.W., Albers K., Schlein C., Sass F., Krott L.M., Schmale H., Gordts P.L., Scheja L, & Heeren J. (2019). PID1 regulates insulin-dependent glucose uptake by controlling intracellular sorting of GLUT4-storage vesicles. Biochimica et biophysica acta. Molecular basis of disease, 1865(6), 1592-1603.
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