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. Author manuscript; available in PMC: 2020 Dec 23.
Published in final edited form as: Sci Signal. 2020 Jun 23;13(637):eaba1015. doi: 10.1126/scisignal.aba1015

Figure 1. TRPML1 channels, are present in vascular SMCs.

Figure 1.

A) RT-qPCR analysis of Mcoln1, Mcoln2, and Mcoln3 mRNA expression levels in homogeneous populations of native cerebral artery SMCs. Data are normalized to Actb, encoding β-actin (N = 3 animals/group). B) RT-qPCR analysis of Mcoln1, Mcoln2, and Mcoln3 mRNA expression levels in cerebral arteries from WT and Mcoln1−/− mice. Data are normalized to Actb (N = 3 animals/group; *P ≤ 0.05). C) RT-qPCR analysis of Mcoln1, Mcoln2, and Mcoln3 mRNA expression levels in mesenteric arteries from WT and Mcoln1−/− mice. Data are normalized to Actb (N= 3 animals/group; *P ≤ 0.05). D) Representative results of Wes protein analysis using cerebral artery lysates from WT and Mcoln1−/− mice. Samples from WT animals probed with a primary antibody against TRPML1 generated a single band at the expected molecular weight of ~60 kDa that was absent in lysates from Mcoln1−/− mice. Lysates were probed for β-actin as a loading control. Representative of 3 independent experiments using tissue from N = 3 mice. All data are shown as mean ± SEM.