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. 2021 Sep 17;62(12):15. doi: 10.1167/iovs.62.12.15

Figure 4.

Figure 4.

Deficient TFEB nuclear translocation in Slc4a11 KO cells. (A) Wes immunoassay of TFEB, Lamin A/C, and GAPDH in nuclear and cytosolic extracts from Slc4a11 WT and KO MCEC. Nuclear membrane proteins, Lamin A/C, and cytoplasmic protein, Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) were used as loading control for the respective fractions and also to rule out cross-contamination between the fractions. (B) Quantification of Wes results from panel A. Mean ± SD. ***P < 0.001. ns = not significant (Student's t-test). (C) Q-PCR of a subset of TFEB regulated CLEAR network genes in Slc4a11 WT and KO MCEC. Blocs1 – Biogenesis of Lysosomal Organelles Complex 1 Subunit 1, Gabarap - GABAA receptor-associated protein 1, Atpv0b – vATPase subunit b, Atpv0c – vATPase subunit C, Gla –Alpha galactosidase A, Ctsd – Cathepsin D, Ctsb- Cathepsin B, and Lamp1- Lysosome-associated membrane glycoprotein 1. Expression normalized to β-actin, *P < 0.05, ***P < 0.001 (Student's t-test). (D) Wes immunoassay of TFEB from Slc4a11 WT and KO corneal endothelial tissue. (E) Quantification of panel D data, mean ± SD, ***P < 0.0001, n = 3 (Student's t-test).