1. ATAD1 physically interacts with the TA protein, GOS28, and is required to limit the level of mislocalized GOS28 on mitochondria in mammals Human dermal fibroblasts (HDFs) stably expressing GFP‐GOS28 were treated with scr or siRNA (#1‐4) against hATAD1, stained with Mitotracker Red, and visualized by fluorescence microscopy.
ATAD1 physically interacts with the TA protein, GOS28, and is required to limit the level of mislocalized GOS28 on mitochondria in mammals Human dermal fibroblasts (HDFs) stably expressing GFP‐GOS28 were treated with scr or siRNA (#1‐4) against hATAD1, stained with Mitotracker Red, and visualized by fluorescence microscopy. Whole‐cell lysate of cells from (A) were immunoblotted using anti‐ATAD1 and actin (loading control) antibodies. Crude mitochondria were extracted from HepG2 cells that stably co‐express GFP‐GOS28 with empty vector (−), HA‐tagged wild‐type ATAD1 (WT), or ATAD1E193Q mutant. ATAD1 was immunoprecipitated using anti‐HA antibody from digitonin‐solubilized lysates and 5% of the crude lysates, and eluates were immunoblotted with anti‐GFP and HA antibodies. Mouse tissue lysates (30 μg protein) from three WT and ATAD1−/− mice were analyzed by immunoblot. S6 ribosomal protein and actin are used as loading controls. The optical densitometry quantification of (D). The values represent the mean ± SEM (***P < 0.001, one‐way ANOVA). Source data are available online for this figure.
Yu‐Chan Chen et al. EMBO J. 2014;33:
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