Figure 3. The K372-E380 salt bridge is required for ATL2 function. (A) Cells transfected with the indicated HA-ATL2 variants were treated 48 h later with siRNAs against ATL2 and ATL3. 72 h after knockdown, cells were fixed and stained with antibodies against the HA epitope and viewed by confocal microscopy. (B) Quantification of the fraction of cells expressing the indicated proteins that had the unbranched ER phenotype. Values represent the means of three independent experiments ± SD. *, P < 0.0005. (C) High level expression of the indicated nonfunctional HA-ATL2 variants also confers a dominant-negative ER phenotype seen here even without ATL2/3 knockdown. Bars, 10 µm.
Figure 3.

The K372-E380 salt bridge is required for ATL2 function. (A) Cells transfected with the indicated HA-ATL2 variants were treated 48 h later with siRNAs against ATL2 and ATL3. 72 h after knockdown, cells were fixed and stained with antibodies against the HA epitope and viewed by confocal microscopy. (B) Quantification of the fraction of cells expressing the indicated proteins that had the unbranched ER phenotype. Values represent the means of three independent experiments ± SD. *, P < 0.0005. (C) High level expression of the indicated nonfunctional HA-ATL2 variants also confers a dominant-negative ER phenotype seen here even without ATL2/3 knockdown. Bars, 10 µm.

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