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. Author manuscript; available in PMC: 2012 Nov 1.
Published in final edited form as: Nature. 2011 Jun 19;476(7360):341–345. doi: 10.1038/nature10234

Figure 4. Impact of point mutations on MCU activity and its sensitivity to Ru360.

Figure 4

a, Schematic of MCU topology across the mitochondrial inner membrane and a multiple sequence alignment of the linker sequence containing a DIME motif. TM1 and TM2 are two transmembrane domains. b, Ca2+ uptake in permeabilized sh-MCU HEK-293 cells transiently expressing MCU mutants. Inset reports linear fits of uptake kinetics between 15 and 25 s, normalized to sh-LACZ (mean ± s.d., n = 3, *P <0.01) c, Ca2+ uptake in HEK-293 cells transiently expressing wild-type MCU or the S259A mutant, in the presence or absence of 0.5 μM Ru360. Inset reports linear fits of uptake kinetics between 30 and 60 s for Ru360-treated cells, and between 15 and 25 s for untreated cells. Uptake rates are normalized to untreated HEK-293 cells (mean ± s.d., n = 3, *P <0.01).