György Csordás

TL;DR: An unexpected dependence of cell function and survival is revealed on the maintenance of proper spacing between the ER and mitochondria, which makes mitochondria prone to Ca2+ overloading and ensuing permeability transition.

TL;DR: These studies provide direct evidence for the existence of high-Ca(2+) microdomains between the ER and mitochondria and suggest an optimal gap width for efficient Ca( 2+) transfer.

TL;DR: Mechanisms that recruit the mitochondrial calcium signal to a pro-apoptotic cascade and the approaches available for assessment of the relevance of the mitochondrial Ca(2+) handling in apoptosis are discussed and a systematic evaluation of the effect of ruthenium red and Ru360, two inhibitors of mitochondrial Ca-2+) uptake on cytosolic [Ca(2+)] and [Ca-2+)].

TL;DR: It is demonstrated that maximal activation of mitochondrial Ca2+ uptake is evoked by IP3‐induced perimitochondrial [Ca2+] elevations, which appear to reach values >20‐fold higher than the global increases of [Ca 2+]c.

TL;DR: The data indicate that MICU1 senses the [Ca(2+)]c to establish the uniporter's threshold and gain, thereby allowing mitochondria to properly decode different inputs.