id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
work_yu4rqhmrpzbvjifxrvgk4rsc6e	David M. Booth	ER Calcium Release is Tuned by Mitochondrial Redox Nanodomains	2015	1	.pdf	application/pdf	1539	107	42	in mouse liver versus heart mitochondria, and a 4.5 fold higher MICU1 to heart mitochondria displayed a decreased threshold and lesser cooperativity nanodomain which developes into a H2O2 transient following IP3 receptormediated ER Ca2þ release and mitochondrial Ca2þ uptake. Pharmacological inhibition showed that the transient was dependent upon ER Ca2þ, mitochondrial as both a messenger and regulator of calcium signaling and are particularly relevant for the control of mitochondrial function. that ROS target mito-motility to control mitochondrial function. Miro1 is Dispensable for Calcium-Mediated Inhibition of Mitochondrial at birth (Nguyen et al., 2014) and fibroblasts (MEFs) derived from Miro1 KO embryos show abnormal mitochondrial distribution, but the calcium-dependent inhibition of motility is unaffected and the respiratory and calcium buffering Imaging in perfused whole heart ex vivo, showed considerable mitochondrial continuity and fusion activity in ventricular CM. adult CM lose mitochondrial fusion activity. Miro1 is Dispensable for Calcium-Mediated Inhibition of Mitochondrial Movement	./cache/work_yu4rqhmrpzbvjifxrvgk4rsc6e.pdf	./txt/work_yu4rqhmrpzbvjifxrvgk4rsc6e.txt