id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
work_2hkskarpjndnvoddv7qcun63wy	Philip A. Gurnev	Alpha-Synuclein Blocks VDAC Suggesting Mechanism of Mitochondrial Regulation and Toxicity in Parkinson Disease	2015	1	.pdf	application/pdf	1557	92	39	Cardiolipin Reorganization and Phase Transition Induced by DynaminRelated Protein 1 Facilitates Mitochondrial Membrane Fission VDAC3 Forms Typical Voltage-Gated, Anion-Selective, and TubulinSensitive Channels The Voltage Dependent Anion Channel (VDAC) forms the major pathway for Both, VDAC1 and VDAC2 reconstituted into planar membranes form voltage-dependent anion-selective channels whose conductance is modulated by dimeric tubulin. mitochondrial membrane potential, or why VDAC3 is predominantly expressed in the short-term high energy demanding cells, such as spermatozoa. cross the mitochondrial outer membrane through the voltage dependent anion Alpha-Synuclein Blocks VDAC Suggesting Mechanism of Mitochondrial the voltage-dependent anion channel (VDAC), the major conduit for ATP VDAC3 Forms Typical Voltage-Gated, Anion-Selective, and Tubulin-Sensitive Channels Channeling of Mitochondrial Energy in Cardiac and Cancer Cells by the Metabolically-Dependent Outer Membrane Potential Alpha-Synuclein Blocks VDAC Suggesting Mechanism of Mitochondrial Regulation and Toxicity in Parkinson Disease Alpha-Synuclein Blocks VDAC Suggesting Mechanism of Mitochondrial Regulation and Toxicity in Parkinson Disease	./cache/work_2hkskarpjndnvoddv7qcun63wy.pdf	./txt/work_2hkskarpjndnvoddv7qcun63wy.txt