Lian Li

TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: The identification of TNF receptor-associated protein 1 (TRAP1), a mitochondrial molecular chaperone also known as heat shock protein 75 (Hsp75), as a cellular substrate for PINK1 kinase is reported, and a novel pathway by which Pink1 phosphorylates downstream effector TRAP1 to prevent oxidative-stress-induced apoptosis is suggested.

TL;DR: Proteomic analyses reveal that the full-length UCH-L1 is a major target of oxidative damage in AD and PD brains, which is extensively modified by carbonyl formation, methionine oxidation, and cysteine oxidation and immunohistochemical studies show that prominent UCH- l1 immunostaining is associated with neurofibrillary tangles and that the level of soluble UCH- L1 protein is inversely proportional to the number of tangles in AD brains.

TL;DR: It is reported thatDJ-1 is oxidatively damaged in the brains of patients with idiopathic PD and AD and association of oxidative damage to DJ-1 with sporadic PD andAD is indicated.