LC3 overexpression reduces Aβ neurotoxicity through increasing α7nAchR expression and autophagic activity in neurons and mice

Neuropharmacology

Volumn 93, Issue , 2015, Pages 243-251

  Hung, Shih Ya ^a,b   Huang, Wei Pang ^c   Liou, Houng Chi ^d   Fu, Wen Mei ^d  

^a CHINA MEDICAL UNIVERSITY HOSPITAL   (Taiwan)

^b CHINA MEDICAL UNIVERSITY   (Taiwan)

^c NATIONAL TAIWAN UNIVERSITY   (Taiwan)

^d NATIONAL TAIWAN UNIVERSITY   (Taiwan)

Author keywords

Apoptosis; Autophagy; A ; LC3; 7nAChR

Indexed keywords

ALPHA BUNGAROTOXIN; AMYLOID BETA PROTEIN; AMYLOID BETA PROTEIN[1-42]; AMYLOID BETA PROTEIN[25-35]; BUNGAROTOXIN RECEPTOR; MEMBRANE PROTEIN; MICROTUBULE ASSOCIATED PROTEIN 1 LIGHT CHAIN 3; UNCLASSIFIED DRUG; ACTIN; AMYLOID BETA-PROTEIN (1-42); AMYLOID BETA-PROTEIN (25-35); BUNGAROTOXIN; CASPASE 3; MAP1LC3 PROTEIN, MOUSE; MICROTUBULE ASSOCIATED PROTEIN; NICOTINIC RECEPTOR BLOCKING AGENT; PEPTIDE FRAGMENT;

ANIMAL CELL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; AUTOPHAGY; CONTROLLED STUDY; DISEASE RESISTANCE; EMBRYO; GENE OVEREXPRESSION; IN VITRO STUDY; IN VIVO STUDY; MOUSE; NERVE CELL; NERVE CELL CULTURE; NEUROPROTECTION; NEUROTOXICITY; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN PROTEIN INTERACTION; ANIMAL; ANIMAL EMBRYO; BRAIN CORTEX; CELL CULTURE; CYTOLOGY; DOSE RESPONSE; DRUG EFFECTS; GENE EXPRESSION REGULATION; GENETICS; HUMAN; METABOLISM; NEUROBLASTOMA; PATHOLOGY; TRANSGENIC MOUSE;

ACTINS; ALPHA7 NICOTINIC ACETYLCHOLINE RECEPTOR; AMYLOID BETA-PEPTIDES; ANIMALS; AUTOPHAGY; BUNGAROTOXINS; CASPASE 3; CELLS, CULTURED; CEREBRAL CORTEX; DOSE-RESPONSE RELATIONSHIP, DRUG; EMBRYO, MAMMALIAN; GENE EXPRESSION REGULATION; HUMANS; MICE; MICE, TRANSGENIC; MICROTUBULE-ASSOCIATED PROTEINS; NEUROBLASTOMA; NEURONS; NICOTINIC ANTAGONISTS; PEPTIDE FRAGMENTS;

EID: 84923866869     PISSN: 00283908     EISSN: 18737064     Source Type: Journal    
DOI: 10.1016/j.neuropharm.2015.02.003     Document Type: Article

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