Corrigendum: mTORC1-independent TFEB activation via Akt inhibition promotes cellular clearance in neurodegenerative storage diseases (Nature Communications (2017) 8 (14338) DOI: 10.1038/ncomms14338);MTORC1-independent TFEB activation via Akt inhibition promotes cellular clearance in neurodegenerative storage diseases

Nature Communications

Volumn 8, Issue , 2017, Pages

  Palmieri, Michela ^a   Pal, Rituraj ^b   Nelvagal, Hemanth R ^c   Lotfi, Parisa ^a   Stinnett, Gary R ^b   Seymour, Michelle L ^b   Chaudhury, Arindam ^b   Bajaj, Lakshya ^a   Bondar, Vitaliy V ^a   Bremner, Laura ^c   Saleem, Usama ^c   Tse, Dennis Y ^d,e   Sanagasetti, Deepthi ^a   Wu, Samuel M ^d   Neilson, Joel R ^b   Pereira, Fred A ^b   Pautler, Robia G ^b   Rodney, George G ^b   Cooper, Jonathan D ^c   Sardiello, Marco ^a  

^a TEXAS CHILDREN S HOSPITAL   (United States)

^b BAYLOR COLLEGE OF MEDICINE   (United States)

^c KING'S COLLEGE LONDON   (United Kingdom)

^d CULLEN EYE INSTITUTE   (United States)

^e HONG KONG POLYTECHNIC UNIVERSITY   (Hong Kong)

Author keywords

[No Author keywords available]

Indexed keywords

8 [4 (1 AMINOCYCLOBUTYL)PHENYL] 9 PHENYL 1,2,4 TRIAZOLO[3,4 F][1,6]NAPHTHYRIDIN 3(2H) ONE; MAMMALIAN TARGET OF RAPAMYCIN COMPLEX 1; PROTEIN KINASE B; PROTEOLIPID; TRANSCRIPTION FACTOR; TRANSCRIPTION FACTOR EB; TREHALOSE; UNCLASSIFIED DRUG; AKT1 PROTEIN, HUMAN; BASIC HELIX LOOP HELIX LEUCINE ZIPPER TRANSCRIPTION FACTOR; CHAPERONE; CLN3 PROTEIN, MOUSE; FUSED HETEROCYCLIC RINGS; MEMBRANE PROTEIN; NEUROPROTECTIVE AGENT; TFEB PROTEIN, HUMAN;

CELLS AND CELL COMPONENTS; ENZYME ACTIVITY; GENE EXPRESSION; INHIBITION; INHIBITOR; LIPID; RODENT; SURVIVAL; TRANSLOCATION;

AMINO ACID SEQUENCE; AMINO ACID SUBSTITUTION; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; ASTROCYTE; AUTOPHAGY; BRAIN CELL; BRAIN CELL CULTURE; BRAIN CORTEX; BRAIN STEM RESPONSE; CELL FUNCTION; CELLULAR CLEARANCE; CELLULAR DISTRIBUTION; CONTROLLED STUDY; DEGENERATIVE DISEASE; DRUG MECHANISM; EMBRYO; ENZYME INHIBITION; ENZYME PHOSPHORYLATION; FIBROBLAST; IN VITRO STUDY; MALE; MOUSE; NEURONAL CEROID LIPOFUSCINOSIS; NEWBORN; NONHUMAN; PHARMACOLOGICAL BLOCKING; PURKINJE CELL; STORAGE DISEASE; THALAMUS NUCLEUS; TRANSCRIPTION INITIATION; ANIMAL; ANTAGONISTS AND INHIBITORS; BRAIN; CELL NUCLEUS; CYTOLOGY; DISEASE MODEL; DRUG EFFECT; GENE KNOCKDOWN; GENETICS; HELA CELL LINE; HUMAN; METABOLISM; NERVE CELL; PATHOLOGY; PHOSPHORYLATION; PHYSIOLOGY; PRIMARY CELL CULTURE; SIGNAL TRANSDUCTION; TRANSGENIC MOUSE;

MUS;

ANIMALS; ASTROCYTES; AUTOPHAGY; BASIC HELIX-LOOP-HELIX LEUCINE ZIPPER TRANSCRIPTION FACTORS; BRAIN; CELL NUCLEUS; DISEASE MODELS, ANIMAL; FIBROBLASTS; GENE KNOCKDOWN TECHNIQUES; HELA CELLS; HETEROCYCLIC COMPOUNDS, 3-RING; HUMANS; MALE; MECHANISTIC TARGET OF RAPAMYCIN COMPLEX 1; MEMBRANE GLYCOPROTEINS; MICE; MICE, TRANSGENIC; MOLECULAR CHAPERONES; NEURODEGENERATIVE DISEASES; NEURONS; NEUROPROTECTIVE AGENTS; PHOSPHORYLATION; PRIMARY CELL CULTURE; PROTO-ONCOGENE PROTEINS C-AKT; SIGNAL TRANSDUCTION; TREHALOSE;

EID: 85011898443     PISSN: None     EISSN: 20411723     Source Type: Journal    
DOI: 10.1038/ncomms15793     Document Type: Erratum

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