Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome

Nature Neuroscience

Volumn 13, Issue 8, 2010, Pages 927-934

  Chakrabarti, Lina ^a   Best, Tyler K ^b   Cramer, Nathan P ^b   Carney, Rosalind S E ^a   Isaac, John T R ^c   Galdzicki, Zygmunt ^b   Haydar, Tarik F ^a,d  

^a CHILDREN'S NATIONAL MEDICAL CENTER   (United States)

^b Uniformed Services University of the Health Sciences and the Walter Reed National Military Medical Center   (United States)

^c NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE   (United States)

^d BOSTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRAIN DISEASE; DEVELOPMENTAL GENE; DOWN SYNDROME; FOREBRAIN; GENE EXPRESSION; GENE REPLICATION; MOUSE; NERVOUS SYSTEM DEVELOPMENT; NONHUMAN; OLIG1 GENE; OLIG2 GENE; PHENOTYPE; PRIORITY JOURNAL; TRISOMY;

ANIMALS; BASIC HELIX-LOOP-HELIX TRANSCRIPTION FACTORS; BLOTTING, WESTERN; BRAIN; BRAIN DISEASES; DISEASE MODELS, ANIMAL; DOWN SYNDROME; EMBRYONIC DEVELOPMENT; IMMUNOHISTOCHEMISTRY; IN SITU HYBRIDIZATION; INHIBITORY POSTSYNAPTIC POTENTIALS; MICE; MICROSCOPY, CONFOCAL; NERVE TISSUE PROTEINS; NEURONS; PATCH-CLAMP TECHNIQUES; REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION;

EID: 77955037842     PISSN: 10976256     EISSN: None     Source Type: Journal    
DOI: 10.1038/nn.2600     Document Type: Article

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