Distinct neuropathologic phenotypes after disrupting the chloride transport proteins ClC-6 or ClC-7/Ostm1

Journal of Neuropathology and Experimental Neurology

Volumn 69, Issue 12, 2010, Pages 1228-1246

  Pressey, Sarah N R ^a   O'Donnell, Kieran J ^a   Stauber, Tobias ^b   Fuhrmann, Jens C ^b   Tyynelä, Jaana ^c   Jentsch, Thomas J ^b   Cooper, Jonathan D ^a  

^a KING'S COLLEGE LONDON   (United Kingdom)

^b MAX DELBRÜCK CENTER FOR MOLECULAR MEDICINE   (Germany)

^c UNIVERSITY OF HELSINKI   (Finland)

Author keywords

Chloride channel; Chloride proton exchanger; Grey lethal; Lysosomal storage disorder; Neuronal ceroid lipofuscinosis Batten disease

Indexed keywords

CARRIER PROTEIN; CLC 6 PROTEIN; CLC 7 PROTEIN; OSTM1 PROTEIN; UNCLASSIFIED DRUG;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL ACTIVATION; CELL LOSS; CENTRAL NERVOUS SYSTEM; CONTROLLED STUDY; DISEASE COURSE; DISEASE SEVERITY; GENE MUTATION; MICROGLIA; MOUSE; NERVE CELL; NEURONAL CEROID LIPOFUSCINOSIS; NEUROPATHOLOGY; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; PROTEIN FUNCTION; THALAMOCORTICAL TRACT;

ANIMALS; CARRIER PROTEINS; CEREBRAL CORTEX; CHLORIDE CHANNELS; MEMBRANE PROTEINS; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; NEURONAL CEROID-LIPOFUSCINOSES; PHENOTYPE; THALAMUS;

EID: 78650177985     PISSN: 00223069     EISSN: None     Source Type: Journal    
DOI: 10.1097/NEN.0b013e3181ffe742     Document Type: Article

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