Mice with disrupted GM2/GD2 synthase gene lack complex gangliosides but exhibit only subtle defects in their nervous system

Proceedings of the National Academy of Sciences of the United States of America

Volumn 93, Issue 20, 1996, Pages 10662-10667

  Takamiya, Kogo ^a,b   Yamamoto, Akihito ^a   Furukawa, Keiko ^a   Yamashiro, Shuji ^a   Shin, Masashi ^a   Okada, Masahiko ^a   Fukumoto, Satoshi ^a   Haraguchi, Masashi ^a   Takeda, Naoki ^b   Fujimura, Koichi ^a   Sakae, Mihoko ^a   Kishikawa, Masao ^a   Shiku, Hiroshi ^c   Furukawa, Koichi ^a   Aizawa, Shinichi ^b  

^a NAGASAKI UNIVERSITY SCHOOL OF MEDICINE   (Japan)

^b KUMAMOTO UNIV SCHOOL OF MEDICINE   (Japan)

^c MIE UNIVERSITY SCHOOL OF MEDICINE   (Japan)

Author keywords

1, 4GalNAc transferase; development; gene knock out

Indexed keywords

GANGLIOSIDE; GANGLIOSIDE GM2; N ACETYLGALACTOSAMINYLTRANSFERASE;

ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; ENZYME ASSAY; EVOKED SOMATOSENSORY RESPONSE; GENE MUTATION; GENE TARGETING; GENETIC RECOMBINATION; MOUSE; NERVOUS SYSTEM DEVELOPMENT; NONHUMAN; PRIORITY JOURNAL; SYNAPTOGENESIS;

ANIMALS; BEHAVIOR, ANIMAL; BRAIN; EVOKED POTENTIALS, SOMATOSENSORY; G(M2) GANGLIOSIDE; GANGLIOSIDES; GENES; MICE; MICE, KNOCKOUT; N-ACETYLGALACTOSAMINYLTRANSFERASES; NERVOUS SYSTEM PHYSIOLOGY; NEURAL CONDUCTION; SOMATOSENSORY CORTEX;

ANIMALIA; MAMMALIA; VERTEBRATA;

EID: 0010492680     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.93.20.10662     Document Type: Article

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