Huntingtin-associated protein 1 (Hap1) mutant mice bypassing the early postnatal lethality are neuroanatomically normal and fertile but display growth retardation

Human Molecular Genetics

Volumn 13, Issue 24, 2004, Pages 3115-3125

  Dragatsis, Ioannis ^a   Zeitlin, Scott ^b   Dietrich, Paula ^a  

^a UNIVERSITY OF TENNESSEE COLLEGE OF MEDICINE   (United States)

^b UNIVERSITY OF VIRGINIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

DNA; HUNTINGTIN; HUNTINGTIN ASSOCIATED PROTEIN 1; POLYPEPTIDE; PROTEIN HAP1; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BEHAVIOR DISORDER; BRAIN DISEASE; CONTROLLED STUDY; DNA REPAIR; EMBRYO; FEEDING BEHAVIOR; FEMALE; FERTILITY; GENE DISRUPTION; GENE TARGETING; GROWTH RETARDATION; LETHALITY; LITTER SIZE; MALE; MOUSE; MOUSE MUTANT; NERVE REGENERATION; NEUROANATOMY; NEWBORN; NONHUMAN; NUCLEOTIDE SEQUENCE; NULL ALLELE; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN FUNCTION; PROTEIN MALNUTRITION; REGULATORY MECHANISM; SUCKLING;

AGE FACTORS; ANIMALS; BODY WEIGHT; GENE TARGETING; HOMOZYGOTE; IN SITU HYBRIDIZATION; MICE; MICE, TRANSGENIC; MUTATION; NERVE TISSUE PROTEINS; NERVOUS SYSTEM; NUCLEAR PROTEINS;

EID: 11044228787     PISSN: 09646906     EISSN: None     Source Type: Journal    
DOI: 10.1093/hmg/ddh328     Document Type: Article

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