Cross linking of polyglutamine domains catalyzed by tissue transglutaminase is greatly favored with pathological-length repeats: Does transglutaminase activity play a role in (CAG)n/Qn-expansion diseases?

Neurochemistry International

Volumn 40, Issue 1, 2002, Pages 53-67

  Cooper, Arthur J L ^a,b   Jeitner, Thomas M ^a,b   Gentile, Vittorio ^c   Blass, John P ^a,b  

^a WEILL CORNELL MEDICAL COLLEGE   (United States)

^b BURKE MEDICAL RESEARCH INSTITUTE   (United States)

^c SECOND UNIVERSITY OF NAPLES   (Italy)

Author keywords

[No Author keywords available]

Indexed keywords

BRAIN ENZYME; CALCIUM ION; CASPASE; HUNTINGTIN; ISOENZYME; MESSENGER RNA; NUCLEAR PROTEIN; POLYGLUTAMINE; PROTEASOME; PROTEIN GLUTAMINE GAMMA GLUTAMYLTRANSFERASE; REPETITIVE DNA;

APOPTOSIS; BRAIN LEVEL; BRAIN TOXICITY; CALCIUM HOMEOSTASIS; CATALYSIS; CONFERENCE PAPER; DEGENERATIVE DISEASE; ENZYME ACTIVITY; ENZYME SUBSTRATE; GENE EXPRESSION; HUMAN; HUNTINGTON CHOREA; MOLECULAR RECOGNITION; MOLECULAR SIZE; NEUROPATHOLOGY; NEUROPROTECTION; NONHUMAN; NUCLEOTIDE REPEAT; PRIORITY JOURNAL; PROTEIN AGGREGATION; PROTEIN CROSS LINKING; PROTEIN DEGRADATION; PROTEIN DOMAIN; PROTEIN FOLDING; PROTEIN PROTEIN INTERACTION; SOLUBILITY;

HUMANS; NEURODEGENERATIVE DISEASES; PEPTIDES; PROTEIN STRUCTURE, TERTIARY; REPETITIVE SEQUENCES, NUCLEIC ACID; TRANSGLUTAMINASES;

EID: 0036134811     PISSN: 01970186     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0197-0186(01)00058-4     Document Type: Conference Paper

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