Human presenilin-1, but not familial Alzheimer's disease (FAD) mutants, facilitate Caenorhabditis elegans Notch signalling independently of proteolytic processing.

Genes and function

Volumn 1, Issue 2, 1997, Pages 149-159

  Baumeister, R ^a   Leimer, U ^a   Zweckbronner, I ^a   Jakubek, C ^a   Grunberg J ^a   Haass, C ^a  

^a UNIVERSITY OF MUNICH   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

MEMBRANE PROTEIN; NOTCH RECEPTOR; PRESENILIN 1; PSEN1 PROTEIN, HUMAN; RECOMBINANT PROTEIN;

ALZHEIMER DISEASE; ANIMAL; ARTICLE; CAENORHABDITIS ELEGANS; GENETICS; HUMAN; HYDROLYSIS; METABOLISM; MUTATION; PHENOTYPE; PLASMID; PROTEIN PROCESSING; TRANSGENIC ANIMAL;

ALZHEIMER DISEASE; ANIMALS; ANIMALS, GENETICALLY MODIFIED; CAENORHABDITIS ELEGANS; HUMANS; HYDROLYSIS; MEMBRANE PROTEINS; MUTATION; PHENOTYPE; PLASMIDS; PRESENILIN-1; PROTEIN PROCESSING, POST-TRANSLATIONAL; RECEPTORS, NOTCH; RECOMBINANT PROTEINS;

EID: 0031108103     PISSN: 13607413     EISSN: None     Source Type: Journal    
DOI: 10.1046/j.1365-4624.1997.00012.x     Document Type: Article

References (0)