Mice with combined gene knock-outs reveal essential and partially redundant functions of amyloid precursor protein family members.

Autor:in

Heber, S; Herms, J; Gajic, V; Hainfellner, J; Aguzzi, A; Rülicke, T; von Kretzschmar, H; von Koch, C; Sisodia, S; Tremml, P; Lipp, H P; Wolfer, D P; Müller, U;

Schlagwörter

Amyloid beta-Protein Precursor/analogs & derivatives; Amyloid beta-Protein Precursor/deficiency; Amyloid beta-Protein Precursor/genetics*; Amyloid beta-Protein Precursor/metabolism; Animals; Blotting, Northern; Blotting, Western; Brain/cytology; Brain/metabolism; Cell Survival/drug effects; Cell Survival/genetics; Cells, Cultured; Crosses, Genetic; Female; Genes, Lethal/genetics; Genetic Complementation Test; Glutamic Acid/metabolism; Glutamic Acid/pharmacology; Heterozygote; Homozygote; Male; Mice; Mice, Knockout; Multigene Family/genetics*; Nerve Tissue Proteins/deficiency; Nerve Tissue Proteins/genetics*; Nerve Tissue Proteins/metabolism; Neurons/cytology; Neurons/drug effects; Neurons/metabolism; Phenotype; RNA, Messenger/metabolism; Synapses/ultrastructure;

ISSN/eISSN

0270-6474 -

PubMed ID

11050115