Literature summary for 3.4.24.11 extracted from

Iijima-Ando, K.; Hearn, S.A.; Granger, L.; Shenton, C.; Gatt, A.; Chiang, H.C.; Hakker, I.; Zhong, Y.; Iijima, K.
Overexpression of neprilysin reduces Alzheimer amyloid-beta42 (Abeta42)-induced neuron loss and intraneuronal Abeta42 deposits but causes a reduction in cAMP-responsive element-binding protein-mediated transcription, age-dependent axon pathology, and premature death in Drosophila (2008), J. Biol. Chem., 283, 19066-19076.

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Cloned(Commentary)

Cloned (Comment)	Organism
transgenic Drosophila melanogaster expressing human neprilysin and amyloid beta42	Homo sapiens

Protein Variants

Protein Variants	Comment	Organism
additional information	in transgenic Drosophila melanogaster expressing human neprilysin and amyloid beta42, neprilysin efficiently suppresses the formation of intraneuronal amyloid beta42 deposits and amyloid beta42-induced neuron loss. Neuronal neprilysin overexpression reduces cAMP-responsive element-binding protein-mediated transcription, causes age-dependent axon degeneration, and shortens the life span of the flies. The mRNA levels of endogenous fly neprilysin genes and phosphoramidon-sensitive neprilysin activity decline during aging in fly brains	Homo sapiens

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	-	expression in Drosophila melanogaster	-

Source Tissue

Source Tissue	Comment	Organism	Textmining

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Release 2023.1 (January 2023)