Literature summary for 3.4.23.45 extracted from

Holler, C.; Webb, R.; Laux, A.; Beckett, T.; Niedowicz, D.; Ahmed, R.; Liu, Y.; Simmons, C.; Dowling, A.; Spinelli, A.; Khurgel, M.; Estus, S.; Head, E.; Hersh, L.; Murphy, M.
BACE2 expression increases in human neurodegenerative disease (2012), Am. J. Pathol., 180, 337-350.

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Application

Application	Comment	Organism
medicine	in patients with preclinical to late-stage Alzheimer's disease, including amnestic mild cognitive impairment, and age-matched controls, cases of frontotemporal dementia, and Down's syndrome, BACE2 protein and enzymatic activity increase as early as preclinical Alzheimer's disease and are found in neurons and astrocytes. Although the levels of total BACE2 mRNA are unchanged, the mRNA for BACE2 splice form C (missing exon 7) increases in parallel with BACE2 protein and activity. BACE1 and BACE2 are strongly correlated with each other at all levels. BACE2 is also elevated in frontotemporal dementia but not in Down's syndrome, even in patients with substantial amyloid beta deposition	Homo sapiens

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	Q9Y5Z0	-	-

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Release 2023.1 (January 2023)