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Literature summary for 3.4.23.46 extracted from

  • Vnencak, M.; Schoelvinck, M.L.; Schwarzacher, S.W.; Deller, T.; Willem, M.; Jedlicka, P.
    Lack of beta-amyloid cleaving enzyme-1 (BACE1) impairs long-term synaptic plasticity but enhances granule cell excitability and oscillatory activity in the dentate gyrus in vivo (2019), Brain Struct. Funct., 224, 1279-1290 .
    View publication on PubMed
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Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
amyloid-beta precursor protein + H2O Mus musculus
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 ?
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 ?

Organism

Organism UniProt Comment Textmining
Mus musculus P56818
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-

Source Tissue

Source Tissue Comment Organism Textmining
brain
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 Mus musculus
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dentate granule cell
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 Mus musculus
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
amyloid-beta precursor protein + H2O
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 Mus musculus ?
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 ?

Synonyms

Synonyms Comment Organism
BACE1
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 Mus musculus
beta-amyloid cleaving enzyme-1
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 Mus musculus

General Information

General Information Comment Organism
malfunction loss of enzyme in the dentate gyrus leads to increased granule cell excitability, indicated by enhanced efficiency of synaptic potentials to generate granule cell spikes. The increase in granule cell excitability is accompanied by prolonged paired-pulse inhibition, altered network gamma oscillations, and impaired synaptic plasticity at entorhinal-dentate synapses of the perforant path Mus musculus
physiological function the enzyme is important for normal dentate gyrus network function Mus musculus