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Literature summary for 3.4.21.68 extracted from

  • Noel, M.; Norris, E.H.; Strickland, S.
    Tissue plasminogen activator is required for the development of fetal alcohol syndrome in mice (2011), Proc. Natl. Acad. Sci. USA, 108, 5069-5074.
    View publication on PubMedView publication on EuropePMC
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Protein Variants

Protein Variants Comment Organism
S481A catalytically inactive tPA Mus musculus

Inhibitors

Inhibitors Comment Organism Structure
PAI-1 ethanol can downregulate the expression of PAI-1, a main inhibitor of tPA in the CNS Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
brain
-
 Mus musculus
-
commercial preparation recombinant enzyme Mus musculus
-
forebrain
-
 Mus musculus
-

Synonyms

Synonyms Comment Organism
Tissue plasminogen activator
-
 Mus musculus
tPA
-
 Mus musculus

General Information

General Information Comment Organism
physiological function ethanol exposure during developmental synaptogenesis can lead to brain defects referred to as fetal alcohol syndrome, which can include mental health problems such as cognitive deficits and mental retardation. Tissue plasminogen activator is implicated in neurodegeneration and is a critical signaling component in FAS. In wild-type mice, ethanol elicits caspase-3 activation, significant forebrain neurodegeneration, and decreases contextual fear conditioning in adults. However, tPA-deficient mice are protected from these neurotoxicities, and this protection can be abrogated by exogenous tPA. The effects of tPA are mediated by the NR2B subunit of the NMDA receptor, but tPA catalytic activity Is not required to promote ethanol-induced neurodegenration Mus musculus