Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 2.4.3.8 extracted from

  • Bernardo, A.; Harrison, F.E.; McCord, M.; Zhao, J.; Bruchey, A.; Davies, S.S.; Jackson Roberts, L.; Mathews, P.M.; Matsuoka, Y.; Ariga, T.; Yu, R.K.; Thompson, R.; McDonald, M.P.
    Elimination of GD3 synthase improves memory and reduces amyloid-beta plaque load in transgenic mice (2008), Neurobiol. Aging, 30, 1777-1791.
    View publication on PubMed
Search for more literature for 2.4.3.8

Application

Application Comment Organism
medicine examination of amyloid beta-ganglioside interactions in neural tissue from mice lacking the gene coding for GD3 synthase, St8sia1, and in a double-transgenic mouse model of Alzheimer’s disease mutated in amyloid precursor protein APP and presenilin PSEN1 cross-bred with GD3 synthase deficient mice. In primary neurons and astrocytes lacking GD3 synthase, amyloid beta-induced cell death and amyloid beta aggregation are inhibited. Like GD3 synthase eficient and APP/PSEN1 double-transgenic mice, APP/PSEN1/GD3 synthase deficient triple-mutant mice are indistinguishable from wild-type mice on casual examination. APP/PSEN1 double-transgenics exhibit robust impairments on a number of reference-memory tasks. In contrast, APP/PSEN1/GD3 synthase deficient triple-mutant mice perform as well as wild-type control and GD3-synthase deficient mice. Consistent with the behavioral improvements, both aggregated and unaggregated amyloid beta and associated neuropathology are almost completely eliminated in triple-mutant mice Mus musculus

Protein Variants

Protein Variants Comment Organism
additional information examination of amyloid beta-ganglioside interactions in neural tissue from mice lacking the gene coding for GD3 synthase, St8sia1, and in a double-transgenic mouse model of Alzheimer’s disease mutated in amyloid precursor protein APP and presenilin PSEN1 cross-bred with GD3 synthase deficient mice. In primary neurons and astrocytes lacking GD3S, amyloid beta-induced cell death and amyloid beta aggregation are inhibited. Like GD3 synthase eficient and APP/PSEN1 double-transgenic mice, APP/PSEN1/GD3 synthase deficient triple-mutant mice are indistinguishable from wild-type mice on casual examination. APP/PSEN1 double-transgenics exhibit robust impairments on a number of reference-memory tasks. In contrast, APP/PSEN1/GD3 synthase deficient triple-mutant mice perform as well as wild-type control and GD3-synthase deficient mice. Consistent with the behavioral improvements, both aggregated and unaggregated amyloid beta and associated neuropathology are almost completely eliminated in triple-mutant mice Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
astrocyte in primary neurons and astrocytes lacking GD3 synthase, amyloid beta-induced cell death and amyloid beta aggregation are inhibited Mus musculus
-
neuron in primary neurons and astrocytes lacking GD3 synthase, amyloid beta-induced cell death and amyloid beta aggregation are inhibited Mus musculus
-