ArticleBiochemical and biophysical research communications2007
Structure nor stability of the transmembrane spanning 6/7 domain of presenilin I correlates with pathogenicity.
Article in Biochemical and biophysical research communications, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Influence of solubilization and AD-mutations on stability and structure of human presenilins.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Since its cloning in 1995, missense point mutations in presenilin I (PS-I) have been shown to be responsible for greater than 70% of the cases of early onset familial Alzheimer's disease (EOFAD), which can affect individuals as early as age 18. PS-I is known to be a component of gamma-secretase, the enzyme responsible for cleavage of the amyloid precursor protein (APP) into 42 amino acid peptides that aggregate to form the plaques surrounding neurons of Alzheimer's patients. It has recently been hypothesized that wild-type (wt) PS-I contains an autoinhibitory module that prevents gamma-secretase cleavage of the APP, while pathogenic PS-I point mutants lack a structure necessary for this inhibition. In this work, spectroscopic data is presented that does not correlate structure or stability of the proposed PS-I autoinhibitory module with pathogenicity.
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What OpenQuestion holds
Registered trials
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