Evidence map›Paper›PMID 29137240›Full record

ArticleOncotarget2017

Mutational re-modeling of di-aspartyl intramembrane proteases: uncoupling physiologically-relevant activities from those associated with Alzheimer's disease.

Anastasia P Grigorenko, Youri K Moliaka, Olga V Plotnikova, Alexander Smirnov, Vera A Nikishina, Andrey Y Goltsov, Fedor Gusev, Tatiana V Andreeva, Omar Nelson, Ilya Bezprozvanny and 1 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 57% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 6 institutions in 2 countries.

Anastasia P GrigorenkoDepartment of Psychiatry, Brudnick Neuropsychiatric Research Institute, University of Massachusetts Medical School, Worcester, MA 01604, USA.
Youri K MoliakaDepartment of Psychiatry, Brudnick Neuropsychiatric Research Institute, University of Massachusetts Medical School, Worcester, MA 01604, USA.
Olga V PlotnikovaDepartment of Psychiatry, Brudnick Neuropsychiatric Research Institute, University of Massachusetts Medical School, Worcester, MA 01604, USA.
Alexander SmirnovDepartment of Psychiatry, Brudnick Neuropsychiatric Research Institute, University of Massachusetts Medical School, Worcester, MA 01604, USA.
Vera A NikishinaDepartment of Psychiatry, Brudnick Neuropsychiatric Research Institute, University of Massachusetts Medical School, Worcester, MA 01604, USA.
Andrey Y GoltsovDepartment of Genomics and Human Genetics, Institute of General Genetics, Russian Academy of Sciences, Moscow, 119991 Russia.
Fedor GusevDepartment of Genomics and Human Genetics, Institute of General Genetics, Russian Academy of Sciences, Moscow, 119991 Russia.
Tatiana V AndreevaDepartment of Genomics and Human Genetics, Institute of General Genetics, Russian Academy of Sciences, Moscow, 119991 Russia.
Omar NelsonDepartment of Physiology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390-9040, USA.
Ilya BezprozvannyDepartment of Physiology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390-9040, USA.
Evgeny I RogaevDepartment of Psychiatry, Brudnick Neuropsychiatric Research Institute, University of Massachusetts Medical School, Worcester, MA 01604, USA.
Institute of Cytology and Genetics · RUUniversity of Massachusetts Chan Medical School · USThe University of Texas Southwestern Medical Center · USLomonosov Moscow State University · RUNeuropsychiatric Research Institute · USVavilov Institute of General Genetics · RU

Funding

Function of intramembrane aspartic proteaseR01AG029360 · NIA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ROGAEV, EVGENY I · 2008 to 2012
$1.6M
Regulation of Presenilin GenesR01NS045854 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ROGAEV, EVGENY I · 2004 to 2008
$1.5M
NIA NIH HHS R01 AG029360NINDS NIH HHS R01 NS045854
6 · The paper itself

Abstract

The intramembrane proteolytic activities of presenilins (PSEN1/PS1 and PSEN2/PS2) underlie production of β-amyloid, the key process in Alzheimer's disease (AD). Dysregulation of presenilin-mediated signaling is linked to cancers. Inhibition of the γ-cleavage activities of PSENs that produce Aβ, but not the ε-like cleavage activity that release physiologically essential transcription activators, is a potential approach for the development of rational therapies for AD. In order to identify whether different activities of PSEN1 can be dissociated, we designed multiple mutations in the evolutionary conserved sites of PSEN1. We tested them

Indexed as

IMPAS/SPPintramembrane aspartyl proteasesmutational re-modellingpresenilinregulated intramembrane proteolysis

Identifiers

PMID29137240
PMCPMC5669866
OpenAlexW2620117313

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.