Evidence map›Paper›PMID 26402097›Full record

ArticleJournal of Alzheimer's disease : JAD2015

Tomoregulin (TMEFF2) Binds Alzheimer's Disease Amyloid-β (Aβ) Oligomer and AβPP and Protects Neurons from Aβ-Induced Toxicity.

Hyun-Seok Hong, Izumi Maezawa, Jitka Petrlova, Xiao-Yan Zhao, John C Voss, Lee-Way Jin

Abstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
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  4. Assessing Aβ-independent effects of Module 42 on immune function in vitro.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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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

6 authors.

Hyun-Seok HongDepartment of Pathology and Laboratory Medicine, University of California Davis Medical Center, Sacramento, CA, USA.
Izumi MaezawaDepartment of Pathology and Laboratory Medicine, University of California Davis Medical Center, Sacramento, CA, USA.
Jitka PetrlovaDepartment of Biochemistry and Molecular Medicine, University of California Davis, Davis, CA, USA.
Xiao-Yan ZhaoBiologics Research-USIC, Bayer Healthcare Pharmaceuticals, San Francisco, CA, USA.
John C VossDepartment of Biochemistry and Molecular Medicine, University of California Davis, Davis, CA, USA.
Lee-Way JinDepartment of Pathology and Laboratory Medicine, University of California Davis Medical Center, Sacramento, CA, USA.

Funding

UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
Inhibition of Alzheimer's Beta-Amyloid Fibril FormationR01AG025500 · NIA · KANSAS STATE UNIVERSITY · PI HUA, DUY H · 2006 to 2009
$1.1M
Identify Abeta Oligomer Inhibitors By Combinatorial ChemistryR21AG031362 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI JIN, LEE-WAY · 2008 to 2009
$355k
The Microglial Kv1.3 Channel in Alzheimer's DiseaseR21AG038910 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI JIN, LEE-WAY, WULFF, HEIKE · 2011 to 2012
$343k
NIA NIH HHS AG010129NIA NIH HHS AG025500NIA NIH HHS AG031362NIA NIH HHS P30 AG010129NIA NIH HHS R01 AG025500NIA NIH HHS R21 AG031362NIA NIH HHS R21 AG038910
6 · The paper itself

Abstract

Amyloid-β (Aβ) protein causes neurotoxicity and its abnormal aggregation into amyloid is a pathological hallmark of Alzheimer's disease (AD). Cellular proteins able to interact with Aβ or its precursor, AβPP (amyloid-β protein precursor), may regulate Aβ production and neurotoxicity. We identified a brain-enriched type I transmembrane protein, tomoregulin (TR), that directly binds Aβ and Aβ oligomers (AβO). TR co-immunoprecipitated with Aβ and AβO in cultured cells and co-localized with amyloid plaques and intraneuronal Aβ in the 5xFAD AD mouse model. TR was also enriched in astrocytic processes reactive to amyloid plaques. Surface plasmon resonance spectroscopy studies showed that the extracellular domain of TR binds to AβO with a high affinity (KD = 76.8 nM). Electron paramagnetic resonance spectroscopy also demonstrated a physical interaction between spin-labeled Aβ and the TR extracellular domain in solution. Furthermore, TR also interacted with AβPP and enhanced its cleavage by α-secretase. Both cellular expression of TR and application of recombinant TR extracellular domain protected N2a neurons from AβO-induced neuronal death. These data provide first evidence that neuronal and astrocytic expression of TR is intimately related to Aβ metabolism and toxicity, and could be neuroprotective through its direct interaction with Aβ and AβPP.

Indexed as

Amyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAnimalsAstrocytesCell Line, TumorCell SurvivalElectron Spin Resonance SpectroscopyFluorescent Antibody TechniqueGene SilencingHumansImmunoprecipitationMembrane ProteinsMice, TransgenicMicroscopy, ConfocalNeoplasm ProteinsNeuronsAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesMembrane ProteinsNeoplasm ProteinsRecombinant ProteinsTMEFF2 protein, humanTmeff2 protein, mouseAlzheimer’s diseaseamyloidbindingneuroprotectionneurotoxicitytomoregulin

Identifiers

PMID26402097
PMCPMC5533101

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.