Evidence map›Paper›PMID 26885753›Full record

ArticleOncotarget2016

Potential role of PCTAIRE-2, PCTAIRE-3 and P-Histone H4 in amyloid precursor protein-dependent Alzheimer pathology.

Dale Chaput, Lisa Kirouac, Stanley M Stevens, Jaya Padmanabhan

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026
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  4. An Update on Neuroaging on Earth and in Spaceflight.International journal of molecular sciences · 2025
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  11. Cyclin-dependent kinases: Masters of the eukaryotic universe.Wiley interdisciplinary reviews. RNA · 2023
    Review
  12. Review
  13. Review
  14. Article
  15. Epigenetics in Alzheimer's Disease.Frontiers in aging neuroscience · 2022
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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

4 authors at 1 institution in 1 country.

Dale ChaputDepartment of Cell Biology, Microbiology, and Molecular Biology, University of South Florida, Tampa, FL, USA.
Lisa KirouacDepartment of Molecular Medicine, USF Health Byrd Alzheimer's Institute, University of South Florida, Tampa, FL, USA.
Stanley M StevensDepartment of Cell Biology, Microbiology, and Molecular Biology, University of South Florida, Tampa, FL, USA.
Jaya PadmanabhanDepartment of Molecular Medicine, USF Health Byrd Alzheimer's Institute, University of South Florida, Tampa, FL, USA.
University of South Florida · US

Funding

UC Irvine Alzheimer's Disease Research Center Induced Pluripotent Stem Cell CoreP50AG016573 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 2000 to 2019
$37.0M
NIA NIH HHS P50 AG016573NIA NIH HHS P50 AG16573
6 · The paper itself

Abstract

Amyloid Precursor Protein (APP) is regulated in a mitosis-specific manner and plays a role in proliferative signaling in cells. Though APP-derived Aβ generation has a well-established role in neurodegeneration, the mechanistic role of APP in this process is not fully understood. Here, we performed an unbiased, comprehensive analysis of the phosphoproteome signature in APP-null neuroblastoma cells (B103) compared to those expressing APP-695 isoform (B103-695) to determine if APP expression affects protein phosphorylation. Stable isotope labeling by amino acids in cell culture (SILAC) followed by mass spectrometry-based phosphoproteomic analysis with PolyMAC identified a total of 2,478 phosphopeptides in the B103 and B103-695 cell culture model system. We observed that phosphorylation of PCTAIRE-2 (CDK17), PCTAIRE-3 (CDK18), and Histone H4 are significantly elevated in B103-695 cells; western blot analysis confirmed overexpression of PCTAIREs and increased phosphorylation of Histone H4. More importantly, analysis of primary neurons treated with Aβ, as well as brain samples from MCI (mild cognitive impaired) and AD patients recapitulated these results, showing increased levels of PCTAIREs and P-Histone H4. These novel findings identify a hitherto uncharacterized mechanism by which APP and/or Aβ may promote AD neurodegeneration, and raises the possibility that their inhibition may protect against pathology development in AD.

Indexed as

Aged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsBlotting, WesternBrainCells, CulturedCognitive DysfunctionCyclin-Dependent KinasesDisease Models, AnimalFemaleHistonesHumansMaleMiceAmyloid beta-PeptidesAmyloid beta-Protein PrecursorCyclin-Dependent KinasesHistonesPCTAIRE-2 protein kinasePCTAIRE-3 protein kinaseA-betaAlzheimer’s diseaseamyloid precursor proteinGerotargetneurodegenerationphosphoproteomics

Identifiers

PMID26885753
PMCPMC4890981
OpenAlexW2277459742

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.