Evidence map›Paper›PMID 23666762›Full record

ArticleNeuromolecular medicine2013

Role of individual MARK isoforms in phosphorylation of tau at Ser²⁶² in Alzheimer's disease.

Gucci Jijuan Gu, Harald Lund, Di Wu, Andries Blokzijl, Christina Classon, Gabriel von Euler, Ulf Landegren, Dan Sunnemark, Masood Kamali-Moghaddam

Abstract read
PubMed Publisher
In one paragraph

Article in Neuromolecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 11% 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

44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 78 citations in OpenAlex.

  1. Association ofFrontiers in medicine · 2025
    Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Increased MyocardialInternational journal of molecular sciences · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. TauCell death & disease · 2024
    Article
  14. Tau Protein Alterations Induced by Hypobaric Hypoxia Exposure.International journal of molecular sciences · 2024
    Review
  15. Tauopathy in AD: Therapeutic Potential of MARK-4.Current Alzheimer research · 2024
    Review
  16. Brain communications · 2024
    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

9 authors at 5 institutions in 3 countries.

Gucci Jijuan GuDepartment of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, 75185, Uppsala, Sweden.
Harald Lund
Di Wu
Andries Blokzijl
Christina Classon
Gabriel von Euler
Ulf Landegren
Dan Sunnemark
Masood Kamali-Moghaddam
Uppsala University · SEKarolinska Institutet · SEScience for Life Laboratory · SEAstraZeneca (Sweden) · SEStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The microtubule-affinity regulating kinase (MARK) family consists of four highly conserved members that have been implicated in phosphorylation of tau protein, causing formation of neurofibrillary tangles in Alzheimer's disease (AD). Understanding of roles by individual MARK isoform in phosphorylating tau has been limited due to lack of antibodies selective for each MARK isoform. In this study, we first applied the proximity ligation assay on cells to select antibodies specific for each MARK isoform. In cells, a CagA peptide specifically and significantly inhibited tau phosphorylation at Ser²⁶² mediated by MARK4 but not other MARK isoforms. We then used these antibodies to study expression levels of MARK isoforms and interactions between tau and individual MARK isoforms in postmortem human brains. We found a strong and significant elevation of MARK4 expression and MARK4-tau interactions in AD brains, correlating with the Braak stages of the disease. These results suggest the MARK4-tau interactions are of functional importance in the progression of AD and the results also identify MARK4 as a promising target for AD therapy.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAnimalsAntibody SpecificityAntigens, BacterialBacterial ProteinsBrainDisease ProgressionFemaleGene Expression Regulation, EnzymologicHumansImmunoenzyme TechniquesMaleMiceNerve Tissue ProteinsAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriMAPT protein, humanMARK4 protein, humanNerve Tissue ProteinsPeptide FragmentsPhosphoserineProtein IsoformsProtein Serine-Threonine KinasesRecombinant Fusion Proteinstau Proteins

Identifiers

PMID23666762
OpenAlexW2062774938

What OpenQuestion holds

Textmetadata
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.