Evidence map›Paper›PMID 28646348›Full record

ArticleNeuroscience bulletin2018

Tau-Induced Ca

Yu-Ping Wei, Jin-Wang Ye, Xiong Wang, Li-Ping Zhu, Qing-Hua Hu, Qun Wang, Dan Ke, Qing Tian, Jian-Zhi Wang

Abstract read
In one paragraph

Article in Neuroscience bulletin, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 28 citations in OpenAlex.

  1. Dual Targeting of Tau Kinases and Autophagy by Abemaciclib Independent of CDK4/6 Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Review
  3. Article
  4. Review
  5. CaMK modulates sensory neural activity to control longevity and proteostasis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. The interaction between dysfunction of vasculature and tauopathy in Alzheimer's disease and related dementias.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Nuclear face of Tau: an inside player in neurodegeneration.Acta neuropathologica communications · 2023
    Review
  11. TRPV1 Modulator Ameliorates Alzheimer-Like Amyloid-Oxidative medicine and cellular longevity · 2022
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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 1 institution in 1 country.

Yu-Ping WeiPathophysiology Department, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Jin-Wang YePathophysiology Department, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Xiong WangPathophysiology Department, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Li-Ping ZhuPathophysiology Department, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Qing-Hua HuPathophysiology Department, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Qun WangPathophysiology Department, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Dan KePathophysiology Department, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Qing TianPathophysiology Department, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. tianq@mail.hust.edu.cn.
Jian-Zhi WangPathophysiology Department, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. wangjz@mail.hust.edu.cn.
Huazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperphosphorylated tau is the major protein component of neurofibrillary tangles in the brains of patients with Alzheimer's disease (AD). However, the mechanism underlying tau hyperphosphorylation is not fully understood. Here, we demonstrated that exogenously expressed wild-type human tau40 was detectable in the phosphorylated form at multiple AD-associated sites in cytoplasmic and nuclear fractions from HEK293 cells. Among these sites, tau phosphorylated at Thr205 and Ser214 was almost exclusively found in the nuclear fraction at the conditions used in the present study. With the intracellular tau accumulation, the Ca

Indexed as

Alzheimer DiseaseCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 4Cell NucleusEnzyme ActivationHEK293 CellsHumansNeuronsPhosphorylationSignal Transductiontau ProteinsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 4CAMK4 protein, humantau ProteinsAlzheimer’s diseaseCaMKIVNuclear calcium signalPhosphorylationTau

Identifiers

PMID28646348
PMCPMC5856708
OpenAlexW2670177371

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.