Evidence map›Paper›PMID 25201987›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Neuronal necrosis is regulated by a conserved chromatin-modifying cascade.

Kai Liu, Lianggong Ding, Yuhong Li, Hui Yang, Chunyue Zhao, Ye Lei, Shuting Han, Wei Tao, Dengshun Miao, Hermann Steller and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. 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
4.2field-weighted citation impact, top 6% 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, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Advancement of epigenetics in stroke.Frontiers in neuroscience · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. CaM kinase II regulates cardiac hemoglobin expression through histone phosphorylation upon sympathetic activation.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

12 authors at 4 institutions in 2 countries.

Kai LiuThe State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Life Sciences, Peking University, Beijing 100871, China;
Lianggong DingThe State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Life Sciences, Peking University, Beijing 100871, China;
Yuhong LiThe State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Life Sciences, Peking University, Beijing 100871, China; Howard Hughes Medical Institute, Department of Internal Medicine, University of Iowa, Iowa City, IA 52242;
Hui YangThe State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Life Sciences, Peking University, Beijing 100871, China;
Chunyue ZhaoThe State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Life Sciences, Peking University, Beijing 100871, China;
Ye LeiThe State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Life Sciences, Peking University, Beijing 100871, China;
Shuting HanThe State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Life Sciences, Peking University, Beijing 100871, China;
Wei TaoThe Education Ministry Key Laboratory of Cell Proliferation and Differentiation, School of Life Sciences, Peking University, Beijing 100871, China;
Dengshun MiaoState Key Laboratory of Reproductive Medicine, Research Center for Bone and Stem Cells, Department of Anatomy, Nanjing Medical University, Nanjing, Jiangsu 210029 China;
Hermann StellerHoward Hughes Medical Institute, Strang Laboratory of Apoptosis and Cancer Biology, The Rockefeller University, New York, NY 10065; and.
Michael J WelshHoward Hughes Medical Institute, Department of Internal Medicine, University of Iowa, Iowa City, IA 52242; michael-welsh@uiowa.edu leiliu@pku.edu.cn.
Lei LiuThe State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Life Sciences, Peking University, Beijing 100871, China; Beijing Institute for Brain Disorders, Department of Neurobiology, Capital Medical University, Youanmen, Beijing 100069, China michael-welsh@uiowa.edu leiliu@pku.edu.cn.
Peking University · CNHoward Hughes Medical Institute · USNanjing Medical University · CNRockefeller University · US

Funding

Pulmonary Toxicology Facility CoreP30ES005605 · NIEHS · UNIVERSITY OF IOWA · PI Brandi Janssen · 1990 to 2026
$40.5M
Proteasome Regulation and Function in Cellular RemodelingR01GM060124 · NIGMS · ROCKEFELLER UNIVERSITY · PI STELLER, HERMANN · 1999 to 2018
$5.4M
Howard Hughes Medical InstituteNIEHS NIH HHS P30 ES005605NIGMS NIH HHS R01 GM060124
6 · The paper itself

Abstract

Neuronal necrosis induced by calcium overload causes devastating brain dysfunction in diseases such as stroke and brain trauma. It has been considered a stochastic event lacking genetic regulation, and pharmacological means to suppress neuronal necrosis are lacking. Using a Drosophila model of calcium overloading, we found JIL-1/mitogen- and stress-activated protein kinase 1/2 is a regulator of neuronal necrosis through phosphorylation of histone H3 serine 28 (H3S28ph). Further, we identified its downstream events including displacement of polycomb repressive complex 1 (PRC1) and activation of Trithorax (Trx). To test the role of JIL-1/PRC1/Trx cascade in mammals, we studied the necrosis induced by glutamate in rat cortical neuron cultures and rodent models of brain ischemia and found the cascade is activated in these conditions and inhibition of the cascade suppresses necrosis in vitro and in vivo. Together, our research demonstrates that neuronal necrosis is regulated by a chromatin-modifying cascade, and this discovery may provide potential therapeutic targets and biomarkers for neuronal necrosis.

Indexed as

AnimalsBiomarkersCalciumChromatinChromosomal Proteins, Non-HistoneDrosophila melanogasterDrosophila ProteinsFemaleHistonesMaleMAP Kinase Signaling SystemMiceMitogen-Activated Protein Kinase 3NecrosisNeuronsPolycomb-Group ProteinsBiomarkersCalciumChromatinChromosomal Proteins, Non-HistoneDrosophila ProteinsHistonesJIL-1 protein, DrosophilaMitogen-Activated Protein Kinase 3Polycomb-Group ProteinsProtein Serine-Threonine Kinasestrx protein, DrosophilaagingepigeneticsH3K4me3histone modificationneurodegeneration

Identifiers

PMID25201987
PMCPMC4183342
OpenAlexW2014133516

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.