Evidence map›Paper›PMID 28274274›Full record

ArticleActa neuropathologica communications2017

A novel form of necrosis, TRIAD, occurs in human Huntington's disease.

Emiko Yamanishi, Kazuko Hasegawa, Kyota Fujita, Shizuko Ichinose, Saburo Yagishita, Miho Murata, Kazuhiko Tagawa, Takumi Akashi, Yoshinobu Eishi, Hitoshi Okazawa

Open access · goldAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta neuropathologica communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.3field-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

24 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
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  11. Oncogenic Pathways in Neurodegenerative Diseases.International journal of molecular sciences · 2022
    Review
  12. Review
  13. Article
  14. Non-Cell Autonomous and Epigenetic Mechanisms of Huntington's Disease.International journal of molecular sciences · 2021
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Intracellular amyloid hypothesis for ultra-early phase pathology of Alzheimer's disease.Neuropathology : official journal of the Japanese Society of Neuropathology · 2021
    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

10 authors at 3 institutions in 1 country.

Emiko YamanishiDepartment of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Kazuko HasegawaDepartment of Neurology, National Hospital Organization, Sagamihara National Hospital, 18-1, Sakura-dai, Minami-ku, Yokosuka, 252-0392, Japan.
Kyota FujitaDepartment of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Shizuko IchinoseResearch Center for Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Saburo YagishitaDepartment of Neurology, National Hospital Organization, Sagamihara National Hospital, 18-1, Sakura-dai, Minami-ku, Yokosuka, 252-0392, Japan.
Miho MurataDepartment of Neurology, National Center of Neurology and Psychiatry, 4-1-1, Ogawahigashimachi, Kodaira, Tokyo, 187-8551, Japan.
Kazuhiko TagawaDepartment of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Takumi AkashiDepartment of Human Pathology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Yoshinobu EishiDepartment of Human Pathology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Hitoshi OkazawaDepartment of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan. okazawa-tky@umin.ac.jp.
Tokyo Medical and Dental University · JPNational Sagamihara Hospital · JPNational Center of Neurology and Psychiatry · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously reported transcriptional repression-induced atypical cell death of neuron (TRIAD), a new type of necrosis that is mainly regulated by Hippo pathway signaling and distinct from necroptosis regulated by RIP1/3 pathway. Here, we examined the ultrastructural and biochemical features of neuronal cell death in the brains of human HD patients in parallel with the similar analyses using mutant Htt-knock-in (Htt-KI) mice. LATS1 kinase, the critical regulator and marker of TRIAD, is actually activated in cortical neurons of postmortem human HD and of Htt-KI mouse brains, while apoptosis promoter kinase Plk1 was inactivated in human HD brains. Expression levels of YAP/YAPdeltaC were decreased in cortical neurons of human HD brains. Ultra-structural analyses revealed extreme enlargement of endoplasmic reticulum (ER), which characterizes TRIAD, in cortical neurons of human HD and those of Htt-KI mice. These biochemical and morphological results support that TRIAD occurs in human and mouse neurons under the HD pathology.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosisBrainCell Cycle ProteinsEndoplasmic ReticulumGene Knock-In TechniquesHumansHuntington DiseaseMice, 129 StrainMice, Inbred C57BLMice, TransgenicNecrosisNeuronsPhosphoproteinsPolo-Like Kinase 1Adaptor Proteins, Signal TransducingCell Cycle ProteinsLATS1 protein, humanLats1 protein, mousePhosphoproteinsPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsTranscription FactorsYAP1 protein, humanYAP-Signaling ProteinsElectron microscopyHippo pathwayHuntington’s diseaseLATSNecrosisNeurodegenerationTEADTRIADYAP

Identifiers

PMID28274274
PMCPMC5341362
OpenAlexW2592656903

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.