Evidence map›Paper›PMID 27124581›Full record

ArticleCell death & disease2016

The hnRNP-Htt axis regulates necrotic cell death induced by transcriptional repression through impaired RNA splicing.

Y Mao, T Tamura, Y Yuki, D Abe, Y Tamada, S Imoto, H Tanaka, H Homma, K Tagawa, S Miyano and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Intracellular amyloid hypothesis for ultra-early phase pathology of Alzheimer's disease.Neuropathology : official journal of the Japanese Society of Neuropathology · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Evaluation of artificial selection in Standard Poodles using whole-genome sequencing.Mammalian genome : official journal of the International Mammalian Genome Society · 2016
    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

11 authors at 2 institutions in 1 country.

Y MaoDepartment of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.
T TamuraDepartment of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.
Y YukiDepartment of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.
D AbeDepartment of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.
Y TamadaDepartment of Computer Science, Graduate School of Information Science and Technology, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
S ImotoLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
H TanakaDepartment of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.
H HommaDepartment of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.
K TagawaDepartment of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.
S MiyanoLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
H OkazawaDepartment of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.
Tokyo Medical and Dental University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we identify signaling network of necrotic cell death induced by transcriptional repression (TRIAD) by α-amanitin (AMA), the selective RNA polymerase II inhibitor, as a model of neurodegenerative cell death. We performed genetic screen of a knockdown (KD) fly library by measuring the ratio of transformation from pupa to larva (PL ratio) under TRIAD, and selected the cell death-promoting genes. Systems biology analysis of the positive genes mapped on protein-protein interaction databases predicted the signaling network of TRIAD and the core pathway including heterogeneous nuclear ribonucleoproteins (hnRNPs) and huntingtin (Htt). RNA sequencing revealed that AMA impaired transcription and RNA splicing of Htt, which is known as an endoplasmic reticulum (ER)-stabilizing molecule. The impairment in RNA splicing and PL ratio was rescued by overexpresion of hnRNP that had been also affected by transcriptional repression. Fly genetics with suppressor or expresser of Htt and hnRNP worsened or ameliorated the decreased PL ratio by AMA, respectively. Collectively, these results suggested involvement of RNA splicing and a regulatory role of the hnRNP-Htt axis in the process of the transcriptional repression-induced necrosis.

Indexed as

ApoptosisAmanitinsAnimalsbeta-Transducin Repeat-Containing ProteinsCell Cycle ProteinsCells, CulturedDrosophilaDrosophila ProteinsEmbryo, MammalianHeterogeneous-Nuclear Ribonucleoprotein Group A-BHeterogeneous-Nuclear RibonucleoproteinsHuntingtin ProteinLarvaNeuronsPolo-Like Kinase 1Protein Serine-Threonine KinasesAmanitinsbeta-Transducin Repeat-Containing ProteinsCell Cycle ProteinsDrosophila ProteinsHeterogeneous-Nuclear Ribonucleoprotein Group A-BHeterogeneous-Nuclear RibonucleoproteinsHnrnpab protein, ratHtt protein, DrosophilaHuntingtin ProteinPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsRibonucleoproteinsTranscription Factors

Identifiers

PMID27124581
PMCPMC4855646
OpenAlexW2345205020

What OpenQuestion holds

Textmetadata
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.