Evidence map›Paper›PMID 27687130›Full record

ArticleScientific reports2016

Differential roles of NF-Y transcription factor in ER chaperone expression and neuronal maintenance in the CNS.

Tomoyuki Yamanaka, Asako Tosaki, Haruko Miyazaki, Masaru Kurosawa, Masato Koike, Yasuo Uchiyama, Sankar N Maity, Hidemi Misawa, Ryosuke Takahashi, Tomomi Shimogori and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Journal of medicinal chemistry · 2026
    Article
  2. The role(s) of NF-Y in development and differentiation.Cell death and differentiation · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. NF-Y (CBF) regulation in specific cell types and mouse models.Biochimica et biophysica acta. Gene regulatory mechanisms · 2017
    Review
  9. 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 6 institutions in 2 countries.

Tomoyuki YamanakaLaboratory of Structural Neuropathology, Doshisha University Graduate School of Brain Science, Kyoto 610-0394, Japan.
Asako TosakiLaboratory for Structural Neuropathology, RIKEN Brain Science Institute, Saitama 351-0198, Japan.
Haruko MiyazakiLaboratory of Structural Neuropathology, Doshisha University Graduate School of Brain Science, Kyoto 610-0394, Japan.
Masaru KurosawaLaboratory for Structural Neuropathology, RIKEN Brain Science Institute, Saitama 351-0198, Japan.
Masato KoikeDepartment of Cell Biology and Neuroscience, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Yasuo UchiyamaDepartments of Cellular and Molecular Neuropathology, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Sankar N MaityDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Hidemi MisawaDivision of Pharmacology, Faculty of Pharmacy, Keio University, Tokyo 105-8512, Japan.
Ryosuke TakahashiDepartment of Neurology, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan.
Tomomi ShimogoriLaboratory for Molecular Mechanisms of Thalamus Development, RIKEN Brain Science Institute, Saitama 351-0198, Japan.
Nobutaka HattoriDepartment of Neurology, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Nobuyuki NukinaLaboratory of Structural Neuropathology, Doshisha University Graduate School of Brain Science, Kyoto 610-0394, Japan.
Juntendo University · JPRIKEN Center for Brain Science · JPDoshisha University · JPKeio University · JPKyoto University · JPThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mammalian central nervous system (CNS) contains various types of neurons with different neuronal functions. In contrast to established roles of cell type-specific transcription factors on neuronal specification and maintenance, whether ubiquitous transcription factors have conserved or differential neuronal function remains uncertain. Here, we revealed that inactivation of a ubiquitous factor NF-Y in different sets of neurons resulted in cell type-specific neuropathologies and gene downregulation in mouse CNS. In striatal and cerebellar neurons, NF-Y inactivation led to ubiquitin/p62 pathologies with downregulation of an endoplasmic reticulum (ER) chaperone Grp94, as we previously observed by NF-Y deletion in cortical neurons. In contrast, NF-Y inactivation in motor neurons induced neuronal loss without obvious protein deposition. Detailed analysis clarified downregulation of another ER chaperone Grp78 in addition to Grp94 in motor neurons, and knockdown of both ER chaperones in motor neurons recapitulated the pathology observed after NF-Y inactivation. Finally, additional downregulation of Grp78 in striatal neurons suppressed ubiquitin accumulation induced by NF-Y inactivation, implying that selective ER chaperone downregulation mediates different neuropathologies. Our data suggest distinct roles of NF-Y in protein homeostasis and neuronal maintenance in the CNS by differential regulation of ER chaperone expression.

Identifiers

PMID27687130
PMCPMC5043352
OpenAlexW2524797119

What OpenQuestion holds

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LicenceCC BY
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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.