Evidence map›Paper›PMID 28978483›Full record

ArticleCell reports2017

Loss of Kdm5c Causes Spurious Transcription and Prevents the Fine-Tuning of Activity-Regulated Enhancers in Neurons.

Marilyn Scandaglia, Jose P Lopez-Atalaya, Alejandro Medrano-Fernandez, Maria T Lopez-Cascales, Beatriz Del Blanco, Michal Lipinski, Eva Benito, Roman Olivares, Shigeki Iwase, Yang Shi and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

84 citing papers in PubMed, 136 citations in OpenAlex.

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  4. Impact of sex chromosomes and gonad type in stress susceptibility in corticostriatal brain regions.Proceedings of the National Academy of Sciences of the United States of America · 2026
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24 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

Marilyn ScandagliaInstituto de Neurociencias (Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas), Molecular Neurobiology and Neuropathology Unit, Av. Santiago Ramón y Cajal s/n, Sant Joan d'Alacant, 03550 Alicante, Spain.
Jose P Lopez-AtalayaInstituto de Neurociencias (Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas), Molecular Neurobiology and Neuropathology Unit, Av. Santiago Ramón y Cajal s/n, Sant Joan d'Alacant, 03550 Alicante, Spain.
Alejandro Medrano-FernandezInstituto de Neurociencias (Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas), Molecular Neurobiology and Neuropathology Unit, Av. Santiago Ramón y Cajal s/n, Sant Joan d'Alacant, 03550 Alicante, Spain.
Maria T Lopez-CascalesInstituto de Neurociencias (Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas), Molecular Neurobiology and Neuropathology Unit, Av. Santiago Ramón y Cajal s/n, Sant Joan d'Alacant, 03550 Alicante, Spain.
Beatriz Del BlancoInstituto de Neurociencias (Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas), Molecular Neurobiology and Neuropathology Unit, Av. Santiago Ramón y Cajal s/n, Sant Joan d'Alacant, 03550 Alicante, Spain.
Michal LipinskiInstituto de Neurociencias (Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas), Molecular Neurobiology and Neuropathology Unit, Av. Santiago Ramón y Cajal s/n, Sant Joan d'Alacant, 03550 Alicante, Spain.
Eva BenitoInstituto de Neurociencias (Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas), Molecular Neurobiology and Neuropathology Unit, Av. Santiago Ramón y Cajal s/n, Sant Joan d'Alacant, 03550 Alicante, Spain.
Roman OlivaresInstituto de Neurociencias (Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas), Molecular Neurobiology and Neuropathology Unit, Av. Santiago Ramón y Cajal s/n, Sant Joan d'Alacant, 03550 Alicante, Spain.
Shigeki IwaseDepartment of Human Genetics, University of Michigan, 5815 Medical Science II, Ann Arbor, MI 48109, USA.
Yang ShiDivision of Newborn Medicine, Boston Children's Hospital, Boston, MA 02115, USA; Department of Cell Biology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.
Angel BarcoInstituto de Neurociencias (Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas), Molecular Neurobiology and Neuropathology Unit, Av. Santiago Ramón y Cajal s/n, Sant Joan d'Alacant, 03550 Alicante, Spain. Electronic address: abarco@umh.es.
Instituto de Neurociencias · ESConsejo Superior de Investigaciones Científicas · ESHarvard University · USUniversity of Michigan–Ann Arbor · US

Funding

Novel epigenetic mechanisms in neuronal development and cognitive functionR01MH096066 · NIMH · BOSTON CHILDREN'S HOSPITAL · PI ARLOTTA, PAOLA, POMEROY, SCOTT LOREN · 2012 to 2022
$6.1M
Neutralizing epigenomes in neurodevelopment disordersR01NS089896 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI IWASE, SHIGEKI · 2015 to 2019
$2.1M
NIMH NIH HHS R01 MH096066NINDS NIH HHS R01 NS089896
6 · The paper itself

Abstract

During development, chromatin-modifying enzymes regulate both the timely establishment of cell-type-specific gene programs and the coordinated repression of alternative cell fates. To dissect the role of one such enzyme, the intellectual-disability-linked lysine demethylase 5C (Kdm5c), in the developing and adult brain, we conducted parallel behavioral, transcriptomic, and epigenomic studies in Kdm5c-null and forebrain-restricted inducible knockout mice. Together, genomic analyses and functional assays demonstrate that Kdm5c plays a critical role as a repressor responsible for the developmental silencing of germline genes during cellular differentiation and in fine-tuning activity-regulated enhancers during neuronal maturation. Although the importance of these functions declines after birth, Kdm5c retains an important genome surveillance role preventing the incorrect activation of non-neuronal and cryptic promoters in adult neurons.

Indexed as

Gene Expression Regulation, DevelopmentalTranscription, GeneticAnimalsDNA-Binding ProteinsDoublecortin Domain ProteinsEnhancer Elements, GeneticFemaleGlial Fibrillary Acidic ProteinHistone DemethylasesHistonesMaleMaze LearningMiceMice, KnockoutMicrotubule-Associated ProteinsNerve Tissue ProteinsDNA-Binding ProteinsDoublecortin Domain ProteinsGlial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouseHistone DemethylasesHistonesKdm5c protein, mouseMicrotubule-Associated ProteinsMtap2 protein, mouseNerve Tissue ProteinsNeuN protein, mouseNeuropeptidesNuclear ProteinsOxidoreductases, N-DemethylatingClaes-Jensen syndromeDNA methylationenhancerepigenetic repressiongermline gene silencinghistone methylationimmediate early geneintellectual disabilitylysine demethylase 5Cspurious transcription

Identifiers

PMID28978483
PMCPMC5679733
OpenAlexW2764116674

What OpenQuestion holds

Textmetadata
LicenceTDM
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.