Evidence map›Paper›PMID 31704914›Full record

ArticleNature communications2019

Regulation of CHD2 expression by the Chaserr long noncoding RNA gene is essential for viability.

Aviv Rom, Liliya Melamed, Noa Gil, Micah Jonathan Goldrich, Rotem Kadir, Matan Golan, Inbal Biton, Rotem Ben-Tov Perry, Igor Ulitsky

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 2 pooled it
4.4field-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

73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 132 citations in OpenAlex.

  1. The Footprint ofCurrent Alzheimer research · 2025
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  14. Antisense oligonucleotide therapies for monogenic disorders.Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V · 2025
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13 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

9 authors at 2 institutions in 1 country.

Aviv RomDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Liliya MelamedDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Noa GilDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Micah Jonathan GoldrichDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Rotem KadirNational Institute for Biotechnology in the Negev and Department of Microbiology, Immunology and Genetics, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Matan GolanDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Inbal BitonDepartment of Veterinary Resources, Weizmann Institute of Science, Rehovot, Israel.
Rotem Ben-Tov PerryDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Igor UlitskyDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel. igor.ulitsky@weizmann.ac.il.ORCID http://orcid.org/0000-0003-0555-6561
Weizmann Institute of Science · ILBen-Gurion University of the Negev · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromodomain helicase DNA binding protein 2 (Chd2) is a chromatin remodeller implicated in neurological disease. Here we show that Chaserr, a highly conserved long noncoding RNA transcribed from a region near the transcription start site of Chd2 and on the same strand, acts in concert with the CHD2 protein to maintain proper Chd2 expression levels. Loss of Chaserr in mice leads to early postnatal lethality in homozygous mice, and severe growth retardation in heterozygotes. Mechanistically, loss of Chaserr leads to substantially increased Chd2 mRNA and protein levels, which in turn lead to transcriptional interference by inhibiting promoters found downstream of highly expressed genes. We further show that Chaserr production represses Chd2 expression solely in cis, and that the phenotypic consequences of Chaserr loss are rescued when Chd2 is perturbed as well. Targeting Chaserr is thus a potential strategy for increasing CHD2 levels in haploinsufficient individuals.

Indexed as

AnimalsChromatin Assembly and DisassemblyDNA-Binding ProteinsGene Expression RegulationGenes, LethalGrowth DisordersHaploinsufficiencyHeterozygoteHomozygoteMiceMice, KnockoutPromoter Regions, GeneticRNA, Long NoncodingRNA, MessengerChd2 protein, mouseDNA-Binding ProteinsRNA, Long NoncodingRNA, Messenger

Identifiers

PMID31704914
PMCPMC6841665
OpenAlexW2984476817

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.