Evidence map›Paper›PMID 27402545›Full record

ReviewEMBO reports2016

CTRL+INSERT: retrotransposons and their contribution to regulation and innovation of the transcriptome.

Jonathan Göke, Huck Hui Ng

Abstract readReview
In one paragraph

Review in EMBO reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

48 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Impact of the 294 bp SINE Insertion in 5'UTR of theAnimals : an open access journal from MDPI · 2025
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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

2 authors.

Jonathan GökeComputational and Systems Biology, Genome Institute of Singapore, Singapore gokej@gis.a-star.edu.sg.ORCID 0000-0002-0825-4991
Huck Hui NgGene Regulation Laboratory, Genome Institute of Singapore, Singapore Department of Biochemistry, National University of Singapore, Singapore Department of Biological Sciences, National University of Singapore, Singapore School of Biological Sciences, Nanyang Technological University, Singapore.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human genome contains millions of fragments from retrotransposons-highly repetitive DNA sequences that were once able to "copy and paste" themselves to other regions in the genome. However, the majority of retrotransposons have lost this capacity through acquisition of mutations or through endogenous silencing mechanisms. Without this imminent threat of transposition, retrotransposons have the potential to act as a major source of genomic innovation. Indeed, large numbers of retrotransposons have been found to be active in specific contexts: as gene regulatory elements and promoters for protein-coding genes or long noncoding RNAs, among others. In this review, we summarise recent findings about retrotransposons, with implications in gene expression regulation, the expansion of gene isoform diversity and the generation of long noncoding RNAs. We highlight key examples that demonstrate their role in cellular identity and their versatility as markers of cell states, and we discuss how their dysregulation may contribute to the formation of and possibly therapeutic response in human cancers.

Indexed as

Gene Expression RegulationRetroelementsTranscriptomeAlternative SplicingAnimalsEndogenous RetrovirusesGenetic MarkersGenome, HumanGenomic InstabilityHumansLong Interspersed Nucleotide ElementsNeoplasmsOncogenesOrgan SpecificityRegulatory Sequences, Nucleic AcidRNA, Long NoncodingGenetic MarkersRetroelementsRNA, Long Noncodingendogenous retroviruslncRNAregulationretrotransposontranscription

Identifiers

PMID27402545
PMCPMC4967949

What OpenQuestion holds

Textmetadata
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.