Evidence map›Paper›PMID 15190191›Full record

ReviewJournal of inherited metabolic disease2004

Retrotransposon-derived elements in the mammalian genome: a potential source of disease.

R Druker, E Whitelaw

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of inherited metabolic disease, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
8.4field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Genetic variation and its role in malignancy.International journal of biomedical science : IJBS · 2011
    Article
  9. Article
  10. Article
  11. Article
  12. Adaptation to diverse nitrogen-limited environments by deletion or extrachromosomal element formation of the GAP1 locus.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. RNA expression microarray analysis in mouse prospermatogonia: identification of candidate epigenetic modifiers.Developmental dynamics : an official publication of the American Association of Anatomists · 2008
    Article
  19. Review
  20. 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

2 authors at 2 institutions in 1 country.

R DrukerSchool of Molecular and Microbial Biosciences, University of Sydney, New South Wales, Australia.
E Whitelaw
University of Sydney · AUUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The plethora of genomic information gathered by the sequencing of the human and mouse genomes has paved the way for a new era of genetics. While in the past we focused mainly on the small percentage of DNA that codes for proteins, we can now concentrate on the remainder, i.e. the noncoding sequences that interrupt and separate genes. This portion of the genome is made up, in most part, of repetitive DNA sequences including DNA transposons, long terminal repeat (LTR) retrotransposons, LINEs (long interspersed nuclear elements) and SINEs (short interspersed nuclear elements). Some of these elements are transcriptionally active and can transpose or retrotranspose around the genome, resulting in insertional mutagenesis that can cause disease. In these cases, insertions have occurred in the coding sequence. However, recent evidence suggests that the main effect of these elements is their ability to influence transcription of neighbouring genes. The elements themselves contain promoters that can initiate transcription of flanking genomic DNA. Furthermore, they are susceptible to epigenetic silencing, which is often stochastic and incomplete, resulting in complex patterns of transcription. This review discusses some diseases in both human and mouse that are caused by these repetitive elements.

Indexed as

Genome, HumanAnimalsGenetic Diseases, InbornHumansMammalsRetroelementsRetroelements

Identifiers

PMID15190191
OpenAlexW2032858746

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.