Evidence map›Paper›PMID 10330146›Full record

ArticleMolecular and cellular biology1999

Regulation of AUF1 expression via conserved alternatively spliced elements in the 3' untranslated region.

G M Wilson, Y Sun, J Sellers, H Lu, N Penkar, G Dillard, G Brewer

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Coupling of alternative splicing and alternative polyadenylation.Acta biochimica et biophysica Sinica · 2024
    Review
  3. Review
  4. Article
  5. Article
  6. RNA Degradation in Neurodegenerative Disease.Advances in neurobiology · 2018
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Expression of two novel alternatively spliced COL2A1 isoforms during chondrocyte differentiation.Matrix biology : journal of the International Society for Matrix Biology · 2008
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

7 authors at 1 institution in 1 country.

G M WilsonDepartment of Microbiology and Immunology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA.
Y Sun
J Sellers
H Lu
N Penkar
G Dillard
G Brewer
Wake Forest University · US

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
POST TRANSCRIPTIONAL REGULATION--ONCOGENE MESSENGER RNAR01CA052443 · NCI · WAKE FOREST UNIVERSITY · PI BREWER, GARY A. · 1990 to 2012
$4.3M
NCI NIH HHS CA 52443NCI NIH HHS P30 CA012197NCI NIH HHS P30 CA 12197NCI NIH HHS R01 CA052443
6 · The paper itself

Abstract

The A+U-rich RNA-binding factor AUF1 exhibits characteristics of a trans-acting factor contributing to the rapid turnover of many cellular mRNAs. Structural mapping of the AUF1 gene and its transcribed mRNA has revealed alternative splicing events within the 3' untranslated region (3'-UTR). In K562 erythroleukemia cells, we have identified four alternatively spliced AUF1 3'-UTR variants, including a population of AUF1 mRNA containing a highly conserved 107-nucleotide (nt) 3'-UTR exon (exon 9) and the adjacent downstream intron (intron 9). Functional analyses using luciferase-AUF1 3'-UTR chimeric transcripts demonstrated that the presence of either a spliceable or an unspliceable intron 9 in the 3'-UTR repressed luciferase expression in cis, indicating that intron 9 sequences may down-regulate gene expression by two distinct mechanisms. In the case of the unspliceable intron, repression of luciferase expression likely involved two AUF1-binding sequences, since luciferase expression was increased by deletion of these sites. However, inclusion of the spliceable intron in the luciferase 3'-UTR down-regulated expression independent of the AUF1-binding sequences. This is likely due to nonsense-mediated mRNA decay (NMD) owing to the generation of exon-exon junctions more than 50 nt downstream of the luciferase termination codon. AUF1 mRNA splice variants generated by selective excision of intron 9 are thus also likely to be subject to NMD since intron 9 is always positioned >137 nt downstream of the stop codon. The distribution of alternatively spliced AUF1 transcripts in K562 cells is consistent with this model of regulated AUF1 expression.

Indexed as

Alternative SplicingGene Expression RegulationHeterogeneous-Nuclear Ribonucleoprotein DUntranslated RegionsBase SequenceBlotting, SouthernDNA PrimersElectrophoresis, Polyacrylamide GelExonsHeLa CellsHeterogeneous Nuclear Ribonucleoprotein D0HumansIntronsK562 CellsLuciferasesModels, GeneticDNA PrimersHeterogeneous-Nuclear Ribonucleoprotein DHeterogeneous Nuclear Ribonucleoprotein D0HNRNPD protein, humanLuciferasesRNA-Binding ProteinsUntranslated Regions

Identifiers

PMID10330146
PMCPMC104365
OpenAlexW2120250962

What OpenQuestion holds

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Read underepoch 390

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.