Evidence map›Paper›PMID 10200312›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Human RNA-specific adenosine deaminase ADAR1 transcripts possess alternative exon 1 structures that initiate from different promoters, one constitutively active and the other interferon inducible.

C X George, C E Samuel

Abstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 201 papers.

0numbers the graph read from it
0cells of the map it votes in
201citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

201 citing papers in PubMed, 352 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Two codes of RNA editing by deamination in human diseases.Experimental & molecular medicine · 2026
    Review
  10. HeterozygousiScience · 2026
    Article
  11. Article
  12. Review
  13. Review
  14. Regulatable In Vivo Gene Expression via Adaptamers.bioRxiv : the preprint server for biology · 2025
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

141 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

2 authors at 2 institutions in 2 countries.

C X GeorgeDepartment of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, CA 93106, USA.
C E Samuel
Institut thématique Génétique, génomique et bioinformatique · FRUniversity of California, Santa Barbara · US

Funding

MECHANISM OF INTERFERON ACTIONR01AI012520 · NIAID · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI SAMUEL, CHARLES E · 1985 to 2009
$3.1M
MECHANISM OF INTERFERON ACTIONR37AI012520 · NIAID · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI SAMUEL, CHARLES E. · 1989 to 1998
–
NIAID NIH HHS AI-12520NIAID NIH HHS R01 AI012520NIAID NIH HHS R37 AI012520
6 · The paper itself

Abstract

RNA-specific adenosine deaminase (ADAR1) catalyzes the deamination of adenosine to inosine in viral and cellular RNAs. Two size forms of the ADAR1 editing enzyme are known, an IFN-inducible approximately 150-kDa protein and a constitutively expressed N-terminally truncated approximately 110-kDa protein. We have now identified alternative exon 1 structures of human ADAR1 transcripts that initiate from unique promoters, one constitutively expressed and the other IFN inducible. Cloning and sequence analyses of 5'-rapid amplification of cDNA ends (RACE) cDNAs from human placenta established a linkage between exon 2 of ADAR1 and two alternative exon 1 structures, designated herein as exon 1A and exon 1B. Analysis of RNA isolated from untreated and IFN-treated human amnion cells demonstrated that exon 1B-exon 2 transcripts were synthesized in the absence of IFN and were not significantly altered in amount by IFN treatment. By contrast, exon 1A-exon 2 transcripts were IFN inducible. Transient transfection analysis with reporter constructs led to the identification of two functional promoters, designated PC and PI. Exon 1B transcripts were initiated from the PC promoter whose activity in transient transfection reporter assays was not increased by IFN treatment. The 107-nt exon 1B mapped 14.5 kb upstream of exon 2. The 201-nt exon 1A that mapped 5.4 kb upstream of exon 2 was initiated from the interferon-inducible PI promoter. These results suggest that two promoters, one IFN inducible and the other not, initiate transcription of the ADAR1 gene, and that alternative splicing of unique exon 1 structures to a common exon 2 junction generates RNA transcripts with the deduced coding capacity for either the constitutively expressed approximately 110-kDa ADAR1 protein (exon 1B) or the interferon-induced approximately 150-kDa ADAR1 protein (exon 1A).

Indexed as

Alternative SplicingTranscription, GeneticAdenosine DeaminaseAmnionBase SequenceCells, CulturedChloramphenicol O-AcetyltransferaseEnzyme InductionExonsFemaleGenomic LibraryHumansInterferonsIntronsMolecular Sequence DataPlacentaADARB1 protein, humanAdenosine DeaminaseChloramphenicol O-AcetyltransferaseInterferonsRecombinant Fusion ProteinsRNA-Binding Proteins

Identifiers

PMID10200312
PMCPMC16382
OpenAlexW2163879429

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.