Evidence map›Paper›PMID 16394130›Full record

ReviewAnnals of the New York Academy of Sciences2005

Development of resistance to RNAi in mammalian cells.

Zhi-Ming Zheng, Shuang Tang, Mingfang Tao

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

23 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Glycine is a competitive antagonist of the TNF receptor mediating the expression of inflammatory cytokines in 3T3-L1 adipocytes.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Article
  6. Ready for Repair? Gene Editing Enters the Clinic for the Treatment of Human Disease.Molecular therapy. Methods & clinical development · 2020
    Review
  7. Review
  8. Double-stranded RNA binding protein, Staufen, is required for the initiation of RNAi in coleopteran insects.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. The impact of unprotected T cells in RNAi-based gene therapy for HIV-AIDS.Molecular therapy : the journal of the American Society of Gene Therapy · 2014
    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

3 authors at 2 institutions in 1 country.

Zhi-Ming ZhengHIV and AIDS Malignancy Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 10 Center Drive, Room 10S 255, Bethesda, MD 20892, USA. zhengt@exchange.nih.gov
Shuang Tang
Mingfang Tao
National Cancer Institute · USNational Institutes of Health · US

Funding

Gene Expression and Post-Transcriptional Regulation of DNA Tumor VirusesZIASC010357 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI ZHENG, ZHI-MING · 2009 to 2025
$24.3M
Viral RNA Splicing and TumorigenesisZ01SC010357 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI ZHENG, ZHI-MING · 2000 to 2008
$1.9M
NCI NIH HHS Z01 SC010357-06
6 · The paper itself

Abstract

The discovery of RNA interference (RNAi) in C. elegans and in plants has revolutionized current approaches to biology and medicine. RNAi silences genes in a sequence-specific manner through the actions of small pieces of double-stranded RNAs (siRNAs and miRNAs). RNAi has been found as a widespread natural phenomenon in eukaryotic cells and is also being used as a powerful experimental tool to explore gene function. Most importantly, it has many potential therapeutic applications. Viral gene-specific siRNAs are theoretically very promising antiviral inhibitors and have been examined in a broad range of medically important viruses. However, many RNA viruses escape RNAi-mediated suppression by counteracting the RNAi machinery through mutation of the targeted region, by encoding viral suppressors, or both. DNA viruses also counteract the RNAi machinery, preferentially using viral suppressors. Cellular factors may also contribute to RNAi resistance; ADAR1 was the first cellular factor found to be responsible for editing-mediated RNAi resistance. Because siRNAs can be used as potent small-molecule inhibitors of any cellular gene, the best way for a cell to maintain expression of essential genes for its long-term survival is to develop a program to resist the detrimental effects of RNAi.

Indexed as

Gene Expression RegulationGenetic TechniquesRNA InterferenceAnimalsCaenorhabditis elegansGene SilencingGenetic VectorsHumansMicroRNAsModels, GeneticRNA, Small InterferingRNA, ViralMicroRNAsRNA, Small InterferingRNA, Viral

Identifiers

PMID16394130
PMCPMC1462965
OpenAlexW2017034172

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.