Evidence map›Paper›PMID 12509140›Full record

ReviewTransgenic research2002

Gene silencing-based disease resistance.

Michael Wassenegger

Abstract readReview
PubMed Publisher
In one paragraph

Review in Transgenic research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

8 citing papers in PubMed, 21 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Michael WasseneggerFraunhofer-Institute for Molecular Biology and Applied Ecology, Am Klopferspitz 18A, 82152 Martinsried, Germany. wassenegger@ime.fraunhofer.de
Fraunhofer Institute for Molecular Biology and Applied Ecology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The definition of a disease is fundamentally difficult, even if one considers only genetically based diseases. In its broadest sense, disease can be defined as any deviation from the norm that results in a physiological disadvantage. Natural selection ensures that the norm for any given species is constantly changing. In addition, some disadvantages are latent and might only manifest under certain environmental conditions. Conversely, an apparent disadvantage can carry a benefit, for example, the disease sickle-cell anemia that is an advantage in malarial areas. Because of the difficulties in giving disease a precise definition, in this review, gene silencing-based disease resistance will be restricted to the description of gene inactivation processes that contribute to maintain the physical fitness of an organism. In this sense, we are concerned with the elimination of invasive nucleic acid expressing. In numerous organisms, a variety of severe diseases are caused by the attack of invasive nucleic acids such as viruses and retroviral or transposable elements. Organisms have developed diverse mechanisms to defend themselves against such attack that include immune responses and apoptosis. Fungi, plants, invertebrates and vertebrates also enlist gene silencing systems to counteract the harmful effects of invasive nucleic acids. In particular, plants that lack interferon and immune responses have established efficient transcriptional and post-transcriptional gene silencing systems. In this review, we describe how plants defend against invasive nucleic acids and focus on the continual evolutionary battle between plants and viruses. In addition, the importance of controlling transposon activity is outlined. Finally, gene silencing-related mechanisms of genomic imprinting and X-chromosome inactivation are discussed in the context of disease resistance.

Indexed as

Gene SilencingAnimalsDosage Compensation, GeneticHumansImmunity, InnatePlantsRNA Interference

Identifiers

PMID12509140
OpenAlexW1524681758

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.