Evidence map›Paper›PMID 11205332›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2001

The reverse transcriptase model of somatic hypermutation.

E J Steele, R V Blanden

Abstract readReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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.

E J SteeleDepartment of Biological Sciences, University of Wollongong, NSW, Australia. ted_steele@uow.edu.au
R V Blanden

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The evidence supporting the reverse transcriptase model of somatic hypermutation is critically reviewed. The model provides a coherent explanation for many apparently unrelated findings. We also show that the somatic hypermutation pattern in the human BCL-6 gene can be interpreted in terms of the reverse transcriptase model and the notion of feedback of somatically mutated sequences to the germline over evolutionary time.

Indexed as

MutationAnimalsDNA-Binding ProteinsHumansImmunoglobulin Variable RegionModels, GeneticProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-6Recombination, GeneticRNA-Directed DNA PolymeraseTranscription FactorsDNA-Binding ProteinsImmunoglobulin Variable RegionProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-6RNA-Directed DNA PolymeraseTranscription Factors

Identifiers

PMID11205332
PMCPMC1087692

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.