Evidence map›Paper›PMID 15710655›Full record

ArticleThe Journal of experimental medicine2005

Identifying protein-protein interactions in somatic hypermutation.

Myron F Goodman, Matthew D Scharff

Abstract readComment
In one paragraph

Article in The Journal of experimental medicine, 2005. 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. Different mutation signatures in DNA polymerase eta- and MSH6-deficient mice suggest separate roles in antibody diversification.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Myron F GoodmanUniversity of Southern California, Los Angeles, CA 90089, USA. mgoodman@usc.edu
Matthew D Scharff

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Somatic hypermutation (SHM) in immunoglobulin genes is required for high affinity antibody-antigen binding. Cultured cell systems, mouse model systems, and human genetic deficiencies have been the key players in identifying likely SHM pathways, whereas "pure" biochemical approaches have been far less prominent, but change appears imminent. Here we comment on how, when, and why biochemistry is likely to emerge from the shadows and into the spotlight to elucidate how the somatic mutation of antibody variable (V) regions is generated.

Indexed as

Somatic Hypermutation, ImmunoglobulinAnimalsDNA-Binding ProteinsDNA-Directed DNA PolymeraseHumansMutS Homolog 2 ProteinProtein BindingProto-Oncogene ProteinsDNA-Binding ProteinsDNA-Directed DNA PolymeraseG-T mismatch-binding proteinMSH2 protein, humanMutS Homolog 2 ProteinProto-Oncogene Proteins

Identifiers

PMID15710655
PMCPMC2213056

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.