Evidence map›Paper›PMID 8570647›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1996

An immunoglobulin mutator that targets G.C base pairs.

J Bachl, M Wabl

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Article
  2. Review
  3. The rate of mutation of a single gene.Nucleic acids research · 2010
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Genome-wide somatic hypermutation.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  9. Article
  10. Somatic hypermutation in human B cell subsets.Springer seminars in immunopathology · 2001
    Review
  11. Expression of error-prone polymerases in BL2 cells activated for Ig somatic hypermutation.Proceedings of the National Academy of Sciences of the United States of America · 2001
    Article
  12. In vivo and in vitro studies of immunoglobulin gene somatic hypermutation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2001
    Review
  13. Article
  14. Article
  15. Article
  16. An experimental solution for the Luria-Delbrück fluctuation problem in measuring hypermutation rates.Proceedings of the National Academy of Sciences of the United States of America · 1999
    Article
  17. Article
  18. A role for RAD51 in the generation of immunoglobulin gene diversity in rabbits.Journal of immunology (Baltimore, Md. : 1950) · 1999
    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

2 authors.

J BachlDepartment of Microbiology and Immunology, University of California, San Francisco 94143-0670, USA.
M Wabl

Funding

GENETIC VARIATION IN B-LYMPHOCYTE ONTOGENYR01GM037699 · NIGMS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI WABL, MATTHIAS R · 1987 to 2000
$284k
NIGMS NIH HHS 1R01 GM37699
6 · The paper itself

Abstract

Hypermutation can be defined as an enhancement of the spontaneous mutation rate which the organism uses in certain types of differentiated cells where a high mutation rate is advantageous. At the immunoglobulin loci this process increases the mutation rate > 10(5)-fold over the normal, spontaneous rate. Its proximate cause is called the immunoglobulin mutator system. The most important function of this system is to improve antibody affinity in an ongoing response; it is turned on and off during the differentiation of B lymphocytes. We have established an in vitro system to study hypermutation by transfecting a rearranged mu gene into a cell line in which an immunoglobulin mutator has been demonstrated. A construct containing the mu gene and the 3' kappa enhancer has all the cis-acting elements necessary for hypermutation of the endogenous gene segments encoding the variable region. The activity of the mutator does not seem to depend strongly on the position of the transfected gene in the genome. The mutator is not active in transformed cells of a later differentiation stage. It is also not active on a transfected lacZ gene. These results are consistent with the specificity of the mutator system being maintained and make it possible to delineate cis and trans mutator elements in vitro. Surprisingly, the mutator preferentially targets G-C base pairs. Two hypotheses are discussed: (i) the immunoglobulin mutator system in mammals consists of several mutators, of which the mutator described here is only one; or (ii) the primary specificity of the system is biased toward mutation of G-C base pairs, but this specificity is obscured by antigenic selection.

Indexed as

Genes, ImmunoglobulinMutagenesisAnimalsAntibodiesAntibody AffinityBase SequenceCell LineCloning, MolecularEnhancer Elements, GeneticHumansImmunoglobulin kappa-ChainsImmunoglobulin mu-ChainsMiceMolecular Sequence DataPoint MutationSequence Analysis, DNAAntibodiesImmunoglobulin kappa-ChainsImmunoglobulin mu-Chains

Identifiers

PMID8570647
PMCPMC40146

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.