Evidence map›Paper›PMID 9115357›Full record

ArticleNucleic acids research1997

Rapid methods for the analysis of immunoglobulin gene hypermutation: application to transgenic and gene targeted mice.

C J Jolly, N Klix, M S Neuberger

Open access · greenAbstract read
In one paragraph

Article in Nucleic acids research, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

76 citing papers in PubMed, 129 citations in OpenAlex.

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  5. Promoter Proximity Defines Mutation Window for VJournal of immunology (Baltimore, Md. : 1950) · 2022
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  16. Cutting Edge: ATM Influences Germinal Center Integrity.Journal of immunology (Baltimore, Md. : 1950) · 2019
    Article
  17. Article
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  20. SAMHD1 enhances immunoglobulin hypermutation by promoting transversion mutation.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article

16 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

C J JollyMedical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK. ccj@mrc-lmb.cam.ac.ui
N Klix
M S Neuberger
MRC Laboratory of Molecular Biology · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypermutation of immunoglobulin genes is a key process in antibody diversification. Little is known about the mechanism, but the availability of rapid facile assays for monitoring immunoglobulin hypermutation would greatly aid the development of culture systems for hypermutating B cells as well as the screening for individuals deficient in the process. Here we describe two such assays. The first exploits the non-randomness of hypermutation. The existence of a mutational hotspot in the Ser31 codon of a transgenic immunoglobulin V gene allowed us to use PCR to detect transgene hypermutation and identify cell populations in which this mutation had occurred. For animals that do not carry immunoglobulin transgenes, we exploited the fact that hypermutation extends into the region flanking the 3'-side of the rearranged J segments. We show that PCR amplification of the 3'-flank of VDJH rearrangements that involve members of the abundantly-used VHJ558 family provides a large database of mutations where the germline counterpart is unequivocally known. This assay was particularly useful for analysing endogenous immunoglobulin gene hypermutation in several mouse strains. As a rapid assay for monitoring mutation in the JH flanking region, we show that one can exploit the fact that, following denaturation/renaturation, the PCR amplified JH flanking region DNA from germinal centre B cells yields mismatched heteroduplexes which can be quantified in a filter binding assay using the bacterial mismatch repair protein MutS -Wagner et al. (1995) Nucleic Acids Res. 23, 3944-3948-. Such assays enabled us, by example, to show that antibody hypermutation proceeds in the absence of the p53 tumour suppressor gene product.

Indexed as

Cell Adhesion MoleculesGenes, ImmunoglobulinLectinsPoint MutationAnimalsAntigens, CDAntigens, Differentiation, B-LymphocyteB-LymphocytesCodonGene RearrangementGenetic VariationImmunoglobulin J-ChainsImmunoglobulin Variable RegionMiceMice, Inbred C57BLMice, Inbred CBAAntigens, CDAntigens, Differentiation, B-LymphocyteCd22 protein, mouseCell Adhesion MoleculesCodonImmunoglobulin J-ChainsImmunoglobulin Variable RegionLectinsSerineSialic Acid Binding Ig-like Lectin 2Tumor Suppressor Protein p53

Identifiers

PMID9115357
PMCPMC146691
OpenAlexW2120490035

What OpenQuestion holds

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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.