ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2001
Transcription, beta-like DNA polymerases and hypermutation.
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 7 papers.
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.
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.
Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Modulation of Pleurodeles waltl DNA polymerase mu expression by extreme conditions encountered during spaceflight.PloS one · 2013Article
- Terminal deoxynucleotidyl transferase: the story of a misguided DNA polymerase.Biochimica et biophysica acta · 2010Review
- Terminal deoxynucleotidyl transferases from elasmobranchs reveal structural conservation within vertebrates.Immunogenetics · 2003Article
- Immunoglobulin somatic hypermutation: double-strand DNA breaks, AID and error-prone DNA repair.Journal of clinical immunology · 2003Review
- Association of DNA polymerase mu (pol mu) with Ku and ligase IV: role for pol mu in end-joining double-strand break repair.Molecular and cellular biology · 2002Article
- DNA double-strand breaks: prior to but not sufficient in targeting hypermutation.The Journal of experimental medicine · 2002Article
- The intrinsic hypermutability of antibody heavy and light chain genes decays exponentially.The EMBO journal · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This paper discusses two aspects of immunoglobulin (Ig) gene hypermutation. In the first approach, a transcription termination signal is introduced in an Ig light chain transgene acting as a mutation substrate, and transgenic lines are generated with control and mutant transgenes integrated in tandem. Analysis of transcription levels and mutation frequencies between mutant and control transgenes clearly dissociates transcription elongation and mutation, and therefore argues against models whereby specific pausing of the RNA polymerase during V gene transcription would trigger an error-prone repair process. The second part reports the identification of two novel beta-like DNA polymerases named Pol lambda and Pol mu, one of which (Pol mu) represents a good candidate for the Ig mutase due to its higher lymphoid expression and its similarity with the lymphoid enzyme terminal deoxynucleotidyl transferase. Peculiar features of the expression of this gene, including an unusual splicing variability and a splicing inhibition in response to DNA-damaging agents, are discussed.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.