Evidence map›Paper›PMID 27047738›Full record

ArticleFEBS open bio2016

Double-strand break repair based on short-homology regions is suppressed under terminal deoxynucleotidyltransferase expression, as revealed by a novel vector system for analysing DNA repair by nonhomologous end joining.

So Maezawa, Saori Nakano, Takaaki Kuniya, Osamu Koiwai, Kotaro Koiwai

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact, top 90% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

5 authors at 1 institution in 1 country.

So MaezawaDepartment of Applied Biological Science Faculty of Science and Technology Tokyo University of Science Noda Chiba Japan.
Saori NakanoDepartment of Applied Biological Science Faculty of Science and Technology Tokyo University of Science Noda Chiba Japan.
Takaaki KuniyaDepartment of Applied Biological Science Faculty of Science and Technology Tokyo University of Science Noda Chiba Japan.
Osamu KoiwaiDepartment of Applied Biological Science Faculty of Science and Technology Tokyo University of Science Noda Chiba Japan.
Kotaro KoiwaiDepartment of Applied Biological Science Faculty of Science and Technology Tokyo University of Science Noda Chiba Japan.
Tokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have constructed a novel, nonhomologous end-joining (NHEJ) assay vector (NAV), containing mKate2, Venus and ccdB genes. Cotransfection of NAV with a construct expressing the restriction enzyme I-SceI generated a double-strand break (DSB) in NAV that excised mKate2 and ccdB. Repair of this DSB produced an intact vector that expressed Venus, a green fluorescent protein. Because cells bearing the repaired NAV lacked the ccdB gene which slows cell proliferation, the cultures were enriched in cells containing repaired DSBs. DNA sequence analysis of the DSB junctions indicated that the repair was carried out mainly by using the closest homology sequence. Use of the NAV yielded rapid results within 3 days after transfection. We then used the NAV to analyse NHEJ in cells overexpressing terminal deoxynucleotidyltransferase (TdT). The results indicated that TdT suppresses DNA repair that is based on short (one- or two-base) homology regions, to efficiently add deoxynucleotides during VDJ recombination in lymphoid cells.

Indexed as

DNA double‐strand breakDNA polymerase XDNA polymerase λDNA polymerase μnonhomologous end joiningterminal deoxynucleotidyltransferase

Identifiers

PMID27047738
PMCPMC4794791
OpenAlexW2294397686

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.