Evidence map›Paper›PMID 29472448›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

Double-stranded DNA break polarity skews repair pathway choice during intrachromosomal and interchromosomal recombination.

Alexanda K Ling, Clare C So, Michael X Le, Audrey Y Chen, Lisa Hung, Alberto Martin

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

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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

6 authors.

Alexanda K LingDepartment of Immunology, University of Toronto, Toronto, ON, Canada M5S1A8.
Clare C SoDepartment of Immunology, University of Toronto, Toronto, ON, Canada M5S1A8.
Michael X LeDepartment of Immunology, University of Toronto, Toronto, ON, Canada M5S1A8.
Audrey Y ChenDepartment of Immunology, University of Toronto, Toronto, ON, Canada M5S1A8.
Lisa HungDepartment of Immunology, University of Toronto, Toronto, ON, Canada M5S1A8.
Alberto MartinDepartment of Immunology, University of Toronto, Toronto, ON, Canada M5S1A8 alberto.martin@utoronto.ca.

Funding

CIHR PJT156330
6 · The paper itself

Abstract

Activation-induced cytidine deaminase (AID) inflicts DNA damage at Ig genes to initiate class switch recombination (CSR) and chromosomal translocations. However, the DNA lesions formed during these processes retain an element of randomness, and thus knowledge of the relationship between specific DNA lesions and AID-mediated processes remains incomplete. To identify necessary and sufficient DNA lesions in CSR, the Cas9 endonuclease and nickase variants were used to program DNA lesions at a greater degree of predictability than is achievable with conventional induction of CSR. Here we show that Cas9-mediated nicks separated by up to 250 nucleotides on opposite strands can mediate CSR. Staggered double-stranded breaks (DSBs) result in more end resection and junctional microhomology than blunt DSBs. Moreover,

Indexed as

DNA Breaks, Double-StrandedDNA End-Joining RepairRecombination, GeneticAnimalsB-LymphocytesChromosomes, MammalianCytidine DeaminaseMiceTranslocation, GeneticCytidine Deaminaseactivation-induced cytidine deaminaseCas9chromosomal translocationclass switch recombinationdouble-stranded DNA repair

Identifiers

PMID29472448
PMCPMC5856553

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.