Evidence map›Paper›PMID 7731791›Full record

ArticleNucleic acids research1995

A modified single-strand annealing model best explains the joining of DNA double-strand breaks mammalian cells and cell extracts.

A L Nicolás, P L Munz, C S Young

Abstract read
In one paragraph

Article in Nucleic acids research, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 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

3 authors.

A L NicolásDepartment of Microbiology, Columbia University, New York, NY 10032, USA.
P L Munz
C S Young

Funding

THE MECHANISMS OF ADENOVIRUS RECOMBINATIONR01GM031452 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI YOUNG, CHARLES S · 1985 to 2003
$1.4M
NIGMS NIH HHS R01 GM31452
6 · The paper itself

Abstract

The joining of DNA double-strand breaks in vivo is frequently accompanied by the loss of a few nucleotides at the junction between the interacting partners. In vitro systems mimic this loss and, on detailed analysis, have suggested two models for the mechanism of end-joining. One invokes the use of extensive homologous side-by-side alignment of the partners prior to joining, while the other proposes the use of small regions of homology located at or near the terminus of the interacting molecules. to discriminate between these two models, assays were conducted both in vitro and in vivo with specially designed substrates. In vitro, molecules with limited terminal homology were capable of joining, but analysis of the junctions suggested that the mechanism employed the limited homology available. In vivo, the substrates with no extensive homology end-joined with equal efficiency to those with extensive homology in two different topological arrangements. Taken together, these results suggest that extensive homology is not a prerequisite for efficient end-joining, but that small homologies close to the terminus are used preferentially, as predicted by the modified single-strand annealing model.

Indexed as

Models, GeneticBase SequenceCell ExtractsDNA RepairDNA, Single-StrandedDNA, ViralHumansMolecular Sequence DataNucleic Acid HybridizationPlasmidsRecombination, GeneticSequence Homology, Nucleic AcidCell ExtractsDNA, Single-StrandedDNA, Viral

Identifiers

PMID7731791
PMCPMC306802

What OpenQuestion holds

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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.