Evidence map›Paper›PMID 32540865›Full record

ArticleG3 (Bethesda, Md.)2020

C-Terminal HA Tags Compromise Function and Exacerbate Phenotypes of

Matan Cohen, Michael Lichten

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in G3 (Bethesda, Md.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 50% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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

2 authors at 1 institution in 1 country.

Matan CohenLaboratory of Biochemistry and Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, 20892, and.ORCID 0000-0002-8501-5695
Michael LichtenLaboratory of Biochemistry and Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, 20892, and michael.lichten@nih.gov.ORCID 0000-0001-9707-2956
National Cancer Institute · US

Funding

Mechanism of Meiotic RecombinationZIABC005268 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LICHTEN, MICHAEL J · 2009 to 2023
$17.3M
6 · The paper itself

Abstract

The Sgs1 helicase and Top3-Rmi1 decatenase form a complex that affects homologous recombination outcomes during the mitotic cell cycle and during meiosis. Previous studies have reported that Sgs1-Top3-Rmi1 function is regulated by SUMOylation that is catalyzed by the Smc5-Smc6-Mms21 complex. These studies used strains in which

Indexed as

Saccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsCell Cycle ProteinsDNA-Binding ProteinsPhenotypeRecQ HelicasesSUMO-1 ProteinSumoylationCell Cycle ProteinsDNA-Binding ProteinsMms21 protein, S cerevisiaeRecQ HelicasesSaccharomyces cerevisiae ProteinsSGS1 protein, S cerevisiaeSMC5 protein, S cerevisiaeSUMO-1 ProteinHA protein tagshomologous recombinationIntramural Research Program of the NIHKey phrases: Sgs1meiosisSmc5-Smc6-Mms21SUMO

Identifiers

PMID32540865
PMCPMC7407464
OpenAlexW3034261778

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.