Evidence map›Paper›PMID 26221032›Full record

ArticleThe Journal of biological chemistry2015

CUX2 protein functions as an accessory factor in the repair of oxidative DNA damage.

Ranjana Pal, Zubaidah M Ramdzan, Simran Kaur, Philippe M Duquette, Richard Marcotte, Lam Leduy, Sayeh Davoudi, Nathalie Lamarche-Vane, Angelo Iulianella, Alain Nepveu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 56 citations in OpenAlex.

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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

10 authors at 5 institutions in 2 countries.

Ranjana PalFrom the Goodman Cancer Research Centre and.
Zubaidah M RamdzanFrom the Goodman Cancer Research Centre and.
Simran KaurFrom the Goodman Cancer Research Centre and Departments of Biochemistry.
Philippe M DuquetteAnatomy and Cell Biology, McGill University, Montreal, Quebec H3A 1A3, Canada.
Richard MarcottePrincess Margaret Cancer Centre, University Health Network, Toronto M5G 1L7, Canada, and.
Lam LeduyFrom the Goodman Cancer Research Centre and.
Sayeh DavoudiDepartments of Biochemistry.
Nathalie Lamarche-VaneAnatomy and Cell Biology, McGill University, Montreal, Quebec H3A 1A3, Canada.
Angelo IulianellaDepartment of Medical Neuroscience, Dalhousie University, Life Science Research Institute, Halifax B3H 4R2, Canada.
Alain NepveuFrom the Goodman Cancer Research Centre and Departments of Biochemistry, Medicine, Oncology, and alain.nepveu@mcgill.ca.
McGill University · CADalhousie University · CAGoodman (Japan) · JPOccupational Cancer Research Centre · CAPrincess Margaret Cancer Centre · CA

Funding

Canadian Institutes of Health Research MOP-326694
6 · The paper itself

Abstract

CUX1 and CUX2 proteins are characterized by the presence of three highly similar regions called Cut repeats 1, 2, and 3. Although CUX1 is ubiquitously expressed, CUX2 plays an important role in the specification of neuronal cells and continues to be expressed in postmitotic neurons. Cut repeats from the CUX1 protein were recently shown to stimulate 8-oxoguanine DNA glycosylase 1 (OGG1), an enzyme that removes oxidized purines from DNA and introduces a single strand break through its apurinic/apyrimidinic lyase activity to initiate base excision repair. Here, we investigated whether CUX2 plays a similar role in the repair of oxidative DNA damage. Cux2 knockdown in embryonic cortical neurons increased levels of oxidative DNA damage. In vitro, Cut repeats from CUX2 increased the binding of OGG1 to 7,8-dihydro-8-oxoguanine-containing DNA and stimulated both the glycosylase and apurinic/apyrimidinic lyase activities of OGG1. Genetic inactivation in mouse embryo fibroblasts or CUX2 knockdown in HCC38 cells delayed DNA repair and increased DNA damage. Conversely, ectopic expression of Cut repeats from CUX2 accelerated DNA repair and reduced levels of oxidative DNA damage. These results demonstrate that CUX2 functions as an accessory factor that stimulates the repair of oxidative DNA damage. Neurons produce a high level of reactive oxygen species because of their dependence on aerobic oxidation of glucose as their source of energy. Our results suggest that the persistent expression of CUX2 in postmitotic neurons contributes to the maintenance of genome integrity through its stimulation of oxidative DNA damage repair.

Indexed as

DNA DamageDNA RepairAnimalsCell LineCerebral CortexDNA-Binding ProteinsDNA GlycosylasesGene Expression RegulationHomeodomain ProteinsHumansMiceNeuronsNuclear ProteinsOxidation-ReductionRatsRepressor ProteinsCUX1 protein, humanCux1 protein, ratCux2 protein, mouseDNA-Binding ProteinsDNA GlycosylasesHomeodomain ProteinsNuclear ProteinsOgg1 protein, mouseOGG1 protein, ratoxoguanine glycosylase 1, humanRepressor ProteinsTranscription Factors8-oxoguanine (8-oxoG)8-oxoguanine glycosylase (OGG1)DNA damageDNA repairoxidative stress

Identifiers

PMID26221032
PMCPMC4566227
OpenAlexW2428764380

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.