Evidence map›Paper›PMID 26208779›Full record

ArticleFree radical biology & medicine2015

SOD2 targeted gene editing by CRISPR/Cas9 yields Human cells devoid of MnSOD.

Kimberly Cramer-Morales, Collin D Heer, Kranti A Mapuskar, Frederick E Domann

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. OCancer cell · 2017
    Trial
  2. Article
  3. Article
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  7. CRISPR editing demonstrates rs10490924 raised oxidative stress in iPSC-derived retinal cells from patients withProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases.International journal of molecular sciences · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

4 authors at 1 institution in 1 country.

Kimberly Cramer-MoralesDepartment of Radiation Oncology, B180 Medical Laboratories, The University of Iowa, Iowa City, IA 52242.
Collin D HeerDepartment of Radiation Oncology, B180 Medical Laboratories, The University of Iowa, Iowa City, IA 52242.
Kranti A MapuskarDepartment of Radiation Oncology, B180 Medical Laboratories, The University of Iowa, Iowa City, IA 52242.
Frederick E DomannDepartment of Radiation Oncology, B180 Medical Laboratories, The University of Iowa, Iowa City, IA 52242. Electronic address: frederick-domann@uiowa.edu.
University of Iowa · US

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Douglas Robert Spitz · 2000 to 2026
$70.0M
Pulmonary Toxicology Facility CoreP30ES005605 · NIEHS · UNIVERSITY OF IOWA · PI Brandi Janssen · 1990 to 2026
$40.5M
TRAINING PROGRAM IN FREE RADICAL AND RADIATION BIOLOGYT32CA078586 · NCI · UNIVERSITY OF IOWA · PI SPITZ, DOUGLAS ROBERT · 1999 to 2024
$5.7M
NCI NIH HHS P30 CA086862NCI NIH HHS T32 CA078586NIEHS NIH HHS P30 ES005605
6 · The paper itself

Abstract

To date no models exist to study MnSOD deficiency in human cells. To address this deficiency, we created a SOD2-null human cell line that is completely devoid of detectable MnSOD protein expression and enzyme activity. We utilized the CRISPR/Cas9 system to generate biallelic SOD2 disruption in HEK293T cells. These SOD2-null cells exhibit impaired clonogenic activity, which was rescued by either treatment with GC4419, a pharmacological small-molecule mimic of SOD, or growth in hypoxia. The phenotype of these cells is primarily characterized by impaired mitochondrial bioenergetics. The SOD2-null cells displayed perturbations in their mitochondrial ultrastructure and preferred glycolysis as opposed to oxidative phosphorylation to generate ATP. The activities of mitochondrial complex I and II were both significantly impaired by the absence of MnSOD activity, presumably from disruption of the Fe/S centers in NADH dehydrogenase and succinate dehydrogenase subunit B by the aberrant redox state in the mitochondrial matrix of SOD2-null cells. By creating this model we provide a novel tool with which to study the consequences of lack of MnSOD activity in human cells.

Indexed as

Oxidative StressBase SequenceBlotting, WesternCell ProliferationCRISPR-Cas SystemsGene Expression RegulationHEK293 CellsHumansMitochondriaMolecular Sequence DataOxidation-ReductionOxidative PhosphorylationRNA EditingSuccinate DehydrogenaseSuperoxide DismutaseSuperoxide Dismutase 2SDHD protein, humanSuccinate DehydrogenaseSuperoxide DismutaseSuperoxide Dismutase 2Electron transportIron metabolismMitochondriaRespirationSuperoxide dismutase

Identifiers

PMID26208779
PMCPMC4890619
OpenAlexW2197588452

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.