Evidence map›Paper›PMID 24145455›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Monoallelic loss of tumor suppressor GRIM-19 promotes tumorigenesis in mice.

Sudhakar Kalakonda, Shreeram C Nallar, Sausan Jaber, Susan K Keay, Ellen Rorke, Raghava Munivenkatappa, Daniel J Lindner, Gary M Fiskum, Dhananjaya V Kalvakolanu

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. [Pathogenic role of NDUFA13 inactivation in spontaneous hepatitis in mice and the mechanism].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  6. Article
  7. Inherited Thyroid Tumors With Oncocytic Change.Frontiers in endocrinology · 2021
    Review
  8. Mitochondrial GRIM-19 deficiency facilitates gastric cancer metastasis through oncogenic ROS-NRF2-HO-1 axis via a NRF2-HO-1 loop.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Heterogeneity of GRIM-19 Expression in the Adult Mouse Brain.Cellular and molecular neurobiology · 2019
    Article
  13. Early loss of mitochondrial complex I and rewiring of glutathione metabolism in renal oncocytoma.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  14. TheGenes · 2018
    Review
  15. Electron leak from NDUFA13 within mitochondrial complex I attenuates ischemia-reperfusion injury via dimerized STAT3.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Sudhakar KalakondaDepartments of Microbiology and Immunology, Anesthesiology, Medicine, and Pathology, Greenebaum Cancer Center, Graduate Program in Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201.
Shreeram C Nallar
Sausan Jaber
Susan K Keay
Ellen Rorke
Raghava Munivenkatappa
Daniel J Lindner
Gary M Fiskum
Dhananjaya V Kalvakolanu
U-M Rogel Cancer CenterApath (United States) · USCleveland Clinic · USUnited States Department of Veterans Affairs · USUniversity of Maryland, Baltimore · US

Funding

Cytokine modulated novel growth inhibitory mechanismsR01CA105005 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI KALVAKOLANU, DHAN V. · 2004 to 2013
$2.7M
NCI NIH HHS CA105005NCI NIH HHS R01 CA105005
6 · The paper itself

Abstract

Gene-associated with retinoid-interferon induced mortality-19 (GRIM-19), a STAT3-inhibitory protein, was isolated as a growth-suppressive gene product using a genome-wide expression knockdown screen. We and others have shown a loss of expression and occurrence of mutations in the GRIM-19 gene in a variety of primary human cancers, indicating its potential role as tumor suppressor. To help investigate its role in tumor development in vivo, we generated a genetically modified mouse in which Grim-19 can be conditionally inactivated. Deletion of Grim-19 in the skin significantly increased the susceptibility of mice to chemical carcinogenesis, resulting in development of squamous cell carcinomas. These tumors had high Stat3 activity and an increased expression of Stat3-responsive genes. Loss of Grim-19 also caused mitochondrial electron transport dysfunction resulting from failure to assemble electron transport chain complexes and altered the expression of several cellular genes involved in glycolysis. Surprisingly, the deletion of a single copy of the Grim-19 gene was sufficient to promote carcinogenesis and formation of invasive squamous cell carcinomas. These observations highlight the critical role of GRIM-19 as a tumor suppressor.

Indexed as

AnimalsCarcinogenesisCarcinoma, Squamous CellDNA PrimersGene ComponentsGene Expression ProfilingGene Knockdown TechniquesGenetic VectorsImmunohistochemistryMiceMice, KnockoutNADH, NADPH OxidoreductasesReal-Time Polymerase Chain ReactionSequence Analysis, RNASTAT3 Transcription FactorDNA PrimersGrim19 protein, mouseNADH, NADPH OxidoreductasesStat3 protein, mouseSTAT3 Transcription Factorcytokinesglucose metabolismimmune responseoxidative phosphorylation

Identifiers

PMID24145455
PMCPMC3831468
OpenAlexW2124172718

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.