Evidence map›Paper›PMID 18571763›Full record

ArticleLung cancer (Amsterdam, Netherlands)2009

Deficiency of a potential 3p21.3 tumor suppressor gene UBE1L (UBA7) does not accelerate lung cancer development in K-rasLA2 mice.

Xiaoyan Yin, Xiuli Cong, Ming Yan, Dong-Er Zhang

Open access · greenAbstract read
In one paragraph

Article in Lung cancer (Amsterdam, Netherlands), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.2field-weighted citation impact, top 43% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Type I IFN induces protein ISGylation to enhance cytokine expression and augments colonic inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  9. Article
  10. Interferon-stimulated gene 15 and the protein ISGylation system.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2011
    Review
  11. ISG15 and immune diseases.Biochimica et biophysica acta · 2010
    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 2 institutions in 1 country.

Xiaoyan YinDepartment of Molecular and Experimental Medicine, Scripps Research Institute, La Jolla, CA 92037, USA.
Xiuli Cong
Ming Yan
Dong-Er Zhang
Scripps Research Institute · USUniversity of California, San Diego · US

Funding

Ubiquitin Like Protein ISG15 ConjugationR01GM066955 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZHANG, DONG-ER · 2003 to 2010
$2.2M
Mechanism of Interferon Response and Resistance in CMLR01CA102625 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZHANG, DONG-ER · 2004 to 2008
$1.1M
NCI NIH HHS CA102625NCI NIH HHS R01 CA102625NIGMS NIH HHS GM066955NIGMS NIH HHS R01 GM066955
6 · The paper itself

Abstract

Genetic lesions in chromosomal region 3p21.3 marks one of the earliest events in human lung cancer development. It is hypothesized that one or more tumor suppressor genes reside in this region. Identification and characterization of these genes are important for the understanding of lung cancer initiation. UBE1L (UBA7) is a long-suspected 3p21.3 residing tumor suppressor gene. It encodes the key enzyme that activates ISGylation, a novel, ubiquitination-like, post-translational protein modification system that is inducible by interferon. It has been implicated that ISGylation plays a variety of biological roles ranging from viral defense to tumor surveillance. Here we tested the possible function of ISGylation during lung cancer development by using the Ube1l-deficient mice and the K-ras(LA2) lung cancer mice. Protein ISGylation levels were largely unchanged during lung cancer progression. Ube1l deficiency neither altered the lung cancer progression nor affected the overall survival of K-ras(LA2) lung cancer mice. Our study suggests that Ube1l is not a tumor suppressor gene in K-ras(LA2) lung cancer mouse model. However, as described in the discussion, additional studies with other lung cancer mouse models will be necessary to elucidate the potential tumor suppressor function of UBE1L in K-RAS mutation independent human lung cancers.

Indexed as

Genes, rasGenes, Tumor SuppressorAnimalsCytokinesLung NeoplasmsLymphomaMiceThymus GlandUbiquitin-Activating EnzymesUbiquitinsCytokinesG1p2 protein, mouseUbiquitin-Activating EnzymesUbiquitins

Identifiers

PMID18571763
PMCPMC3137380
OpenAlexW2023911934

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.