Evidence map›Paper›PMID 26104890›Full record

ArticleZhongguo fei ai za zhi = Chinese journal of lung cancer2015

PR-Set7 is Degraded in a Conditional Cul4A Transgenic Mouse Model of Lung Cancer.

Yang Wang, Zhidong Xu, Jian-Hua Mao, David Hsieh, Alfred Au, David M Jablons, Hui Li, Liang You

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

Article in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2015. 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 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. The emerging role for Cullin 4 family of E3 ligases in tumorigenesis.Biochimica et biophysica acta. Reviews on cancer · 2019
    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

8 authors at 4 institutions in 2 countries.

Yang WangThoracic Surgery Department, Beijing Chao-Yang Hospital, Capital University of Medical Science, Beijing 100020, China.
Zhidong XuThoracic Oncology Laboratory, Department of Surgery, Comprehensive Cancer Center, University of California, San Francisco, CA 94143, USA.
Jian-Hua MaoLife Sciences Division, Lawrence Berkeley National Laboratory, University of California, Berkeley, CA 94720, USA.
David HsiehThoracic Oncology Laboratory, Department of Surgery, Comprehensive Cancer Center, University of California, San Francisco, CA 94143, USA.
Alfred AuDivision of Diagnostic Pathology, Comprehensive Cancer Center, University of California, San Francisco, CA 94143, USA.
David M JablonsThoracic Oncology Laboratory, Department of Surgery, Comprehensive Cancer Center, University of California, San Francisco, CA 94143, USA.
Hui LiThoracic Surgery Department, Beijing Chao-Yang Hospital, Capital University of Medical Science, Beijing 100020, China.
Liang YouThoracic Oncology Laboratory, Department of Surgery, Comprehensive Cancer Center, University of California, San Francisco, CA 94143, USA.
Beijing Chao-Yang Hospital · CNUCSF Helen Diller Family Comprehensive Cancer Center · USUniversity of California, San Francisco · USLawrence Berkeley National Laboratory · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMaintenance of genomic integrity is essential to ensure normal organismal development and to prevent diseases such as cancer. PR-Set7 (also known as Set8) is a cell cycle regulated enzyme that catalyses monomethylation of histone 4 at Lys20 (H4K20me1) to promote chromosome condensation and prevent DNA damage. Recent studies show that CRL4CDT2-mediated ubiquitylation of PR-Set7 leads to its degradation during S phase and after DNA damage. This might occur to ensure appropriate changes in chromosome structure during the cell cycle or to preserve genome integrity after DNA damage.

methodsWe developed a new model of lung tumor development in mice harboring a conditionally expressed allele of Cul4A. We have therefore used a mouse model to demonstrate for the first time that Cul4A is oncogenic in vivo. With this model, staining of PR-Set7 in the preneoplastic and tumor lesions in AdenoCre-induced mouse lungs was performed. Meanwhile we identified higher protein level changes of γ-tubulin and pericentrin by IHC.

resultsThe level of PR-Set7 down-regulated in the preneoplastic and adenocarcinomous lesions following over-expression of Cul4A. We also identified higher levels of the proteins pericentrin and γ-tubulin in Cul4A mouse lungs induced by AdenoCre.

conclusionsPR-Set7 is a direct target of Cul4A for degradation and involved in the formation of lung tumors in the conditional Cul4A transgenic mouse model.

Indexed as

AnimalsCell CycleCullin ProteinsDisease Models, AnimalDown-RegulationHistone-Lysine N-MethyltransferaseHistonesHumansLungLung NeoplasmsMiceMice, TransgenicProteolysisTubulinCUL4A protein, humanCullin ProteinsHistone-Lysine N-MethyltransferaseHistonesKMT5a protein, mouseTubulin

Identifiers

PMID26104890
PMCPMC5999902
OpenAlexW2200949963

What OpenQuestion holds

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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.