Evidence map›Paper›PMID 21952639›Full record

ArticleCell cycle (Georgetown, Tex.)2011

NIRF constitutes a nodal point in the cell cycle network and is a candidate tumor suppressor.

Tsutomu Mori, Daisuke D Ikeda, Toshihiko Fukushima, Seiichi Takenoshita, Hideo Kochi

Open access · hybridAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2011. 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
1.5field-weighted citation impact, top 19% 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, 47 citations in OpenAlex.

  1. Review
  2. Review
  3. UHRF2 accumulates in early GCell cycle (Georgetown, Tex.) · 2024
    Article
  4. Review
  5. Article
  6. The Role of SUMO E3 Ligases in Signaling Pathway of Cancer Cells.International journal of molecular sciences · 2022
    Review
  7. Article
  8. The UHRF protein family in epigenetics, development, and carcinogenesis.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2022
    Review
  9. Observational
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Early human embryos are naturally aneuploid-can that be corrected?Journal of assisted reproduction and genetics · 2017
    Review
  18. Article
  19. Article
  20. Article
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

5 authors at 1 institution in 1 country.

Tsutomu MoriDepartment of Human Lifesciences, Fukushima Medical University School of Nursing, Fukushima, Japan. tmori@fmu.ac.jp
Daisuke D Ikeda
Toshihiko Fukushima
Seiichi Takenoshita
Hideo Kochi
Fukushima Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In biological networks, a small number of "hub" proteins play critical roles in the network integrity and functions. The cell cycle network orchestrates versatile cellular functions through interactions between many signaling modules, whose defects impair diverse cellular processes, often leading to cancer. However, the network architecture and molecular basis that ensure proper coordination between distinct modules are unclear. Here, we show that the ubiquitin ligase NIRF (also known as UHRF2), which induces G1 arrest, interacts with multiple cell cycle proteins including cyclins (A2, B1, D1 and E1), p53 and pRB, and ubiquitinates cyclins D1 and E1. Consistent with its versatility, a bioinformatic network analysis demonstrated that NIRF is an intermodular hub protein that is responsible for the coordination of multiple network modules. Notably, intermodular hubs are frequently associated with oncogenesis. Indeed, we detected loss of heterozygosity of the NIRF gene in several kinds of tumors. When a cancer outlier profile analysis was applied to the Oncomine database, loss of the NIRF gene was found at statistically significant levels in diverse tumors. Importantly, a recurrent microdeletion targeting NIRF was observed in non-small cell lung carcinoma. Furthermore, NIRF is immediately adjacent to the single nucleotide polymorphism rs719725, which is reportedly associated with the risk of colorectal cancer. These observations suggest that NIRF occupies a prominent position within the cell cycle network, and is a strong candidate for a tumor suppressor whose aberration contributes to the pathogenesis of diverse malignancies.

Indexed as

Carcinoma, Non-Small-Cell LungCell Cycle ProteinsCell LineChromosomes, Human, Pair 9Cyclin A2Cyclin B1Cyclin D1Cyclin EG1 Phase Cell Cycle CheckpointsGene DeletionHumansRecombinant Fusion ProteinsRetinoblastoma ProteinTumor Suppressor Protein p53UbiquitinationUbiquitin-Protein LigasesCell Cycle ProteinsCyclin A2Cyclin B1Cyclin D1Cyclin ERecombinant Fusion ProteinsRetinoblastoma ProteinTumor Suppressor Protein p53Ubiquitin-Protein LigasesUHRF2 protein, human

Identifiers

PMID21952639
PMCPMC3233626
OpenAlexW2024204000

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.