Evidence map›Paper›PMID 20404349›Full record

ArticleThe Journal of biological chemistry2010

Regulation of cyclin B2 expression and cell cycle G2/m transition by menin.

Ting Wu, Xiuli Zhang, Xiaohua Huang, Yuqing Yang, Xianxin Hua

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

40 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Menin in Cancer.Genes · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. The role of menin in bone pathology.Endocrine connections · 2022
    Review
  9. Article
  10. Review
  11. Upregulation of Cyclin B2 (American journal of cancer research · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  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 3 institutions in 2 countries.

Ting WuDepartment of Biomedical Sciences, School of Life Science,Medical College, Xiamen University, Xiamen 361005, China.
Xiuli Zhang
Xiaohua Huang
Yuqing Yang
Xianxin Hua
Xiamen University · CNCancer Research Institute · USUPMC Hillman Cancer Center · US

Funding

Function of tumor suppressor gene meninR01CA100912 · NCI · UNIVERSITY OF PENNSYLVANIA · PI HUA, XIANXIN · 2004 to 2008
$1.4M
Beta Cell Regeneration by an Epigenetic PathwayR01DK097555 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI HUA, XIANXIN · 2013 to 2016
$1.4M
Regulation of apoptosis by meninR01CA113962 · NCI · UNIVERSITY OF PENNSYLVANIA · PI HUA, XIANXIN · 2005 to 2009
$1.4M
NCI NIH HHS R01 CA100912NCI NIH HHS R01-CA-100912NCI NIH HHS R01 CA113962NCI NIH HHS R01-CA-113962NIDDK NIH HHS R01 DK097555
6 · The paper itself

Abstract

Multiple endocrine neoplasia type 1 (MEN1) results from mutations in tumor suppressor gene Men1, which encodes nuclear protein menin. Menin up-regulates certain cyclin-dependent kinase inhibitors through increasing histone H3 lysine 4 (H3K4) methylation and inhibits G(0)/G(1) to S phase transition. However, little is known as to whether menin controls G(2)/M-phase transition, another important cell cycle checkpoint. Here, we show that menin expression delays G(2)/M phase transition and reduces expression of Ccnb2 (encoding cyclin B2). Menin associates with the promoter of Ccnb2 and reduces histone H3 acetylation, a positive chromatin marker for gene transcription, at the Ccnb2 locus. Moreover, Men1 ablation leads to an increase in cyclin B2 expression, histone H3 acetylation at the Ccnb2 locus, and G(2)/M transition. In contrast, knockdown of cyclin B2 diminishes the number of cells at M phase and reduces cell proliferation. Furthermore, menin interferes with binding of certain positive transcriptional regulators, such as nuclear factor Y (NF-Y), E2 factors (E2Fs), and histone acetyltransferase CREB (cAMP-response element-binding protein)-binding protein (CBP) to the Ccnb2 locus. Notably, MEN1 disease-related mutations, A242V and L22R, abrogate the ability of menin to repress cyclin B2 expression and G(2)/M transition. Both of the mutants fail to reduce the acetylated level of the Ccnb2 locus. Together, these results suggest that menin-mediated repression of cyclin B2 is crucial for inhibiting G(2)/M transition and cell proliferation through a previously unrecognized molecular mechanism for menin-induced suppression of MEN1 tumorigenesis.

Indexed as

Gene Expression Regulation, NeoplasticAcetylationAnimalsCell ProliferationCell SeparationCyclin B2FibroblastsFlow CytometryG2 PhaseHistonesMiceMutationPromoter Regions, GeneticProto-Oncogene ProteinsTranscription, GeneticCyclin B2HistonesMen1 protein, mouseProto-Oncogene Proteins

Identifiers

PMID20404349
PMCPMC2881754
OpenAlexW1991269237

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.