Evidence map›Paper›PMID 21127195›Full record

ArticleCancer research2011

The tumor suppressor protein menin inhibits AKT activation by regulating its cellular localization.

Yan Wang, Atsushi Ozawa, Shadia Zaman, Nijaguna B Prasad, Settara C Chandrasekharappa, Sunita K Agarwal, Stephen J Marx

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 112 citations in OpenAlex.

  1. Article
  2. Article
  3. Menin in Cancer.Genes · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Observational
  13. Article
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  15. Review
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  19. Article
  20. Molecular Genetic Studies of Pancreatic Neuroendocrine Tumors: New Therapeutic Approaches.Endocrinology and metabolism clinics of North America · 2018
    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

7 authors at 5 institutions in 2 countries.

Yan WangMetabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland 20892, USA. wangyan@mail.nih.gov
Atsushi Ozawa
Shadia Zaman
Nijaguna B Prasad
Settara C Chandrasekharappa
Sunita K Agarwal
Stephen J Marx
Gunma University · JPCancer Genetics (United States) · USJohns Hopkins University · USNational Human Genome Research Institute · USNational Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

NHGRI/DIR Genomics CoreZICHG200346 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI CHANDRASEKHARAPPA, SETTARA · 2010 to 2025
$14.5M
POSITIONAL CLONING OF THE MEN1 GENEZIAHG000029 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI CHANDRASEKHARAPPA, SETTARA · 2009 to 2025
$13.3M
Hyperparathyroidism-- Etiology, Diagnosis And TreatmentZIADK043006 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI JHA, SMITA · 2011 to 2025
$8.9M
Pathophysiology Of Multiple Endocrine Neoplasia Type 1ZIEDK043009 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI MARX, STEPHEN · 2009 to 2012
$1.0M
MEN1 as a Tumor Suppressor GeneZIEDK043321 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI MARX, STEPHEN · 2009 to 2012
$1.0M
Molecular Pathways of the MEN1 GeneZIJDK043322 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI MARX, STEPHEN · 2009 to 2012
$1.0M
Molecular Pathways of the MEN1 GeneZ01DK043322 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI MARX, STEPHEN · 2007 to 2008
$896k
Intramural NIH HHS Z01 DK043322
6 · The paper itself

Abstract

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder associated mainly with tumors of multiple endocrine organs. Mutations in the MEN1 gene that encodes for the menin protein are the predominant cause for hereditary MEN1 syndrome. Though menin is a tumor suppressor, its molecular mechanism of action has not been defined. Here, we report that menin interacts with AKT1 in vitro and in vivo. Menin downregulates the level of active AKT and its kinase activity. Through interaction with AKT1, menin suppresses both AKT1-induced proliferation and antiapoptosis in nonendocrine and endocrine cells. Confocal microscopy analysis revealed that menin regulates AKT1 in part by reducing the translocation of AKT1 from the cytoplasm to the plasma membrane during growth factor stimulation. Our findings may be generalizable to other cancers, insofar as we found that loss of menin expression was also associated with AKT activation in a mouse model of pancreatic islet adenoma. Together, our results suggest menin as an important novel negative regulator of AKT kinase activity.

Indexed as

Adenoma, Islet CellAnimalsCell Growth ProcessesCell MembraneEnzyme ActivationHEK293 CellsHumansMiceMicroscopy, ConfocalPancreatic NeoplasmsProto-Oncogene ProteinsProto-Oncogene Proteins c-aktTransfectionAKT1 protein, humanMEN1 protein, humanMen1 protein, mouseProto-Oncogene ProteinsProto-Oncogene Proteins c-akt

Identifiers

PMID21127195
PMCPMC3076053
OpenAlexW2138980361

What OpenQuestion holds

Textmetadata
LicenceTDM
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.