Evidence map›Paper›PMID 29367689›Full record

ArticleScientific reports2018

Repression of Akt3 gene transcription by the tumor suppressor RIZ1.

Qingnan Liu, Xiaotian Qu, Xiaolei Xie, Pei He, Shi Huang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.3field-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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. SP1 activates AKT3 to facilitate the development of diabetic nephropathy.Journal of endocrinological investigation · 2025
    Article
  4. Article
  5. The antagonistic effect of FTO on METTL14 promotes AKT3 mJournal of cancer research and clinical oncology · 2024
    Article
  6. Review
  7. 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.

Qingnan LiuCenter for Medical Genetics, School of Life Sciences, Central South University, Changsha, Hunan, China.
Xiaotian QuCenter for Medical Genetics, School of Life Sciences, Central South University, Changsha, Hunan, China.
Xiaolei XieCenter for Medical Genetics, School of Life Sciences, Central South University, Changsha, Hunan, China.
Pei HeCenter for Medical Genetics, School of Life Sciences, Central South University, Changsha, Hunan, China.
Shi HuangCenter for Medical Genetics, School of Life Sciences, Central South University, Changsha, Hunan, China. huangshi@sklmg.edu.cn.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RIZ1 has been studied as a tumor suppressor and may play a role in metabolic diseases related to the Western style diet, such as cancer and obesity. The Akt pathway is known to play a role in both cancer and obesity, and a link between Akt and RIZ1 has also been found. To better understand the role of RIZ1 in obesity and cancer, we investigated how RIZ1 regulates the expression of Akt3. We found that overexpression of RIZ1 in HEK293 cells reduced the expression of Akt3 protein. Luciferase reporter activity of Akt3 gene promoter was significantly reduced in cells co-transfected with RIZ1. Recombinant proteins of RIZ1 was able to bind the Akt3 promoter in vitro, and chromatin immunoprecipitation assay also demonstrated the ability of RIZ1 binding to the Akt3 promoter in vivo. Overexpression of RIZ1 increased H3K9 methylation on the Akt3 promoter. These results identify Akt3 as a target of RIZ1 regulation and expand our understanding of the Akt pathway in cancer and obesity.

Indexed as

Transcription, GeneticChromatin ImmunoprecipitationDNADNA-Binding ProteinsHEK293 CellsHistone-Lysine N-MethyltransferaseHumansNuclear ProteinsPromoter Regions, GeneticProtein BindingProto-Oncogene Proteins c-aktTranscription FactorsAKT3 protein, humanDNADNA-Binding ProteinsHistone-Lysine N-MethyltransferaseNuclear ProteinsPRDM2 protein, humanProto-Oncogene Proteins c-aktTranscription Factors

Identifiers

PMID29367689
PMCPMC5784169
OpenAlexW2805068201

What OpenQuestion holds

Textmetadata
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.