Evidence map›Paper›PMID 36437247›Full record

ArticleCell death & disease2022

Activation of orphan receptor GPR132 induces cell differentiation in acute myeloid leukemia.

Chunyang Yi, Jiacheng He, Dan Huang, Yumiao Zhao, Chan Zhang, Xiyun Ye, Ying Huang, Ruth Nussinov, Junke Zheng, Mingyao Liu and 1 more

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

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

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  8. Molecular principles underlying aggressive cancers.Signal transduction and targeted therapy · 2025
    Review
  9. A human gutScience (New York, N.Y.) · 2024
    Article
  10. Article
  11. Review
  12. 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

11 authors at 4 institutions in 4 countries.

Chunyang Yi *Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Jiacheng He *Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.ORCID 0000-0002-5264-2983
Dan Huang *Department of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yumiao ZhaoShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Chan ZhangShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Xiyun YeShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Ying HuangNMPA Key Laboratory of Rapid Drug Inspection Technology, Guangdong Institute for Drug Control, 766 Shenzhou Road, Guangzhou, 510663, China.
Ruth NussinovComputational Structural Biology Section, Basic Science Program, Frederick National Laboratory for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702, USA.
Junke ZhengDepartment of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China. zhengjunke@shsmu.edu.cn.
Mingyao LiuShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China. myliu@bio.ecnu.edu.cn.ORCID 0000-0001-7339-5048
Weiqiang LuShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China. wqlu@bio.ecnu.edu.cn.ORCID 0000-0003-1349-6597
East China Normal University · CNShanghai Jiao Tong University · CNGuangdong Institute for Drug Control · CNTel Aviv University · IL

Funding

NCI NIH HHS HHSN261201500003CNCI NIH HHS HHSN261201500003I
6 · The paper itself

Abstract

Blocked cellular differentiation is a critical pathologic hallmark of acute myeloid leukemia (AML). Here, we showed that genetic activation of the orphan GPCR GPR132 significantly induced cell differentiation of AML both in vitro and in vivo, indicating that GPR132 is a potential trigger of myeloid differentiation. To explore the therapeutic potential of GPR132 signaling, we screened and validated a natural product 8-gingerol (8GL) as a GPR132 agonist. Notably, GPR132 activation by 8GL promoted differentiation and reduced colony formation in human AML cell lines with diverse genetic profiles. Mechanistic studies revealed that 8GL treatment inhibits the activation of the mammalian target of rapamycin (mTOR), a regulator of AML cell differentiation blockade, via activating GPR132-G

Indexed as

Cell DifferentiationLeukemia, Myeloid, AcuteReceptors, G-Protein-CoupledAnimalsCarrier ProteinsCell Cycle ProteinsHumansMammalsMiceSignal TransductionTOR Serine-Threonine KinasesCarrier ProteinsCell Cycle ProteinsG2A receptorReceptors, G-Protein-CoupledTOR Serine-Threonine Kinases

Identifiers

PMID36437247
PMCPMC9701798
OpenAlexW4310273463

What Socratic 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 Socratic graph.