Evidence map›Paper›PMID 25164432›Full record

ArticleJournal of cellular and molecular medicine2014

Heterodimerization of apelin receptor and neurotensin receptor 1 induces phosphorylation of ERK(1/2) and cell proliferation via Gαq-mediated mechanism.

Bo Bai, Xin Cai, Yunlu Jiang, Emmanouil Karteris, Jing Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. The Apelinergic System in Kidney Disease: Novel Perspectives.International journal of molecular sciences · 2025
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Orthogonal Peptide-Templated Labeling Elucidates Lateral ETChembiochem : a European journal of chemical biology · 2022
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Apelinergic System Structure and Function.Comprehensive Physiology · 2017
    Review
  15. Article
  16. Article
  17. 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 2 institutions in 2 countries.

Bo BaiNeurobiology Institute, Jining Medical University, Jining, Shandong, China.
Xin Cai
Yunlu Jiang
Emmanouil Karteris
Jing Chen
Jining Medical University · CNBrunel University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dimerization of G protein-coupled receptors (GPCRs) is crucial for receptor function including agonist affinity, efficacy, trafficking and specificity of signal transduction, including G protein coupling. Emerging data suggest that the cardiovascular system is the main target of apelin, which exerts an overall neuroprotective role, and is a positive regulator of angiotensin-converting enzyme 2 (ACE2) in heart failure. Moreover, ACE2 cleaves off C-terminal residues of vasoactive peptides including apelin-13, and neurotensin that activate the apelin receptor (APJ) and neurotensin receptor 1 (NTSR1) respectively, that belong to the A class of GPCRs. Therefore, based on the similar mode of modification by ACE2 at peptide level, the homology at amino acid level and the capability of forming dimers with other GPCRs, we have been suggested that APJ and NTSR1 can form a functional heterodimer. Using co-immunoprecipitation, BRET and FRET, we provided conclusive evidence of heterodimerization between APJ and NTSR1 in a constitutive and induced form. Upon agonist stimulation, hetrodimerization enhanced ERK(1/2) activation and increased proliferation via activation of Gq α-subunits. These novel data provide evidence for a physiological role of APJ/NTSR1 heterodimers in terms of ERK(1/2) activation and increased intracellular calcium and induced cell proliferation and provide potential new pharmaceutical targets for cardiovascular disease.

Indexed as

Cell ProliferationApelin ReceptorsBlotting, WesternCells, CulturedFlow CytometryGTP-Binding Protein alpha Subunits, Gq-G11HEK293 CellsHumansHuman Umbilical Vein Endothelial CellsImmunoenzyme TechniquesImmunoprecipitationMicroscopy, ConfocalMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphorylationProtein MultimerizationApelin ReceptorsAPLNR protein, humanGTP-Binding Protein alpha Subunits, Gq-G11MAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3neurotensin type 1 receptorReceptors, G-Protein-CoupledReceptors, NeurotensinRNA, MessengerRNA, Small Interferingapelin receptorERK 1/2G protein-coupled receptorheterodimerizationneurotensin receptor 1resonance energy transfer

Identifiers

PMID25164432
PMCPMC4244021
OpenAlexW2124731208

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.