Evidence map›Paper›PMID 30405161›Full record

ArticleScientific reports2018

Cellular signaling and gene expression profiles evoked by a bivalent macrocyclic peptide that serves as an artificial MET receptor agonist.

Wenyu Miao, Katsuya Sakai, Naoya Ozawa, Takumi Nishiuchi, Yoshinori Suzuki, Kenichiro Ito, Tomomi Morioka, Masataka Umitsu, Junichi Takagi, Hiroaki Suga and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Cyclic Peptide-Based Biologics Regulating HGF-MET.International journal of molecular sciences · 2020
    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

11 authors at 3 institutions in 1 country.

Wenyu MiaoDivision of Tumor Dynamics and Regulation, Cancer Research Institute, Kanazawa University, Kakuma, Kanazawa, 920-1192, Japan.
Katsuya SakaiDivision of Tumor Dynamics and Regulation, Cancer Research Institute, Kanazawa University, Kakuma, Kanazawa, 920-1192, Japan.
Naoya OzawaDepartment of Chemistry, Graduate School of Science, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Takumi NishiuchiDivision of Functional Genomics, Advanced Science Research Center, Kanazawa University, Takaramachi, Kanazawa, 920-0934, Japan.
Yoshinori SuzukiDivision of Tumor Dynamics and Regulation, Cancer Research Institute, Kanazawa University, Kakuma, Kanazawa, 920-1192, Japan.
Kenichiro ItoDepartment of Chemistry, Graduate School of Science, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Tomomi MoriokaDepartment of Chemistry, Graduate School of Science, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Masataka UmitsuLaboratory of Protein Synthesis and Expression, Institute for Protein Research, Osaka University, Osaka, 565-0871, Japan.
Junichi TakagiLaboratory of Protein Synthesis and Expression, Institute for Protein Research, Osaka University, Osaka, 565-0871, Japan.
Hiroaki SugaDepartment of Chemistry, Graduate School of Science, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.ORCID http://orcid.org/0000-0002-5298-9186
Kunio MatsumotoDivision of Tumor Dynamics and Regulation, Cancer Research Institute, Kanazawa University, Kakuma, Kanazawa, 920-1192, Japan. kmatsu@staff.kanazawa-u.ac.jp.
Kanazawa University · JPThe University of Tokyo · JPProtein Research Foundation · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-native ligands for growth factor receptors that are generated by chemical synthesis are applicable to therapeutics. However, non-native ligands often regulate cellular signaling and biological responses in a different manner than native ligands. Generation of surrogate ligands comparable to native ligands is a challenging need. Here we investigated changes in signal transduction and gene expression evoked by a bivalent macrocyclic peptide (aMD5-PEG11) capable of high-affinity binding to the MET/hepatocyte growth factor (HGF) receptor. Binding of aMD5-PEG11 to the MET extracellular region was abolished by deletion of the IPT3-IPT4 domain, indicating the involvement of IPT3-IPT4 in the binding of aMD5-PEG11 to the MET receptor. aMD5-PEG11 induced dimerization and activation of the MET receptor and promoted cell migration that was comparable to induction of these activities by HGF. Signal activation profiles indicated that aMD5-PEG11 induced phosphorylation of intracellular signaling molecules, with a similar intensity and time dependency as HGF. In 3-D culture, aMD5-PEG11 as well as HGF induced epithelial tubulogenesis and up-regulated the same sets of functionally classified genes involved in multicellular organism development. Thus, a non-native surrogate ligand that consisted of a bivalent macrocyclic peptide can serve as an artificial MET receptor agonist that functionally substitutes for the native ligand, HGF.

Indexed as

TranscriptomeCell LineComputational BiologyGene Expression ProfilingGene Expression RegulationMolecular StructurePeptides, CyclicProtein BindingProtein Interaction Domains and MotifsProtein MultimerizationProto-Oncogene Proteins c-metReceptors, ArtificialSignal TransductionPeptides, CyclicProto-Oncogene Proteins c-metReceptors, Artificial

Identifiers

PMID30405161
PMCPMC6220203
OpenAlexW2899398134

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.