Evidence map›Paper›PMID 27982020›Full record

ArticleCancer gene therapy2017

Intrabody targeting vascular endothelial growth factor receptor-2 mediates downregulation of surface localization.

E Alirahimi, A Ashkiyan, F Kazemi-Lomedasht, K Azadmanesh, M Hosseininejad-Chafi, M Habibi-Anbouhi, R Moazami, M Behdani

Abstract read
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In one paragraph

Article in Cancer gene therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Iranian journal of basic medical sciences · 2022
    Article
  6. Article
  7. Review
  8. Iranian journal of basic medical sciences · 2020
    Article
  9. Article
  10. Review
  11. Antiangiogenic effects of oridonin.BMC complementary and alternative medicine · 2017
    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

8 authors at 2 institutions in 1 country.

E AlirahimiBiotechnology Research Center, Venom & Biotherapeutics Molecules Laboratory, Pasteur Institute of Iran, Tehran, Iran.
A AshkiyanBiotechnology Research Center, Venom & Biotherapeutics Molecules Laboratory, Pasteur Institute of Iran, Tehran, Iran.
F Kazemi-LomedashtBiotechnology Research Center, Venom & Biotherapeutics Molecules Laboratory, Pasteur Institute of Iran, Tehran, Iran.
K AzadmaneshVirology Department, Pasteur Institute of Iran, Tehran, Iran.
M Hosseininejad-ChafiBiotechnology Research Center, Venom & Biotherapeutics Molecules Laboratory, Pasteur Institute of Iran, Tehran, Iran.
M Habibi-AnbouhiNational Cell Bank, Pasteur Institute of Iran, Tehran, Iran.
R MoazamiBiotechnology Research Center, Venom & Biotherapeutics Molecules Laboratory, Pasteur Institute of Iran, Tehran, Iran.
M BehdaniBiotechnology Research Center, Venom & Biotherapeutics Molecules Laboratory, Pasteur Institute of Iran, Tehran, Iran.
Biotechnology Research Center · IRPasteur Institute of Iran · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis is among the most important mechanisms that helps cancer cells to survive, grow and undergo metastasis. Therefore, inhibiting angiogenesis will suppress tumor growth. Vascular endothelial growth factor (VEGF) and its receptor (VEGFR) are believed to be important players of angiogenesis. The goal of this study was to evaluate the success of a novel nanobody against VEGFR2 in tethering its target inside the endoplasmic reticulum and preventing its transport to the cell membrane. Nanobody sequence was cloned in a mammalian vector in fusion with green fluorescent protein and a KDEL retention signal. After transfection of 293KDR cells with this expression vector, surface localization of VEGFR2 was monitored by flow cytometry. This study demonstrates that our intrananobody is effective in targeting VEGFR2 receptor, and therefore, it is a powerful tool to downregulate a surface-exposed target protein, and in this capacity, it has potential to be used as a therapeutic protein to inhibit growth of tumors.

Indexed as

Cell LineCell MembraneDown-RegulationFlow CytometryGene ExpressionGene OrderHumansPlasmidsProtein TransportRecombinant Fusion ProteinsSingle-Domain AntibodiesTransfectionVascular Endothelial Growth Factor Receptor-2Recombinant Fusion ProteinsSingle-Domain AntibodiesVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID27982020
OpenAlexW2561470434

What OpenQuestion holds

Textmetadata
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.