Evidence map›Paper›PMID 26796342›Full record

ArticleeLife2016

Transmembrane chemokines act as receptors in a novel mechanism termed inverse signaling.

Kirsten Hattermann, Henrike Gebhardt, Sebastian Krossa, Andreas Ludwig, Ralph Lucius, Janka Held-Feindt, Rolf Mentlein

Open access · goldAbstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Infection and immunity · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. The Role of CXCL16 in the Pathogenesis of Cancer and Other Diseases.International journal of molecular sciences · 2021
    Review
  8. Article
  9. KLF7 promotes pancreatic cancer growth and metastasis by up-regulating ISG expression and maintaining Golgi complex integrity.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  10. Article
  11. Review
  12. CD11cFrontiers in immunology · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

7 authors at 3 institutions in 1 country.

Kirsten HattermannDepartment of Anatomy, University of Kiel, Kiel, Germany.
Henrike GebhardtDepartment of Anatomy, University of Kiel, Kiel, Germany.
Sebastian KrossaDepartment of Structural Biology, Institute of Zoology, Kiel, Germany.
Andreas LudwigInstitute for Pharmacology and Toxicology, RWTH Aachen University, Aachen, Germany.
Ralph LuciusDepartment of Anatomy, University of Kiel, Kiel, Germany.
Janka Held-FeindtDepartment of Neurosurgery, University Medical Center Schleswig-Holstein, Kiel, Germany.
Rolf MentleinDepartment of Anatomy, University of Kiel, Kiel, Germany.
Kiel University · DERWTH Aachen University · DEUniversity Hospital Schleswig-Holstein · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transmembrane chemokines CX3CL1/fractalkine and CXCL16 are widely expressed in different types of tumors, often without an appropriate expression of their classical receptors. We observed that receptor-negative cancer cells could be stimulated by the soluble chemokines. Searching for alternative receptors we detected that all cells expressing or transfected with transmembrane chemokine ligands bound the soluble chemokines with high affinity and responded by phosphorylation of intracellular kinases, enhanced proliferation and anti-apoptosis. This activity requires the intracellular domain and apparently the dimerization of the transmembrane chemokine ligand. Thus, shed soluble chemokines can generate auto- or paracrine signals by binding and activating their transmembrane forms. We term this novel mechanism "inverse signaling". We suppose that inverse signaling is an autocrine feedback and fine-tuning system in the communication between cells that in tumors supports stabilization and proliferation.

Indexed as

Signal TransductionApoptosisCell Line, TumorCell ProliferationChemokine CX3CL1Chemokine CXCL16Chemokines, CXCHumansProtein BindingProtein MultimerizationReceptors, ScavengerChemokine CX3CL1Chemokine CXCL16Chemokines, CXCCX3CL1 protein, humanCXCL16 protein, humanReceptors, Scavengercell biologyCellular communicationChemokineshumanreceptorssignal transduction

Identifiers

PMID26796342
PMCPMC4739769
OpenAlexW2286637453

What OpenQuestion holds

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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.