Evidence map›Paper›PMID 25854920›Full record

ArticleGenes & development2015

Senescent cells communicate via intercellular protein transfer.

Anat Biran, Meirav Perelmutter, Hilah Gal, Dominick G A Burton, Yossi Ovadya, Ezra Vadai, Tamar Geiger, Valery Krizhanovsky

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
–field-weighted citation impact
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

80 citing papers in PubMed, 131 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. The states of senescent cells.Biochemical Society transactions · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Molecular hallmarks of ageing in amyotrophic lateral sclerosis.Cellular and molecular life sciences : CMLS · 2024
    Review
  17. Review
  18. Review
  19. Review
  20. Review

20 more citing papers are in PubMed but not listed here.

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.

Anat BiranDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel;
Meirav PerelmutterDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel;
Hilah GalDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel;
Dominick G A BurtonDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel;
Yossi OvadyaDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel;
Ezra VadaiDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel;
Tamar GeigerSackler School of Medicine, Tel Aviv University, Tel-Aviv 69978, Israel.
Valery KrizhanovskyDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel; valery.krizhanovsky@weizmann.ac.il.
Weizmann Institute of Science · ILTel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mammalian cells mostly rely on extracellular molecules to transfer signals to other cells. However, in stress conditions, more robust mechanisms might be necessary to facilitate cell-cell communications. Cellular senescence, a stress response associated with permanent exit from the cell cycle and the development of an immunogenic phenotype, limits both tumorigenesis and tissue damage. Paradoxically, the long-term presence of senescent cells can promote tissue damage and aging within their microenvironment. Soluble factors secreted from senescent cells mediate some of these cell-nonautonomous effects. However, it is unknown whether senescent cells impact neighboring cells by other mechanisms. Here we show that senescent cells directly transfer proteins to neighboring cells and that this process facilitates immune surveillance of senescent cells by natural killer (NK) cells. We found that transfer of proteins to NK and T cells is increased in the murine preneoplastic pancreas, a site where senescent cells are present in vivo. Proteomic analysis and functional studies of the transferred proteins revealed that the transfer is strictly dependent on cell-cell contact and CDC42-regulated actin polymerization and is mediated at least partially by cytoplasmic bridges. These findings reveal a novel mode of intercellular communication by which senescent cells regulate their immune surveillance and might impact tumorigenesis and tissue aging.

Indexed as

ActinsAnimalsCell CommunicationCellular SenescenceFibroblastsKiller Cells, NaturalLymphocyte ActivationMicePancreasPolymerizationProtein Transportrho GTP-Binding ProteinsT-LymphocytesActinsrho GTP-Binding Proteinsactin polymerizationcellular senescencecytoplasmic bridgesnatural killer cells

Identifiers

PMID25854920
PMCPMC4403256
OpenAlexW2086653505

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.