Evidence map›Paper›PMID 16357222›Full record

ArticleGenes & development2005

Inactivation of S6 ribosomal protein gene in T lymphocytes activates a p53-dependent checkpoint response.

Sanda Sulic, Linda Panic, Martina Barkic, Mladen Mercep, Miljana Uzelac, Sinisa Volarevic

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing 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

82 citing papers in PubMed, 514 citations in OpenAlex.

  1. Single cell RNA-seq analysis of hematopoietic cell types in 22q11.2 deletion syndrome reveals significant changes to non-T cells.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2025
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  7. Ribosomal Protein S6: A Potential Therapeutic Target against Cancer?International journal of molecular sciences · 2021
    Review
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  16. Suboptimal T-cell receptor signaling compromises protein translation, ribosome biogenesis, and proliferation of mouse CD8 T cells.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  17. Article
  18. Review
  19. Regulatory module involving FGF13, miR-504, and p53 regulates ribosomal biogenesis and supports cancer cell survival.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  20. The Evolution of the Ribosomal Protein-MDM2-p53 Pathway.Cold Spring Harbor perspectives in medicine · 2016
    Review

22 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

6 authors at 2 institutions in 1 country.

Sanda SulicDepartment of Molecular Medicine and Biotechnology, School of Medicine, University of Rijeka, Croatia.
Linda Panic
Martina Barkic
Mladen Mercep
Miljana Uzelac
Sinisa Volarevic
Pliva (Croatia) · HRUniversity of Rijeka · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ribosome biogenesis has been associated with regulation of cell growth and cell division, but the molecular mechanisms that integrate the effect of ribosome biogenesis on these processes in mammalian cells remain unknown. To study the effect of impaired ribosome functions in vivo, we conditionally deleted one or two alleles of the 40S ribosomal protein S6 gene in T cells in the mouse. While complete deletion of S6 abrogated T-cell development, hemizygous expression did not have any effect on T-cell maturation in the thymus, but inhibited the accumulation of T cells in the spleen and lymph nodes, as a result of their decreased survival in the peripheral lymphoid organs. Additionally, TCR-mediated stimulation of S6-heterozygous T cells induced a normal increase in their size, but cell cycle progression was impaired. Genetic inactivation of p53 tumor suppressor rescued development of S6-homozygous null thymocytes and proliferative defect of S6-heterozygous T cells. These results demonstrate the existence of a p53-dependent checkpoint mechanism that senses changes in the fidelity of the translational machinery to prevent aberrant cell division or eliminate defective T cells in vivo. Failure to activate this checkpoint response could potentially lead to a development of pathological processes such as tumors and autoimmune diseases.

Indexed as

Cell CycleCell DifferentiationAnimalsAutoimmune DiseasesLymphocyte ActivationLymphoid TissueMiceMice, TransgenicNeoplasmsProtein BiosynthesisReceptors, Antigen, T-CellRibosomal Protein S6RibosomesT-LymphocytesTumor Suppressor Protein p53Receptors, Antigen, T-CellRibosomal Protein S6Tumor Suppressor Protein p53

Identifiers

PMID16357222
PMCPMC1315409
OpenAlexW2140899494

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.