Evidence map›Paper›PMID 42327758›Full record

ArticleFrontiers in immunology2026

SLy1-deficiency results in functional impaired, exhausted and senescent NK cells.

Lisa Rebmann, Victoria Schwenck, Carolin Blumendeller, Isabelle Grund, Jannika Botzenhardt, Sandra Beer-Hammer

Abstract read
In one paragraph

Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Lisa RebmannDepartment of Pharmacology, Experimental Therapy and Toxicology, Institute of Experimental and Clinical Pharmacology and Pharmacogenomic and ICePhA, University of Tübingen, Tübingen, Germany.
Victoria SchwenckDepartment of Pharmacology, Experimental Therapy and Toxicology, Institute of Experimental and Clinical Pharmacology and Pharmacogenomic and ICePhA, University of Tübingen, Tübingen, Germany.
Carolin BlumendellerDepartment of Pharmacology, Experimental Therapy and Toxicology, Institute of Experimental and Clinical Pharmacology and Pharmacogenomic and ICePhA, University of Tübingen, Tübingen, Germany.
Isabelle GrundDepartment of Pharmacology, Experimental Therapy and Toxicology, Institute of Experimental and Clinical Pharmacology and Pharmacogenomic and ICePhA, University of Tübingen, Tübingen, Germany.
Jannika BotzenhardtDepartment of Pharmacology, Experimental Therapy and Toxicology, Institute of Experimental and Clinical Pharmacology and Pharmacogenomic and ICePhA, University of Tübingen, Tübingen, Germany.
Sandra Beer-HammerDepartment of Pharmacology, Experimental Therapy and Toxicology, Institute of Experimental and Clinical Pharmacology and Pharmacogenomic and ICePhA, University of Tübingen, Tübingen, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: SLy1 is an emerging adapter protein, exclusively expressed in lymphocytes. In NK cells it serves as ribosomal stabilizer and plays an important role for their maturation, survival and functionality. SLy1-deficient (SLy1 Objective: This study aimed to analyze phenotypical and functional characteristics of SLy1- and p53-deficient NK cells and to understand which impairments depend on both proteins. Results: We established a SLy1 Conclusion: In brief, we demonstrated that SLy1 is indispensable for adequate numbers of viable, activatable NK cells with an intact cytolytic capacity, and that those phenotypic alterations are p53-mediated. Furthermore, the absence of SLy1 leads to senescence and exhaustion of NK cells in an p53-independant manner. These findings correlate with the recently shown association of human SLy1-mutations with specific types of common variable immunodeficiencies. We therefore strongly recommend testing for mutations in the gene locus, especially in patients with unclear immunodeficiencies.

Indexed as

Adaptor Proteins, Vesicular TransportCellular SenescenceKiller Cells, NaturalAnimalsCytotoxicity, ImmunologicImmune System ExhaustionMiceMice, Inbred C57BLMice, KnockoutRibosomal ProteinsTumor Suppressor Protein p53Adaptor Proteins, Vesicular TransportRibosomal ProteinsSLY1 protein, mouseTumor Suppressor Protein p53exhaustionNK cellsp53ribosomesenescenceSLy1/SASH3

Identifiers

PMID42327758
PMCPMC13275445

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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.