ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Rpl22 Loss Selectively Impairs αβ T Cell Development by Dysregulating Endoplasmic Reticulum Stress Signaling.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 47 citations in OpenAlex.
- Loss of ribosomal protein RPL22 restricts African swine fever virus replication by inducing PERK-dependent ER stress.Emerging microbes & infections · 2026Article
- p97-mediated proteostasis is a checkpoint for late-stage thymocyte positive selection.Cellular & molecular immunology · 2026Article
- The Effect of Training on the Expression of Protein and Metabolites in the Plasma Exosomes of theAnimals : an open access journal from MDPI · 2026Article
- Integrated multi-omics analysis reveals dendritic cell centered regulatory networks and therapeutic targets in necrotizing enterocolitis.Frontiers in immunology · 2026Article
- Ribosomal protein control of hematopoietic stem cell transformation through regulation of metabolism.Cell reports · 2025Article
- Role of NK cells in immune escape in patients with classical paroxysmal nocturnal haemoglobinuria.Clinical and translational medicine · 2025Article
- Epstein-Barr virus functional RNAs as part of its immune evasion strategy: a role for EBER1?Open biology · 2025Review
- Ribosomal RNA transcription regulates splicing through ribosomal protein RPL22.Cell chemical biology · 2025Article
- Ribosomal proteins: the missing piece in the inflammation puzzle?Molecular and cellular biochemistry · 2025Review
- TMED4 facilitates regulatory T cell suppressive function via ROS homeostasis in tumor and autoimmune mouse models.The Journal of clinical investigation · 2024Article
- HDAC1 Promotes Mitochondrial Pathway Apoptosis and Inhibits the Endoplasmic Reticulum Stress Response in High Glucose-Treated Schwann Cells via Decreased U4 Spliceosomal RNA.Neurochemical research · 2024Article
- Navigating the landscape of the unfolded protein response in CD8Frontiers in immunology · 2024Review
- RPL11 promotes non-small cell lung cancer cell proliferation by regulating endoplasmic reticulum stress and cell autophagy.BMC molecular and cell biology · 2023Article
- Reducing the aneuploid cell burden - cell competition and the ribosome connection.Disease models & mechanisms · 2022Review
- KLF16 enhances stress tolerance of colorectal carcinomas by modulating nucleolar homeostasis and translational reprogramming.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Article
- Loss of Ribosomal Protein Paralog Rpl22-like1 Blocks Lymphoid Development without Affecting Protein Synthesis.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Preventing translational inhibition from ribosomal protein insufficiency by a herpes simplex virus-encoded ribosome-associated protein.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Ribosome Biogenesis and Cancer: Overview on Ribosomal Proteins.International journal of molecular sciences · 2021Review
- Endoplasmic Reticulum Quality Control in Immune Cells.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Although ribosomal proteins (RP) are thought to primarily facilitate biogenesis of the ribosome and its ability to synthesize protein, emerging evidence suggests that individual RP can perform critical regulatory functions that control developmental processes. We showed previously that despite the ubiquitous expression of the RP ribosomal protein L22 (Rpl22), germline ablation of Rpl22 in mice causes a selective, p53-dependent block in the development of αβ, but not γδ, T cell progenitors. Nevertheless, the basis by which Rpl22 loss selectively induces p53 in αβ T cell progenitors remained unclear. We show in this study that Rpl22 regulates the development of αβ T cells by restraining endoplasmic reticulum (ER) stress responses. In the absence of Rpl22, ER stress is exacerbated in αβ, but not γδ, T cell progenitors. The exacerbated ER stress in Rpl22-deficient αβ T lineage progenitors is responsible for selective induction of p53 and their arrest, as pharmacological induction of stress is sufficient to induce p53 and replicate the selective block of αβ T cells, and attenuation of ER stress signaling by knockdown of protein kinase R-like ER kinase, an ER stress sensor, blunts p53 induction and rescues development of Rpl22-deficient αβ T cell progenitors. Rpl22 deficiency appears to exacerbate ER stress by interfering with the ability of ER stress signals to block new protein synthesis. Our finding that Rpl22 deficiency exacerbates ER stress responses and induces p53 in αβ T cell progenitors provides insight into how a ubiquitously expressed RP can perform regulatory functions that are selectively required by some cell lineages but not others.
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