ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Rpl22 Loss Impairs the Development of B Lymphocytes by Activating a p53-Dependent Checkpoint.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Suppression of pre-B cell colony formation by catecholamine oxidation.Journal of immunology (Baltimore, Md. : 1950) · 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
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- A Csde1-Strap complex regulates plasma cell differentiation by coupling mRNA translation and decay.Nature communications · 2025Article
- Article
- RPL22 is a tumor suppressor in MSI-high cancers and a splicing regulator of MDM4.Cell reports · 2024Article
- RPL22 is a tumor suppressor in MSI-high cancers and a key splicing regulator of MDM4.bioRxiv : the preprint server for biology · 2023Article
- Loss of Ribosomal Protein Paralog Rpl22-like1 Blocks Lymphoid Development without Affecting Protein Synthesis.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Ribosomal proteins and human diseases: molecular mechanisms and targeted therapy.Signal transduction and targeted therapy · 2021Review
- MYSM1 maintains ribosomal protein gene expression in hematopoietic stem cells to prevent hematopoietic dysfunction.JCI insight · 2020Article
- Cancer-mutated ribosome protein L22 (RPL22/eL22) suppresses cancer cell survival by blocking p53-MDM2 circuit.Oncotarget · 2017Article
- EZH2 Regulates the Developmental Timing of Effectors of the Pre-Antigen Receptor Checkpoints.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- ER fatalities-The role of ER-mitochondrial contact sites in yeast life and death decisions.Mechanisms of ageing and development · 2017Review
- Rpl22 Loss Selectively Impairs αβ T Cell Development by Dysregulating Endoplasmic Reticulum Stress Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Probing the mechanisms underlying human diseases in making ribosomes.Biochemical Society transactions · 2016Review
- Ribosomal Protein Rpl22 Controls the Dissemination of T-cell Lymphoma.Cancer research · 2016Article
- Splicing-Mediated Autoregulation Modulates Rpl22p Expression in Saccharomyces cerevisiae.PLoS genetics · 2016Article
- Role of ribosomal protein mutations in tumor development (Review).International journal of oncology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Although ribosomal proteins facilitate the ribosome’s core function of translation, emerging evidence suggests that some ribosomal proteins are also capable of performing tissue-restricted functions either from within specialized ribosomes or from outside of the ribosome. In particular, we have previously demonstrated that germline ablation of the gene encoding ribosomal protein Rpl22 causes a selective and p53-dependent arrest of ab T cell progenitors at the b-selection checkpoint. We have now identified a crucial role for Rpl22 during early B cell development. Germline ablation of Rpl22 results in a reduction in the absolute number of B-lineage progenitors in the bone marrow beginning at the pro–B cell stage. Although Rpl22-deficient pro–B cells are hyporesponsive to IL-7, a key cytokine required for early B cell development, the arrest of B cell development does not result from disrupted IL-7 signaling. Instead, p53 induction appears to be responsible for the developmental defects, as Rpl22 deficiency causes increased expression of p53 and activation of downstream p53 target genes, and p53 deficiency rescues the defect in B cell development in Rpl22-deficient mice. Interestingly, the requirement for Rpl22 in the B cell lineage appears to be developmentally restricted, because Rpl22-deficient splenic B cells proliferate normally in response to Ag receptor and Toll receptor stimuli and undergo normal class-switch recombination. These results indicate that Rpl22 performs a critical, developmentally restricted role in supporting early B cell development by preventing p53 induction.
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Registered trials
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.