| Year | Reference (first author, journal) | Publication date | URL/DOI | System (human cell lines/organism) | What was measured/approach | Key finding about RPL18A/eL20 | Quantitative/statistical detail if present in extracted text | Relevance to functional annotation (translation/biogenesis/localization/disease) |
|---|---|---|---|---|---|---|---|---|
| 2021 | Miller, *WIREs RNA* | Jul 2021 | https://doi.org/10.1002/wrna.1613 | HCV IRES in in vitro translation assays; host ribosome context not further specified in snippet | Review summarizing prior experimental work on viral translation; cites in vitro translation assays | eL20/RPL18A was reported to interact with HCV IRES RNA, and adding eL20 protein to in vitro translation extracts moderately stimulated HCV IRES activity (pqac-00000003, pqac-00000004) | “moderately stimulated” HCV IRES activity; no numerical value in snippet (pqac-00000003) | Direct evidence for a translation-related role of eL20/RPL18A beyond generic structural annotation; supports RNA interaction capability in the 60S context (pqac-00000003, pqac-00000004) |
| 2022 | Luan, *Nucleic Acids Research* | 2022 (month not visible in snippet) | https://doi.org/10.1093/nar/gkac053 | Human A549, U2OS, Neuro-2a, HUVECs mentioned in study methods; genome-wide RP knockdown framework | Ribo-seq/RNA-seq after knockdown of 75 human ribosomal proteins; CRISPR-Cas9 comparison; polysome profiling | Although RPL18A is not singled out in the extracted text, the study shows that deficiency of 60S ribosomal proteins causes stronger growth inhibition than 40S RP deficiency through p53 signaling, and that RPs entering ribosome biogenesis in the nucleus are enriched among those affecting cell-cycle/p53 pathways (pqac-00000005, pqac-00000006) | 60S vs 40S: more DTGs after 60S RP deficiency (*t* test, **P** = 0.018); greater p53 protein increase for Group 1 RPs (**P** = 4.2e−07); more elevated p53 target genes (**P** = 1.657e−15); enrichment for nucleus-entering RPs (hypergeometric **P** = 0.00034) (pqac-00000005) | Indirect but relevant evidence for likely pathway context of RPL18A as a 60S RP involved in nuclear ribosome biogenesis and ribosomal-stress/p53 responses (pqac-00000005, pqac-00000006) |
| 2023 | Zhang, *Cell* | May 25, 2023 | https://doi.org/10.1016/j.cell.2023.04.026 | K562 and HEK293T cells mentioned in extracted methods/discussion | Cysteine-focused chemical proteomics plus functional genomics to identify anticancer drug targets and ROS-sensitive proteins | RPL18A contained a ROS-controlled cysteine site (C22) identified among sites for ROS-controlled translation in the study’s integrated proteogenomic framework (as summarized in retrieved evidence) (pqac-00000000, pqac-00000001, pqac-00000002) | Specific residue reported: C22 in RPL18A; no effect size for RPL18A itself in extracted snippet (pqac-00000000) | Recent evidence linking RPL18A to redox-sensitive translational regulation at the residue level; suggests possible post-translational modulation rather than changing its core ribosomal identity (pqac-00000000, pqac-00000001, pqac-00000002) |
| 2024 | Lindahl, *International Journal of Molecular Sciences* | Oct 17, 2024 | https://doi.org/10.3390/ijms252011186 | General eukaryotic ribosome biology | Perspective/review on ribosome heterogeneity and ribosome assembly | The review states that in eukaryotes ribosome assembly begins in the nucleolus, continues in the nucleoplasm, and is completed after export to the cytoplasm (pqac-00000009) | No RPL18A-specific quantitative detail in snippet (pqac-00000009) | Indirect localization/biogenesis context for all cytoplasmic RPs including RPL18A: nucleolus → nucleoplasm → cytoplasm maturation pathway (pqac-00000009) |
| 2025 | Kim, *Scientific Reports* | Jul 2025 | https://doi.org/10.1038/s41598-025-10316-3 | *Caenorhabditis elegans* rpl-20, ortholog of mammalian RPL18a/eL20 | Genetics plus ribosome profiling in an orthologous animal model | rpl-20/RPL18a-eL20 is a 60S large-subunit component; a conserved missense mutation reduced 60S biogenesis and 80S ribosomes, caused slow growth, and a full deletion was early larval lethal (pqac-00000007, pqac-00000016) | Conserved Gly82→Arg in worm (Gly79 in mammals); 60S amount “markedly reduced”; full deletion caused homozygous early larval lethality; suppression stronger as homozygote than heterozygote (pqac-00000016) | Strong orthology-based support that eL20 is essential for 60S biogenesis and organismal viability; useful when direct human mechanistic studies are sparse (pqac-00000007, pqac-00000016) |


*Table: This table compiles the most relevant retrieved sources that explicitly mention RPL18A/eL20 or provide closely related functional context. It helps distinguish direct evidence on RPL18A from broader ribosomal-protein background relevant to annotating its role in translation, ribosome biogenesis, localization, and stress-related pathways.*