RPL22 (Ribosomal Protein L22)

Sdcbp and Rpl22 were most abundantly expressed in Microglia, and Ppia in Oligodendrocytes, while Sec61g exhibited lower overall expression, all showing high activity in immune metabolic pathways. Bioinformatics analysis and experimental verification indicate that Sdcbp, Ppia, and Sec61g are associated with ferroptosis and immune infiltration in IS, and hold promise as therapeutic targets for IS treatment.

In addition, an analysis of the response of MRPL22 to anticancer drugs in public databases revealed its relevance to a range of drugs and compounds. In summary, this study integrated diverse interdisciplinary methodologies, thereby offering insights into the mechanism of the inhibition of PCa by the aNDs and the regulatory role of MRPL22 in the ribosomal pathway.

Lin28b promotes a substantial increase in lipid content, upon which the survival of Rpl22-deficient leukemias depends. Altogether, these findings reveal that Rpl22 insufficiency enhances the leukemia potential of HSCs through regulation of FAO and promotes leukemogenesis through Lin28b promotion of lipid synthesis.

Our study revealed a positive feedback loop between RPL22L1 and Myc that drove LUAD progression.

This work provides the first evidence that RPL22 deficiency is an easily measured indicator of a unique subset of MLH1 deficient endometrial cancers that can be characterized as immune low. Our work suggests that patients with RPL22 deficient tumors could represent poor candidates for CD8+ T cell-based immunotherapies, a current frontline therapy for MLH1 deficient endometrial cancers.

We identified some differentially expressed genes relevant to oncogenic signaling and immunosuppressive tumor-associated macrophages. These findings provide novel insights into factors affecting prognosis in patients with residual disease after NAC for early-stage TNBC.

This analysis identified a blood-based 7-gene signature shared between LUAD and microbial lung infections, associated with immunosuppressive microenvironment features, suggesting a potential link between infection-driven inflammation and tumor-promoting immune modulation.

Notably, RPL22-dependent alternative splicing is reversed by Pol I inhibition, revealing a non-canonical ribotoxic stress-initiated tumor suppressive pathway. This study uncovers a robust mechanism linking rRNA synthesis activity to splicing, coordinated by the ribosomal protein RPL22.

Tamoxifen administration into PdgfraCreERT:Rpl22HA and PlpCreERT:Rpl22HA mice led to widespread HA reporter expression in oligodendrocyte precursor cells (OPCs) and oligodendrocytes, respectively, throughout the brain and spinal cord...This suggests a potential regulation of gene expression in OPCs in demyelinated lesions, in which Rpl22HA translation may be prevented until oligodendrocyte differentiation occurs. Overall, the RiboTag reporter demonstrates high sensitivity and stability, and its potential application should be carefully considered in relation to the experimental model, timeline in which it will be used, and cell tracking conditions.

RPL22's effect on MDM4 and other mRNA splicing events is a striking example. A better understanding of the mechanisms involved could guide the development of improved cancer treatments.

In contrast, IFN-β signaling appeared less critical. These findings highlight the inflammatory role of OLCs in EAE, suggesting OLCs as a potential therapeutic target for mitigating neuroinflammation in MS and related disorders.

Predominant hypomethylation of MRPs and RPs disrupted mitochondrial function, contributed to oxidative phosphorylation (OXPHOS) and metabolic reprogramming, favoring cancer cell survival. The survival analysis validated the clinical relevance of these hub genes, with high-expression cohorts exhibiting poor overall survival (OS) outcomes enlightened their relevance in LUAD pathogenesis and presented the potential for developing novel targeted therapeutic strategies.