Ask about this productRelated genes to: Rpsa antibody
- Gene:
- RPSA NIH gene
- Name:
- ribosomal protein SA
- Previous symbol:
- LAMR1
- Synonyms:
- LRP, 37LRP, p40, SA
- Chromosome:
- 3p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-03
- Date modifiied:
- 2019-04-23
Related products to: Rpsa antibody
Related articles to: Rpsa antibody
- Streptococcus suis serotype 2 is a significant zoonotic pathogen that poses a serious threat to the health of humans and various animals. Ribosomal protein S1 (RPSA), acting as a key virulence factor, mediates SS2 adhesion to host cells and facilitates its penetration of the blood-brain barrier. In this study, we expressed the SS2 RPSA recombinant protein and used it to immunize BALB/c mice. Through screening, we obtained a high-affinity hybridoma clone and produced a specific anti-RPSA monoclonal antibody (designated mAb-RPSA-5E2). We found that mAb-RPSA-5E2 exhibited potent antibacterial activity, significantly inhibiting the proliferation of SS2 in vitro. In SS2-challenged mice, treatment with mAb-RPSA-5E2 significantly reduced mortality and alleviated pathological damage in the lung and brain tissues. Furthermore, evaluating the immunoprotective effect of the SS2-RPSA protein as a subunit vaccine revealed that this vaccine provided good protection against SS2 infection. These findings indicate that RPSA is a promising candidate target for developing SS2 subunit vaccines and targeted therapeutic biologics. KEY POINTS: • The SS2 RPSA monoclonal antibody can inhibit the proliferation of SS2 in vitro. • The SS2 RPSA monoclonal antibody can reduce the mortality rates of mice. • The SS2-RPSA subunit vaccine provides significant immunoprotective effects in mice. - Source: PubMed
Publication date: 2026/04/17
Liu XiaoPeng BoLv FangWen GuangyuanJin SijiaWang DanZhang JianwuFan YunpengYin YupengXiao Shuqi - The 5' untranslated region (5' UTR) of messenger RNAs (mRNAs) plays a central role in regulating protein synthesis initiation, particularly through the Kozak sequence and upstream open reading frames (uORFs). Genetic variants within these regulatory elements could affect translation, altering gene expression and contributing to clinical phenotypes in humans. We developed a computational method called 5ULTRA (5' Untranslated Region Annotation) for analysis of whole-exome sequencing and whole-genome sequencing data to detect, annotate, and prioritize 5' UTR variants with potential translation impact. 5ULTRA identifies single-nucleotide variants, indels, and splicing variants that affect uORFs by creating or disrupting start/stop codons and that alter Kozak sequence strength of either the uORFs or the main coding sequence. 5ULTRA incorporates recent uORF databases and provides comprehensive annotations. 5ULTRA implements a machine-learning score to prioritize candidate variants with predicted effects on translation and also provides specific mechanistic predictions. The score correlates strongly with experimentally measured protein-level effects of 5' UTR variants. We applied 5ULTRA to multiple genetics datasets across diverse disease contexts, identifying candidate variants including potential cancer-driving somatic mutations predicted to decrease ABI1 level or increase NRAS abundance; common variants associated with traits such as multiple sclerosis, lung function, and cardiovascular function, by altering protein levels of TAGAP, VRTN, and SPAAR, respectively; and rare germline variants in our cohort, including a splicing variant of RPSA leading to 5' UTR sequence alteration that causes congenital asplenia and a variant of TNF that could predispose to tuberculosis. - Source: PubMed
Publication date: 2026/03/24
Chaldebas MatthieuPonsin KhorenBohlen JonathanConil ClementMourelatos HaralambosStenson Peter DCooper David NAbel LaurentCasanova Jean-LaurentCobat AurélieZhang Peng - The liver is a primary target for recombinant adeno-associated viral (rAAV) vectors, yet the influence of serotype, sex, and liver zonation on transduction and transcriptomic changes remains incompletely understood. This proof-of-concept study employs spatial transcriptomics alongside single-nucleus RNA sequencing to map the spatial distribution and impacts of rAAV2- and rAAV9-CMV-EGFP vectors in male and female mouse livers. Spatial transcriptomics provided precise transgene mapping and highlighted that CMV-EGFP rAAV vectors deregulate hepatocellular lipid metabolism, the circadian clock, and the immune/stress response with sex specific differences. Lipid metabolism genes (Elovl3, Chka, Irs2, Ppard), were consistently deregulated across all zones of the liver lobule in male and female rAAV2- and rAAV9-CMV-EGFP-treated mice, while Srebf1, Tlcd4, Cpt2, and Acot1 exhibited sex-specific patterns. Circadian clock modulators (Dbp, Tef, Arntl, Nfil3, Nr1d1/Nr1d2) were altered independently of zonation. The study found sex-specific downregulation of immune and stress-response genes and pathways, including Gadd45g and hypoxia pathways. TGF-β and EGFR pathways were upregulated sex-independently. Spatial transcriptomics further enabled examination of transgene and rAAV entry factor co-expression, identifying known and novel factors like Rpsa, Dpp4, Sdc1, and solute carrier proteins, highlighting its role in supporting targeted screening. Our findings demonstrate spatial transcriptomics as a powerful tool in gene therapy research and reveal novel rAAV vector effects on liver biology. - Source: PubMed
Publication date: 2026/03/11
Amberg BettinaKöchl FabianKumpesa NadinePrasad MeganaBochner FilipHernández-Obiols MarOtteneder Michael BStalder LucasShaffo FrancesNowrouzi AliMarkusic DavidHaegel HélèneXicluna RebeccaSultan MarcJacobsen BjörnRottenberg SvenValdeolivas AlbertoSchwalie Petra CHahn Kerstin - Cellular senescence remodels the microenvironment via SASP, and immune inflammation promotes carcinogenesis through DNA damage and immune remodeling; the “senescence-inflammation” vicious cycle formed by these two processes is a core driver of cancer development and progression, yet its mechanism in prostate cancer progression remains unclear. The regulatory mechanisms of “senescence-inflammation” related genes in prostate cancer were revealed, targeted drugs were predicted, and new insights were provided for the clinical treatment of prostate cancer. In this study, gene expression profile data of prostate cancer were obtained from the Gene Expression Omnibus (GEO). Differentially expressed genes were screened out through bioinformatics analysis and verified by experiments; GO and KEGG analyses were used to explore the prostate cancer-specific biological processes and signaling pathways involved, immune infiltration characteristics were revealed by combining immune infiltration tools with single-cell technology, and finally, drugs with therapeutic potential were predicted through core gene target analysis. Prostate cancer-related differentially expressed genes were found to number 203. Notable hub genes included ACTB, RPLP0, TOP2A, TXN, HSP90B1, TAGLN, RPSA, and ANXA2. According to enrichment analysis, apoptosis, cellular senescence, inflammation, and the initiation of immunological responses are the main factors contributing to the development of bladder cancer. The immunological processes of prostate cancer are significantly influenced by memory B cells, CD8 T cells, follicular helper T cells, M1 macrophages, monocytes, and NK cells, as confirmed by immune infiltration and single-cell data. Furthermore, hub genes were found to be significantly expressed in a variety of immune cells by single-cell studies; monocytes and macrophages in particular exhibited high levels of ACTB, RPLP0, RPSA, and ANXA2. We next used Western blotting, PCR, and immunohistochemistry to evaluate these genes’ expression in clinical samples. Lastly, Miconazole, Fostamatinib, Quercetin, Resveratrol, and Regorafenib were shown to be possible important drugs or ingredients for the treatment of prostate cancer by our drug-target interaction prediction analysis. We clarified the mechanism by which immune-inflammatory and aging-related genes contribute to the pathogenesis of prostate cancer. We identified and validated four core genes, namely TXN, TOP2A, ANXA2, and HSP90B1, and predicted potential therapeutic agents, specifically resveratrol and regorafenib. These findings provide a theoretical basis for research on the molecular mechanisms of prostate cancer and its clinical treatment. - Source: PubMed
Publication date: 2026/03/07
Wang YingLiu QinYi MeiLiu YanHe Ji'ang'shuZhang Han Chao - Various echocardiographic views are used to assess left ventricular wall thickness (LVWT), but whether these measurements are interchangeable remains unclear. - Source: PubMed
Novo Matos JoseLuis Fuentes Virginia