RPL11 Polyclonal Antibody, ALEXA FLUOR 594 Conjugated
- Known as:
- RPL11 Polyclonal Antibody, ALEXA FLUOR 594 Conjugated
- Catalog number:
- bs-5715r-a594
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Bioss
- Gene target:
- RPL11 Polyclonal Antibody ALEXA FLUOR 594 Conjugated
Related genes to: RPL11 Polyclonal Antibody, ALEXA FLUOR 594 Conjugated
- Gene:
- RPL11 NIH gene
- Name:
- ribosomal protein L11
- Previous symbol:
- -
- Synonyms:
- L11, uL5
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-23
- Date modifiied:
- 2019-04-23
Related products to: RPL11 Polyclonal Antibody, ALEXA FLUOR 594 Conjugated
Related articles to: RPL11 Polyclonal Antibody, ALEXA FLUOR 594 Conjugated
- Sialidase Neu4 is a glycosidase that removes sialic acids from nonreducing ends of sugar chains. Recently, Mexican tetra Neu4 (AmNeu4) was identified as a nuclear-localized sialidase. However, the subnuclear localization and biological functions of AmNeu4 have remained unclear. This study demonstrated that AmNeu4 localized in the nucleolus and investigated the significance of its nuclear localization signal (NLS) for the nucleolar localization. Green fluorescent protein (GFP) fused to NLS localized to the nucleolus. Additionally, deletion of the NLS in AmNeu4 abolished its nucleolar localization, and insertion of additional lysine/arginine residues into AmNeu4's NLS induced exclusive nucleolar localization. These results indicated that the nucleolar localization of AmNeu4 was mediated by its NLS. The proliferation of AmNeu4-overexpressing HeLa cells was significantly reduced compared with that of the mock-transfected cells. Moreover, enzymatically inactive AmNeu4 also suppressed cell growth, indicating that the enzymatic activity of AmNeu4 is not required for the suppression of cell growth. We hypothesized that the suppressed cell proliferation is mediated by protein-protein interactions involving AmNeu4. By immunoprecipitation assay, ribosomal proteins L5 and L11 (RPL5 and RPL11, respectively) were identified as AmNeu4 interacting partners. C-MYC protein levels were lower in AmNeu4-overexpressing cells than in mock cells, and these reduced levels were restored by RPL11 knockdown. Coimmunoprecipitation assay further revealed that RPL11 bound to C-MYC in AmNeu4-overexpressing cells. These results suggest that the interaction between AmNeu4 and RPL5/RPL11 delays cell growth through destabilizing C-MYC. - Source: PubMed
Publication date: 2026/05/29
Hyodo ToshikiYamate SatsukiChen XiaoyingKomatsu MasaharuShiozaki Kazuhiro - Diabetic retinopathy (DR) develops via complex interactions of multiple risk factors and molecular pathways. However, the association between oxidative stress-related genes (OSRGs) and DR progression remains poorly understood. We analyzed two DR datasets (GSE221521, GSE189005) and 986 OSRGs. Differentially expressed genes (DEGs) from GSE221521 were intersected with OSRGs to generate candidate genes; those with protein-protein interaction (PPI) network associations were defined as candidate hub genes. Machine learning further filtered final hub genes, which underwent cross-dataset expression validation. Biomarkers were identified by receiver operating characteristic (ROC) curve analysis (AUC > 0.7) and subjected to nomogram construction, functional annotation, and immune correlation analysis. We obtained 52 candidate genes, 39 of which had PPI interactions. Machine learning yielded 13 final hub genes; CD36, DDIT3, E2F2, NFATC4, and RPL11 showed consistent expression trends across datasets. CD36, DDIT3, E2F2, and RPL11 (AUC > 0.7) were validated as biomarkers, with robust DR predictive performance in nomograms. These genes were enriched in ribosome and spliceosome pathways. Immune infiltration analysis identified three differential cell types: M0 macrophages, monocytes, and activated memory CD4 + T cells. CD36, DDIT3, E2F2, and RPL11 are potential diagnostic biomarkers for DR. The present bioinformatic findings provide preliminary clues for subsequent exploration of DR pathogenesis. - Source: PubMed
Publication date: 2026/05/22
Niu LiangjieZhang YifanXia HuikaWang Jianmin - To study the effects of different concentrations of glutathione peroxidase (GSH-Px) on sperm motility and viability, structural integrity, antioxidant capacity and metabolic enzyme activity after frozen semen of sheep, and to evaluate the expression of differential proteins. - Source: PubMed
Publication date: 2026/05/07
Wang KexinZhou QianWang YupingShen ZhixingLi JunLi XueShi ShengrongYan YiningZhang ChunxiangShi LeiRen Youshe - BackgroundPost-marketing surveillance indicates a possible link between omeprazole consumption and changes in cognitive abilities; however, existing observational studies have yielded conflicting outcomes. This highlights the lack of consensus and underscores the imperative for further systematic investigation to elucidate this relationship.ObjectiveThis investigation thoroughly examined the connection between omeprazole administration and reported memory issues, with the goal of supplying empirical support for evaluating the medication's safety profile and determining its risk-benefit balance in clinical practice.MethodsWe employed a range of analytical approaches, including descriptive statistics, multivariable logistic regression, and receiver operating characteristic curve analysis, to systematically evaluate the association between omeprazole use and memory function. Network pharmacology further characterized omeprazole's molecular targets and pathways linked to memory deficits.ResultsIn the National Health and Nutrition Examination Survey (NHANES) analysis, it revealed a significant positive association between omeprazole consumption and memory impairment (OR [95% CI] = 3.51 [1.87, 6.59]). Through network pharmacology, 342 core targets related to Alzheimer's disease were identified. The top 10 potential binding targets of omeprazole-UBA52, RPL23, RPS18, RPL4, RPL15, RPL11, RPS6, EGFR, RPL13, and RPS20-exhibited strong binding affinities. The enrichment analysis implies a role for omeprazole in causing memory issues, possibly by affecting processes like carboxylic acid metabolism and membrane transportation.ConclusionsMounting research from both large-scale population studies and drug safety surveillance reports paints a clear picture: regular omeprazole consumption appears to hike the chances of experiencing cognitive hiccups related to memory function. - Source: PubMed
Publication date: 2026/03/25
Zhang HaoZeng Qi YuLiu CuiWu YouLiu Jiang KeWang Fei HuiLuo Xi - Alzheimer’s Disease represents the most significant form of neurodegenerative disease worldwide with progressive dementia and synaptic dysfunction. Though the accumulation of β-amyloid and hyperphosphorylated tau protein is the most observed pathological feature of AD, the emergence of ribosomal dysfunction and oxidative stress has recently gained interest. In this study, we conducted a comprehensive multi-omics investigation, which included transcriptomic, proteomic, and lipidomic analyses, on cortical region from 5xFAD mice, a transgenic model of AD. Gene and protein expression analysis demonstrated ribosomal pathways were largely affected in the cortex. Histological and immunohistochemistry imaging showed increased amyloid-β and tau pathology leading to extensive cortical neurodegeneration. RNAseq analysis revealed increased oxidative RNA damage, indicating a potential mechanism of ribosomal stress. Elevated expression of RPL11, RPL6, and other large ribosomal subunit proteins was observed, consistent with impaired protein synthesis. This dysregulation may contribute to neurodegenerative processes in AD. Among the large subunit ribosomal proteins, Rpl29 were downregulated at the gene expression level in AD, although its protein expression revealed a statistically insignificant rise. Comparison between the transcriptome and proteome demonstrated evidence of impaired translation, suggesting failed translational control. Lipidomic analyses revealed alterations in the levels of phospholipids, sphingolipids and lipid mediators in AD that is closely linked to the alterations in the neuroinflammatory pathways at the transcriptomic and proteomics levels. Multi-omics integration demonstrates that ribosomal dysregulation, oxidative stress, and protein homeostasis are affected, leading to neuronal damage in AD. According to this study, ribosomal malfunction plays a significant role in the pathophysiology of AD and serve as a potential target for therapeutic interventions. - Source: PubMed
Publication date: 2026/02/23
Agrawal KirtiEgbejiogu Blessing CAdeyelu TolulopeBurk DavidMurray Kermit KWalls AlexJones KatarinaCampagna Shawn RFrancis JosephGhosh SujoyOgundele Olalekan MGartia Manas Ranjan