Human Polyclonal RPL11 Ab
- Known as:
- Human Polyclonal RPL11 Antibody
- Catalog number:
- a6407
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal RPL11
Related genes to: Human Polyclonal RPL11 Ab
- 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: Human Polyclonal RPL11 Ab
Related articles to: Human Polyclonal RPL11 Ab
- 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 - Oral squamous cell carcinoma (OSCC) is one of the most common malignant tumors worldwide. This necessitates the development of innovative drugs with high efficiency, low toxicity, and good tolerance. Bitter melon extract has been reported to have potent anticancer activity against OSCC. We evaluated the effects of nine triterpenoids from bitter melon extract on OSCC using cell counting kit-8 (CCK-8) proliferation and Transwell migration assays. Among the nine triterpenoids, momordicine I (MI) exhibited the strongest anticancer activity against OSCC. Animal experiments also showed that MI inhibited OSCC cell growth in vivo. Additionally, MI decreased the mitochondrial membrane potential and promoted apoptosis in OSCC. RNA-sequencing (RNA-seq) analysis revealed that MI induced an unfolded protein response (UPR) and endoplasmic reticulum (ER) stress, which was confirmed by western blotting and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cellular thermal shift assay (CETSA) and mass spectrometry (MS) analysis, combined with molecular docking, identified ribosomal proteins (ribosomal protein L7 (RPL7), RPL11, RPL12, RPL18, RPL30, RPL38, RPS13, and RPS25) as MI targets. By targeting ribosomal proteins, MI likely disrupts ribosome-mediated protein folding, leading to the UPR and ER stress. In summary, MI targets ribosomal proteins to induce ER stress and inhibit OSCC, highlighting its therapeutic potential. - Source: PubMed
Publication date: 2025/12/22
Kong JianluZhu ZiyuHu YijieZhou SiyiGu TianyiShen XiaoWang HuimingYu MengfeiLiu Yu - Hereditary anemias are a cause of nonimmune hydrops fetalis (NIHF). Our objective was to review the spectrum of hereditary anemia genes in NIHF diagnosed by exome sequencing (ES). - Source: PubMed
Publication date: 2026/02/03
Makhamreh Mona MRice Stephanie MShivashankar KavyaBrewer Casey JMcLaren Rodney ABerger Seth IAl-Kouatly Huda B - Diabetic retinopathy (DR) is a leading microvascular complication of diabetes mellitus, causing irreversible vision loss in adults worldwide. However, the molecular mechanisms underlying DR pathogenesis-especially the crosstalk between core genes, immune microenvironment, and environmental factors remains incompletely elucidated. This knowledge gap hinders the development of effective preventive and therapeutic strategies for DR, making it urgent to identify key molecular targets and regulatory pathways. - Source: PubMed
Publication date: 2025/11/26
Zhang JianYang Xin