RPL11 antibody (FITC)
- Known as:
- RPL11 (anti-) (fluorecein)
- Catalog number:
- orb103412
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- RPL11 antibody (FITC)
Related genes to: RPL11 antibody (FITC)
- 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 antibody (FITC)
Related articles to: RPL11 antibody (FITC)
- BYSL gene encodes the bystin-like (BYSL) protein, a nucleolar protein involved in eukaryotic ribosome biogenesis and essential for 40S ribosomal subunit synthesis. Although BYSL upregulation has been implicated in hepatocellular carcinoma, its mechanistic contribution to tumor progression remains undefined. We observed that BYSL is consistently upregulated across multiple cancer types and is associated with adverse clinicopathological features and poor prognosis, with the strongest clinical relevance observed in hepatocellular carcinoma through the integrative transcriptomic and proteomic analyses. BYSL-knockout suppresses malignant phenotypes, including proliferation, migration, and invasion, and induced G1/S arrest and apoptosis. Mechanistically, loss of BYSL disrupts nucleolar homeostasis and reduces global protein synthesis, thereby activating the RPL5/RPL11-MDM2-p53 axis, leading to p53 stabilization and tumor suppression. Importantly, MYC directly bound to the BYSL promoter and transcriptionally activated its expression, whereas co-targeting BYSL and MYC produced more synergistic antitumor effects than either intervention alone. Collectively, our study reveals that BYSL acts as a pivotal downstream mediator of MYC-regulated ribosome biogenesis and promotes hepatocellular carcinoma progression. Our findings suggest that BYSL may represent a potential therapeutic target for hepatocellular carcinoma; nevertheless, additional in vivo preclinical studies are warranted to validate its translational prospects. - Source: PubMed
Publication date: 2026/08/10
Zhao HeyuanLiu HuiyingLiu XiaHe LiangmeiJiang ShupingZhong HaijianKatanaev Vladimir LLi Yumei - Neoporphyra haitanensis and Neopyropia yezoensis are two economically important seaweeds in Asia, yet their germplasm identification is often hindered by high phenotypic plasticity and limited molecular resources. To address this, we utilized a genome skimming strategy on five No. haitanensis and two Ny. yezoensis cultivars to retrieve their plastome information (including whole plastome sequences, plastome-divergent hotspots, and plastome-derived SSRs) and to identify genome-wide polymorphic nuclear SSRs. The plastomes of No. haitanensis (201,110-201,310 bp) were markedly larger than those of Ny. yezoensis (191,974 bp), a difference largely driven by expansions in intergenic regions. Gene annotation identified 253 genes in No. haitanensis and 256 in Ny. yezoensis, with the latter uniquely containing two additional hypothetical ORFs (ORF33 and ORF35) and an extra rRNA gene (rrfB). Further comparative analysis revealed seven hypervariable regions (π > 0.1), five of which-apcE-tatC, psbW-trnR, psbX-accD, trnW-rpl11, and ycf32-rpl32-are intergenic spacers with strong potential as species-discriminatory barcodes. We also characterized 26-30 chloroplast-derived SSRs and identified notable interspecific variations in their repeat-type profiles. Importantly, we developed 230 and 505 high-quality polymorphic nuclear SSRs for No. haitanensis and Ny. yezoensis, respectively, predominantly trinucleotide repeats, offering a robust toolset for fine-scale genetic analyses. Phylogenetic reconstruction using 201 shared plastid protein-coding genes clearly separated the two species into distinct clades, supporting their independent evolutionary trajectories, and further revealed intraspecific genetic differentiation, particularly with the cultivar ZD-1 forming a distinct branch within No. haitanensis. This study provides comprehensive genomic resources-including complete plastomes, hypervariable regions, and polymorphic SSR markers-that will facilitate germplasm identification, phylogenetic studies, and molecular breeding in Porphyra sensu lato. - Source: PubMed
Publication date: 2026/07/20
Zhang CongcongGao ZhicongWang HaotianZhou WeiDeng YinyinYang RuiChen HaiminChen JuanjuanZhu Shanshan - The rising incidence of resistance to conventional chemical insecticides necessitates the development of novel, sustainable pest management strategies. RNA interference (RNAi) offers a highly specific alternative; however, its practical application in lepidopteran pests is often limited by low efficacy due to rapid dsRNA degradation, inefficient transport of dsRNA to the site of action, and suboptimal target gene selection. While nanoformulated dsRNA has been shown to improve RNAi efficiency, delivery enhancement alone does not consistently result in high mortality. In the current study, we used PLL/EGCG/dsRNA nanoformulations to improve RNAi-based control of . We first validated the effectiveness of nanoparticle-mediated RNAi in by targeting the inhibitor of apoptosis (IAP) gene. Nanoformulated dsRNA targeting IAP resulted in substantial gene silencing, with an 80% reduction in target gene mRNA levels and 63% larval mortality, confirming that improved dsRNA delivery can significantly enhance RNAi efficacy in lepidopterans. We extended our analysis to evaluate an additional 14 candidate genes selected from recent genome-wide RNAi screens that identified superior RNAi targets. Orthologs of these genes in S. frugiperda, including proteasome subunit β-type 4 (BT4) and 60S ribosomal protein L11 (RPL11), were targeted using PLL/EGCG/dsRNA nanoformulations. Although these genes induced moderate larval mortality, their effects were consistently lower than those observed with IAP, indicating that IAP remains a more effective RNAi target among the genes evaluated in . - Source: PubMed
Publication date: 2026/06/30
Moola Anil KumarPalli Subba Reddy - Oxidized low-density lipoprotein (ox-LDL) and inflammation cause endothelial dysfunction in coronary heart disease (CHD). Although ribosomal protein S5 (RPS5) has been linked to cardiovascular disease, the mechanism by which it functions in the endothelium and its relationship to NF-κB signaling remain unknown. RPS5 was chosen as the hub gene for CHD after differential expression analysis was done on the GSE68506 dataset. The human coronary artery endothelial cells (HCAECs) injury model was established by ox-LDL. In vitro experiments were performed to evaluate the changes in RPS5 expression, apoptosis, inflammatory markers, vascular protective factors, cell proliferation, and Endothelial-to-Mesenchymal Transition (EndMT). Combining the dual luciferase reporter gene assay and the NF-κB nuclear translocation immunofluorescence assay, the effect of RPS5 on the NF-κB pathway was evaluated. Seven ribosomal genes (RPL11, RPL8, RPS13, RPS20, RPS3, RPS5, RPS8) were downregulated in coronary artery disease (CAD) samples in the GSE68506 dataset. In vitro, ox-LDL injury similarly reduced RPS5 expression in HCAECs. Functionally, RPS5 knockdown inhibits cell proliferation and enhances apoptosis and EndMT, while RPS5 overexpression has the opposite effect. Mechanistically, RPS5 overexpression diminished NF-κB nuclear accumulation, lowered κB-WT reporter activity, and reduced the phosphorylation levels of IKKα/β, IκBα, and p65. It also reduced pro-inflammatory mediators and decreased VEGF and HSP70. The pathway dependency was confirmed when LPS-induced NF-κB activation reversed these effects. Through the NF-κB signaling pathway, RPS5 plays a crucial role in controlling inflammation, apoptosis, EndMT, and vascular protection factors in injured HCAECs. Endothelial damage in CHD may be treatable by focusing on the RPS5-NF-κB axis. - Source: PubMed
Publication date: 2026/07/13
Han SuxiaLi WanqiuHuang YanXu YifeiSong HaihanQi Weigang - : Radioresistance is a critical challenge in the treatment of esophageal squamous cell carcinoma (ESCC). Histone lysine-specific demethylase 4D (KDM4D) has been implicated in DNA damage response; however, its role in regulating ESCC radiosensitivity remained unclear. We hypothesized KDM4D modulates radiosensitivity through the c-Myc/checkpoint kinase 1 (CHK1) pathway. : To investigate the role of KDM4D in ESCC radiosensitivity and to elucidate the underlying molecular mechanisms. : KDM4D expression was analyzed in tumor samples from 32 ESCC patients who received neoadjuvant radiotherapy. ESCC cell lines with KDM4D knockdown or overexpression were subjected to irradiation, and radiosensitivity was evaluated. Chromatin immunoprecipitation-polymerase chain reaction (ChIP-PCR), luciferase assay, and xenograft models were used to explore the underlying mechanisms. : Elevated KDM4D expression was associated with improved response to radiotherapy and prolonged progression-free survival (PFS). KDM4D knockdown significantly reduced radiation-induced apoptosis. Mechanistically, KDM4D promoted the demethylation of histone H3 lysine 9 trimethylation (H3K9me3), thereby activating S1 RNA-binding domain-containing protein 1 (SRBD1). SRBD1 subsequently upregulated ribosomal protein L11 (RPL11), which suppressed c-Myc expression, thereby downregulating wild-type p53-induced phosphatase 1 (WIP1) and CHK1. Rescue experiments and xenograft studies further verified this regulatory axis. : KDM4D enhances ESCC radiosensitivity through the SRBD1/RPL11/c-Myc/WIP1/CHK1 pathway, highlighting its potential as both a diagnostic biomarker and a therapeutic target. - Source: PubMed
Publication date: 2026/05/15
Gao ZhenhuaHan XiaoyunYuan Shuanghu