NOL5A Blocking Peptide
- Known as:
- NOL5A Blocking Peptide
- Catalog number:
- 33r-2386
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- NOL5A Blocking Peptide
Related genes to: NOL5A Blocking Peptide
- Gene:
- NOP56 NIH gene
- Name:
- NOP56 ribonucleoprotein
- Previous symbol:
- NOL5A
- Synonyms:
- SCA36
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-21
- Date modifiied:
- 2014-11-18
Related products to: NOL5A Blocking Peptide
Related articles to: NOL5A Blocking Peptide
- Short tandem repeat expansions are associated with over 50 diseases, many with primary neurological presentations. Despite the prevalence of short tandem repeat expansion disorders, genetically diagnosing these conditions is complicated by a lack of efficient and comprehensive diagnostic screening approaches. We integrated a new short tandem repeat genotyping tool, STRipy, into the analytical workflow for short-read sequencing data generated by the comprehensive neurological disease gene panel used in the Diagnostic Genomics Department, PathWest Laboratory Medicine. We tested STRipy on Versions 6 and 7 of the panel. Version 6 already included probes covering five short tandem repeat expansion loci in the following genes: , , , and . Additional probes targeting 13 neurological disease short tandem repeat expansion loci were designed and included in Version 7. All expansions detected by STRipy were validated and sized using PCR-based diagnostic techniques. Four hundred and eighteen patients with ataxia were tested on Version 6 of the panel, and 61 (14.6%) had reportable pathogenic variants, including 11 patients with pathogenic repeat expansions detected by STRipy. Sixty-seven ataxia patients were tested on Version 7 of the panel, and 15 (22.4%) had reportable pathogenic variants, including three repeat expansions detected by STRipy. Therefore, STRipy contributed 18.0% and 20.0% of the solved cases from Version 6 and 7 of the ataxia subpanels, respectively. STRipy accurately identified and sized loci with shorter pathogenic repeat thresholds where the expansion was smaller than the read length. In addition to increased diagnostic yield, implementation of STRipy into diagnostic analysis pipelines has streamlined clinical diagnosis of short tandem repeat expansion disorders. - Source: PubMed
Publication date: 2026/03/16
Scriba Carolin KFolland ChiaraBlack MichaelBaker JessicaAbromeit DanielSaw SamanthaChiew Mei-TingGooding RebeccaLaing Nigel GDavis Mark RRavenscroft Gianina - Folate (FA), essential for DNA synthesis, repair and methylation, is predominantly stored and metabolized in the liver. Dysregulation of folate intake and metabolism is strongly implicated in the pathogenesis of hepatocellular carcinoma (HCC). Although small nucleolar RNAs (snoRNAs) have shown promise as diagnostic and prognostic biomarkers in HCC, the impact of folate deficiency on their expression landscape remains uncharacterized. Here, by performing snoRNA-seq in folate-deficient HepG2 cells, we systematically identified 26 differentially expressed snoRNAs for the first time. Functional enrichment analysis indicated that downregulated snoRNAs were closely associated with cell proliferation pathways. From these, we selected SNORD1B, highly expressed in HCC tissues, correlated with poor prognosis, and significantly suppressed upon 28-day FA deprivation for mechanistic investigation. We demonstrated that FA deficiency coordinately downregulated SNORD1B and its host gene SNHG16 ( < 0.05), with strong positive correlation (R = 0.5104, = 0.0465). This downregulation led to markedly reduced 2′-O-methylation at the G4362 site of 28S rRNA ( < 0.01) and impaired ribosomal activity. Expression of snoRNA-binding proteins (FBL, NOP58, NOP56) as well as IL-6 and CDK1 were significantly suppressed ( < 0.05), alongside decreased TP53 protein levels ( < 0.001). Functional assays confirmed that FA deficiency potently inhibited HepG2 proliferation and migration ( < 0.01). Our findings reveal a previously unrecognized mechanism: folate deficiency attenuates SNORD1B-dependent 2′-O-methylation of 28S rRNA, resulting in ribosomal dysfunction and suppression of global protein synthesis, thereby inhibiting HCC cell proliferation and migration. This study provides novel insight into the epigenetic-ribosomal axis of FA-mediated tumor suppression and highlights snoRNAs as potential therapeutic targets in HCC. - Source: PubMed
Publication date: 2026/03/23
Song XinxinKong DeyuZi YongjiaoWang XuNi Juan - : Recent findings underscore the importance of ribosome biogenesis, a complex molecular machinery, in cancer biology, highlighting opportunities for targeted treatment strategies. Here, we revealed that dysregulation of ribosome biogenesis is a distinctive feature of non-small lung cancer (NSCLC). However, further investigation is required to pinpoint which specific processes within this complex pathway are aberrant in this malignancy. : The expression levels and clinical significance of NOP56 in NSCLC were investigated by microarray analysis, qPCR, TCGA and GEO datasets. Function assays were conducted to explore the biological role of NOP56 in NSCLC cells. The mechanisms that mediate the upregulation of NOP56 were investigated by bisulfite DNA sequencing, luciferase reporter assay, chromatin immunoprecipitation and TCGA datasets. The downstream pathway of NOP56 was explored by RNA sequencing, qPCR, Western blot and luciferase reporter assay. : High expression of NOP56 was detected in NSCLC tissues and was associated with poor prognosis. Functional assays revealed that overexpression of NOP56 promoted NSCLC cellular proliferation, metastasis and ribosome biogenesis in vitro, and further accelerated tumorigenesis in vivo. Mechanistically, NOP56 activates MYC signaling by regulating IRES-dependent translation, which in turn transcriptionally upregulated NOP56 expression, creating a positive feedback loop. Additionally, hypomethylation also contributed to the upregulation of NOP56 in NSCLC. : Our study demonstrated that NOP56/MYC forms a positive feedback loop that enhances ribosome biogenesis and drives the progression of NSLSC, positioning NOP56 a promising therapeutic target for this malignancy. - Source: PubMed
Publication date: 2026/02/26
Zhu ChengjieZhang XuanchangZhang YiWei XiaoweiShang Yan - M2 macrophages significantly contribute to the advancement of prostate cancer (PCa). This research aims to pinpoint M2 macrophage-associated genes (M2RGs) by leveraging single-cell analyses, with a focus on evaluating their prognostic and therapeutic implications in PCa. - Source: PubMed
Publication date: 2026/02/27
Wu ZhikaiLi JianxinHu JintaoLai CongLi ZhuohangYu HaoYuan ZhihanDai MingzhouShi JuanyiLiu ChengXu Kewei - Chromosome dynamics, recombination, and nucleolar organization intersect during meiotic prophase I, yet how the recombination context influences nucleolar architecture remains unclear. We analyzed the nucleolar pool of Cdc14 in under matched prophase I gating and a uniform, frame-based operational definition of transient two-focus episodes. In a prophase-arrest reference, Cdc14-mCherry formed a predominant single nucleolar focus with occasional, reversible two-focus episodes that Nop56-GFP placed within the nucleolar compartment (nucleolar splitting). Splitting rose sharply when interhomolog recombination was compromised and remained elevated when Spo11 catalytic activity was abolished, indicating that increased DSB formation is not required and pointing instead to the homolog engagement state as a key variable. Population checkpoint readouts did not map onto the phenotype: Hop1 phosphorylation differed strongly across genotypes, yet splitting remained high in recombination-defective and DSB-free contexts and low in the reference. Timing analyses showed that events concentrated early and declined in the reference, whereas recombination-defective and DSB-free backgrounds retained activity into later windows across thresholds. We propose that nucleolar splitting reflects a rheological response of the nucleolus to chromosome-scale forces that vary with homolog engagement, consistent with contributions from DSB-independent chromosome dynamics such as telomere clustering, telomere-led rapid prophase movements, and centromere coupling/pairing. Together, these data support the nucleolus as a mesoscale, mechanically sensitive readout of meiotic chromosome dynamics. - Source: PubMed
Publication date: 2026/01/15
Rodríguez-Jiménez PatriciaAlonso-Ramos PaulaAcosta IsabelÁlvarez-Melo DavidCarballo Jesús A