RRN3 antibody - C-terminal region (ARP34462_P050)
- Known as:
- RRN3 (anti-) - C-terminal region (ARP34462_P050)
- Catalog number:
- arp34462_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RRN3 antibody - C-terminal region (ARP34462_P050)
Related genes to: RRN3 antibody - C-terminal region (ARP34462_P050)
- Gene:
- RRN3 NIH gene
- Name:
- RRN3 homolog, RNA polymerase I transcription factor
- Previous symbol:
- -
- Synonyms:
- DKFZp566E104, TIF-IA
- Chromosome:
- 16p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-08-19
- Date modifiied:
- 2015-07-22
Related products to: RRN3 antibody - C-terminal region (ARP34462_P050)
Related articles to: RRN3 antibody - C-terminal region (ARP34462_P050)
- RRN3 is a nucleolar protein required for ribosome biogenesis, but its role in cancer remains insufficiently defined. This study aimed to systematically evaluate the clinical relevance, molecular characteristics, immune-related features, and biological function of RRN3 across cancers, with a particular focus on gastric cancer (GC). - Source: PubMed
Publication date: 2026/05/22
He RuofanXing QingqingLiu SongyiLin ShiweiLin XiangYe Jianxin - Early growth response 1 (EGR1) was identified as a positive regulator in Pol II- and Pol Ⅲ-directed transcription. Whether EGR1 modulates Pol Ⅰ-directed transcription remains unknown. Here, we report that EGR1 is present in the nucleoli of several cancer cell lines. EGR1 positively regulates the synthesis of Pol Ⅰ products and the proliferation of HeLa, HePG2, and AGS cells both in vitro and in vivo. EGR1 silencing increased R-loop formation and lncRNA PAPAS expression, which inversely correlated with Pol Ⅰ product levels. Mechanistically, EGR1 enhances the recruitment of Pol I transcription machinery factors to the rDNA promoter through interactions with these factors. The EGR1 DNA-binding domain mediates the interaction between EGR1 and Pol I machinery components. EGR1 activates RRN3 gene transcription by binding to the RRN3 gene promoter. Thus, EGR1 promotes Pol Ⅰ-directed transcription and cancer cell growth by both interacting with Pol I machinery factors and controlling RRN3 expression. - Source: PubMed
Publication date: 2026/01/09
Song XiaoyeXia WenxinZhang JiandongWu ZhongyuZeng HuatingYang YouWang YeYu DeenZhao ShashaGuo BaoqiangDeng Wensheng - Stress-induced alternative processing of mRNA is emerging as an essential mechanism to drive almost every hallmark of cancer. Through a genome-wide screening based on an abnormal transcriptional readthrough event favoring the malignant progression of ovarian carcinoma (OC), we identified novel mRNA processing regulators including RRN3, an essential factor for the transcriptional initiation of rRNA. The long-read RNA sequencing and PAR-CLIP analyses revealed that RRN3 was involved in the usage of alternative polyadenylation (APA) sites, resulting in the altered stability of autophagy-related mRNAs. More interestingly, we discovered that nutrient-deprivation-induced phosphorylation of RRN3 at serine 199 was sufficient to divert RRN3 out of the nucleolus to the nuclear plasma, where RRN3 regulated the APA of autophagy mRNAs, such as OPTN, to enhance their stability and eventually promoted autophagy. Further in vivo experiments showed that nutrient-stress-triggered switch of RRN3 from rRNA transcription to APA regulation was essential for the growth and dissemination of OC in mice. - Source: PubMed
Publication date: 2025/11/21
Lv JianyingWang ShuoLiu TianxiangLiu YiBai YutingQu Wei-AoDing JixuanChen ZhiqiangLiu YanhuaChen YananLi JiaLi JianDing WeiPiao YongjunXiang RongZeng BeileiWang LonglongShi Yi - Aberrant upregulation of RNA polymerase I (Pol I) transcription and its dedicated machinery plays a pivotal role in tumor progression and chemoresistance. RRN3, a Pol I-specific transcription initiation factor, is frequently overexpressed in malignancies contributing to oncogenic processes. Despite the therapeutic potential of Pol I transcription inhibition, existing inhibitors lack specificity and are associated with DNA damage, mutagenicity, and toxicity, limiting their clinical utility. To fully realize the potential of Pol I-targeted cancer therapies, selective Pol I transcription inhibitors with minimal off-target effects are essential. - Source: PubMed
Publication date: 2025/10/20
Sarkar Shashanka ShekharSharma MansiKarmakar ArpitaJahan KousarSaproo SheetanshuBiswas SoumojitNautiyal SakshiRoy IpsitaBharatam P VNaidu Srivatsava - Ribosome biogenesis is essential for the rapid proliferation and life cycle transitions of Plasmodium falciparum, the causative agent of malaria. In eukaryotes, ribosomal RNA synthesis is carried out by RNA polymerase I (Pol I), highly specialized transcriptional machinery. This review provides a comparative analysis of Pol I transcription apparatus in yeast and humans, serving as a reference framework to examine its evolutionary divergence in P. falciparum and related apicomplexans and alveolates. Bioinformatic analyses revealed that some of these organisms lack any identifiable homologues or orthologs of several canonical eukaryotic transcription factors essential for Pol I-mediated transcription, including initiation factor RRN3, activator UBF, and all specific subunits of the promoter recognition complexes. Interestingly, the parasite retains core Pol I subunits, incorporating unique parasite-specific structural domains characterized through AI-based protein complex modeling of P. falciparum Pol I. These adaptations may compensate for the absence of traditional regulatory factors, enabling the parasite to employ distinct mechanisms for promoter recognition and transcription initiation. The substantial differences between parasite and host Pol I transcription machinery create potential targets for therapeutic intervention with parasite-specific elements representing potential drug targets. By integrating evolutionary, structural, and functional perspectives, this review advances our understanding of Pol I transcription in alveolates and its implications for the development of novel antimalarial strategies. - Source: PubMed
Mair GunnarDaiß Julia LEngel ChristophPanov Konstantin I