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)
- Neural stem cells (NSCs) are the basis of neurogenesis and neural regeneration and are widely used as models for drug test and disease therapy. However, how NSCs self-renewal is modulated is not fully understood. In this study, we show that cytoskeletal Filamin A (FLNA) acts as a negative regulator in NSCs proliferation or self-renew. FLNA can be localized to the nucleoli of both NE-4C and C17.2 cell lines. FLNA silencing activated the expression of Pol Ⅰ products. In contrast, FLNA overexpression dampened rDNA transcription, suggesting that FLNA suppresses NSCs proliferation by downregulating Pol Ⅰ-directed transcription. Mechanistically, FLNA downregulates Pol I-directed transcription by inhibiting RRN3 expression and the occupancies of the Pol I transcription machinery factors at the rDNA promoter. In addition, FLNA suppresses NSCs proliferation by maintaining high levels of P53 and PTEN expression. Finally, we show that FLNA silencing does not affect the identity of neural stem cells, but inhibits neuronal differentiation from neural stem cells. These findings provide a novel insight into the mechanisms by which FLNA negatively regulates NSCs self-renew. - Source: PubMed
Publication date: 2026/07/21
Wu ZihuiZhou XiangyuSong XiaoyeWang YeYu DeenZhao ShashaDeng Wensheng - 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