Ask about this productRelated genes to: RFC5 Blocking Peptide
- Gene:
- RFC5 NIH gene
- Name:
- replication factor C subunit 5
- Previous symbol:
- -
- Synonyms:
- RFC36
- Chromosome:
- 12q24.23
- Locus Type:
- gene with protein product
- Date approved:
- 1994-10-14
- Date modifiied:
- 2016-10-05
Related products to: RFC5 Blocking Peptide
Related articles to: RFC5 Blocking Peptide
- Sliding clamps like PCNA are crucial processivity factors for replicative polymerases, requiring specific clamp loaders for loading onto DNA. The human alternative clamp loader CTF18-RFC interacts with the leading strand polymerase Pol ε and loads PCNA onto primer/template DNA using its RFC pentameric module. Here, we provide a structural characterization of the human CTF18-RFC complex and its interaction with PCNA. Our cryo-EM data support that the Ctf8 and Dcc1 subunits of CTF18-RFC, which form the regulatory module interacting with Pol ε, are flexibly tethered to the RFC module. A 2.9 Å cryo-EM structure shows the RFC module bound to PCNA in an autoinhibited conformation similar to the canonical RFC loader, marking the initial step of the clamp-loading reaction. The unique RFC1 (Ctf18) large subunit of CTF18-RFC, which based on the cryo-EM map shows high relative flexibility, is anchored to PCNA through an atypical low-affinity PIP box in the AAA+ domain and engages the RFC5 subunit using a novel β-hairpin at the disordered N-terminus. We show that deletion of this β-hairpin impairs the CTF18-RFC-PCNA complex stability, slows down clamp loading, and decreases the rate of primer synthesis by Pol ε. Our research identifies distinctive structural characteristics of the human CTF18-RFC complex, providing insights into its role in PCNA loading and the stimulation of leading strand synthesis by Pol ε. - Source: PubMed
Publication date: 2026/02/23
Briola Giuseppina RTehseen MohammadAl-Amodi AmaniYoung GraceDanazumi Ammar UNguyen Phong QuocSavva Christos GHedglin MarkHamdan Samir MDe Biasio Alfredo - Diffuse large B-cell lymphoma (DLBCL) is a heterogeneous disease that requires more reliable prognostic biomarkers. In this study, bioinformatic analysis identified replication factor C 5 (), one of the DNA repair-related gene, as a potential novel oncogene in DLBCL. Analysis of public datasets and immunohistochemical staining showed that expression was significantly higher in tumor samples than in normal samples. High expression was associated with worse prognostic clinical features. Notably, there was a difference in overall survival (OS) between the high- and low- expression groups. Multivariate Cox regression analyses showed that was an independent risk factor associated with poorer OS. Furthermore, correlations were observed between expression in DLBCL and TIME(Tumor Immune Microenvironment), as well as immune cell infiltration, cytokine levels, cytokine receptor expression, and immune checkpoint activity. Gene set enrichment analysis (GSEA) analysis revealed that the elevated expression group showed significant enrichment in multiple tumor signaling pathways. These results suggest that may contribute to the pathogenesis of DLBCL by modulating these critical molecular pathways. Our findings indicate that may be a novel prognostic biomarker for DLBCL. - Source: PubMed
Publication date: 2025/12/07
Tian ZuguoLiu ShuiyuWeng ChunlanRen Mingqiang - The capacity of tumor cells to repair DNA damage is closely associated with their resistance to radiotherapy and chemotherapy. Our investigation demonstrated elevated RFC5 levels within nasopharyngeal carcinoma (NPC) cells and is involved in DNA damage repair. Mechanistic studies revealed that high RFC5 expression in NPC cells reduces the formation of micronuclei during cisplatin treatment, thereby suppressing cGAS-STING signaling activation and limiting inflammatory mediator production, which in turn promotes tumor progression. In in vivo experiments, tumors with high RFC5 expression showed reduced secretion of IFN-γ and TNF-α by CD8T cells in the tumor immune microenvironment, along with enhanced PD-1, LAG-3, and CTLA-4 expression, leading to T cell exhaustion. Our findings suggest that RFC5 enhances the repair of cisplatin-induced DNA damage and promotes immune evasion, suggesting RFC5 is a promising therapeutic candidate for enhancing treatment outcomes in radiotherapy and chemotherapy. - Source: PubMed
Publication date: 2025/11/04
Han YumoMiao MengyuShan YingZhou YongPan SiZhu RuiYuan LingZhu ZiyuZhang Jie - Sliding clamps like PCNA are crucial processivity factors for replicative polymerases, requiring specific clamp loaders for loading onto DNA. The human alternative clamp loader CTF18-RFC interacts with the leading strand polymerase Pol ε and loads PCNA onto primer/template DNA using its RFC pentameric module. Here, we provide a structural characterization of the human CTF18-RFC complex and its interaction with PCNA. Our cryo-EM data support that the Ctf8 and Dcc1 subunits of CTF18-RFC, which form the regulatory module interacting with Pol ε, are flexibly tethered to the RFC module. A 2.9 Å cryo-EM structure shows the RFC module bound to PCNA in an autoinhibited conformation similar to the canonical RFC loader, marking the initial step of the clamp-loading reaction. The unique RFC1 (Ctf18) large subunit of CTF18-RFC, which based on the cryo-EM map shows high relative flexibility, is anchored to PCNA through an atypical low-affinity PIP box in the AAA+ domain and engages the RFC5 subunit using a novel β-hairpin at the disordered N-terminus. We show that deletion of this β-hairpin impairs the CTF18-RFC-PCNA complex stability, slows down clamp loading, and decreases the rate of primer synthesis by Pol ε. Our research identifies distinctive structural characteristics of the human CTF18-RFC complex, providing insights into its role in PCNA loading and the stimulation of leading strand synthesis by Pol ε. - Source: PubMed
Publication date: 2025/11/05
Briola Giuseppina RTehseen MuhammadAl-Amodi AmaniYoung GraceDanazumi Ammar UNguyen Phong QuocSavva Christos GHedglin MarkHamdan Samir MDe Biasio Alfredo - Olaparib exhibits antitumor effects in castration-resistant prostate cancer patients with germline mutations in DNA repair genes. We previously reported that simvastatin reduced the expression of DNA repair genes in PC-3 cells. The efficacy of combination therapy using olaparib and simvastatin as "BRCAness" in castration-resistant and taxane-resistant prostate cancers was evaluated in this study. - Source: PubMed
Publication date: 2025/03/21
Sekine YoshitakaOka DaisukeOhtsu AkiraNakayama HiroshiMiyao TakeshiMiyazawa YoshiyukiArai SeijiKoike HidekazuMatsui HiroshiShibata YasuhiroSuzuki Kazuhiro