Ask about this productRelated genes to: RC3H2 Blocking Peptide
- Gene:
- RC3H2 NIH gene
- Name:
- ring finger and CCCH-type domains 2
- Previous symbol:
- MNAB
- Synonyms:
- FLJ20301, FLJ20713, RNF164
- Chromosome:
- 9q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-20
- Date modifiied:
- 2016-10-05
Related products to: RC3H2 Blocking Peptide
Related articles to: RC3H2 Blocking Peptide
- Amyotrophic lateral sclerosis (ALS) is characterized by motor neuron degeneration and is in many cases associated with mutations in genes encoding RNA-binding proteins (RBPs), including fused in sarcoma (FUS) and heterogeneous nuclear ribonuclearprotein A1 (hnRNPA1). These mutations often cause cytoplasmic mislocalization and aggregation of these typically nuclear proteins. Current treatment options for ALS are limited, highlighting the need for new therapeutic strategies. Here, we demonstrate an approach using circular RNAs (circRNAs) to target disease-associated RBPs for degradation. We designed circRNAs containing binding sites for both the target RBPs (FUS or hnRNPA1) and ring finger and CCCH-type domains 2 (RC3H2), an RNA-binding E3 ubiquitin ligase. Through RNA immunoprecipitations and protein analyses, we show that these circRNAs can form ternary complexes with their target RBPs and RC3H2. Importantly, we observed significant reductions in steady-state protein levels of ALS-associated FUS-P525L (20%) and hnRNPA1-P288S (30%) mutants when treated with their respective targeting circRNAs. These findings provide proof of concept for using circRNAs as scaffolds to promote the degradation of disease-associated RBPs, establishing a foundation for developing advanced RNA-based therapeutic strategies for ALS and potentially other RBP-related diseases. - Source: PubMed
Publication date: 2025/06/26
Hollensen Anne KruseSørensen Matilde HelboThomsen Sofie VesterbækThomsen Henriette SylvainDamgaard Christian Kroun - Hepatocellular carcinoma (HCC), a leading cause of cancer-related mortality, is commonly treated with doxorubicin (DOX). However, its effectiveness varies significantly among patients. - Source: PubMed
Publication date: 2025/06/04
Shilbayeh Sireen Abdul RahimKhedr Naglaa FAlshabeeb Mohammad AAlsaleh Abdulmonem AliAlanizi Abdalrhman HamdanAbd El-Baset Omnia AWerida Rehab H - Atopic dermatitis is a common inflammatory skin disease which is treated with narrowband ultraviolet B (NB-UVB). Exploring the critical targeted genes in patients by UV radiation is the main aim of this study. Gene expression profiles of lesional and non-lesional skin samples of atopic dermatitis patients after treatment with NB-UVB and the non-irradiated samples were extracted from the Gene Expression Omnibus (GEO) database and analyzed via protein-protein interaction (PPI) network analysis to find the critical targeted genes. A total of 357 significant differentially expressed genes (DEGs) were included in the PPI network. CTNNB1, SRSF1, YWHAB, SMC3, GNB2, ARF3, UBL7, RAB2A, YWHAE, EIF5B, SNRPE, PPIG, RC3H2, CFL1, SMARCB1. LAPTM5, PRPF40A, and RBBP4 were introduced as hub-bottlenecks. In conclusion, five central genes including SMC3, ARF3, EIF5B, SMARCB1, and LAPTM5 were highlighted as the critical genes in response to NB-UVB radiation in the skin of the treated atopic dermatitis patients. The introduced crucial genes are involved in essential cellular functions such as apoptosis, cell cycle, cell proliferation, and inflammation. It seems that applied NB-UVB radiation is a suitable therapeutic method for atopic dermatitis disease. - Source: PubMed
Publication date: 2024/07/30
Rezaei Tavirani MostafaBandarian FatemehRazi FaridehRazzaghi ZahraArjmand BabakRostami Nejad Mohammad - Reactive oxygen species (ROS) are highly reactive and their accumulation causes oxidative damage to cells. Cells maintain survival upon mild oxidative stress with anti-oxidative systems, such as the kelch-like ECH-associated protein 1 (Keap1)-nuclear factor erythroid 2-related factor 2 (Nrf2) system. On the other hand, upon severe oxidative stress, cells undergo regulated cell death, including apoptosis, for eliminating damaged cells. To execute efficient cell death, cells need to turn off the anti-oxidant systems, while triggering cell death. However, it remains unknown how cells orchestrate these two conflicting systems under excessive oxidative stress. Herein, we show that when cells are exposed to excessive oxidative damage, an E3 ubiquitin ligase Roquin-2 (also known as RC3H2) plays a key role in switching cell fate from survival to death by terminating activation of transforming growth factor-β-activated kinase 1 (TAK1), a positive regulator for Nrf2 activation. Roquin-2 interacted with TAK1 via four cysteine residues in TAK1 (C96, C302, C486, and C500) that are susceptible to oxidative stress and participate in oligomer formation via disulfide bonds, promoting K48-linked polyubiquitination and degradation of TAK1. Nrf2 was inactivated upon lethal oxidative stress in wild-type mouse embryonic fibroblast (MEF) cells, whereas it sustained activation and conferred resistance to Roquin-2 deficient cells, which was reversed by pharmacological or genetic inhibition of TAK1. These data demonstrate that in response to excessive ROS exposure, Roquin-2 promotes ubiquitination and degradation of TAK1 to suppress Nrf2 activation, and thereby contributes to an efficient cell death, providing insight into the pathogenesis of oxidative stress-related diseases, including cancer. - Source: PubMed
Publication date: 2024/05/08
Hirata YusukeNakata YuyaKomatsu HiromuKudoh YukiTakahashi MikiTaguchi SomaNoguchi TakuyaMatsuzawa Atsushi - Suicide is a societal and public health concern of global scale. Identifying genetic risk factors for suicide attempt can characterize underlying biology and enable early interventions to prevent deaths. Recent studies have described common genetic variants for suicide-related behaviors. Here, we advance this search for genetic risk by analyzing the association between suicide attempt and uncommon variation exome-wide in a large, ancestrally diverse sample. - Source: PubMed
Publication date: 2023/12/21
Wilkerson Matthew DHupalo DanielGray Joshua CZhang XijunWang JiaweiGirgenti Matthew JAlba CamilleSukumar GauthamanLott Nathaniel MNaifeh James AAliaga PabloKessler Ronald CTurner ClessonPollard Harvey BDalgard Clifton LUrsano Robert JStein Murray B