Ask about this productRelated genes to: ADARB1 antibody
- Gene:
- ADARB1 NIH gene
- Name:
- adenosine deaminase RNA specific B1
- Previous symbol:
- -
- Synonyms:
- ADAR2, DRADA2, ADAR2g, DRABA2, RED1, hRED1, ADAR2a-L1, ADAR2a-L2, ADAR2a-L3, ADAR2a, ADAR2b, ADAR2c, ADAR2d
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-02
- Date modifiied:
- 2019-01-18
Related products to: ADARB1 antibody
Related articles to: ADARB1 antibody
- Adenosine-to-inosine (A-to-I) RNA editing has been found to function in various neurological disorders; however, the role of A-to-I RNA editing in retinitis pigmentosa (RP) remains unclear. - Source: PubMed
Publication date: 2026/05/15
Ren Chun-YanZhang Yi-ChenYao JinPingGuo TaoChang LeiChen Jian-HuanLiu Yanshan - The adenosine deaminase acting on RNA (ADAR) enzymes deaminate adenosine to inosine in double-stranded (ds)RNA. Mammals express two catalytically active enzymes: ADAR1, which is ubiquitously expressed and essential for innate immune homeostasis, and ADAR2, which is enriched in the brain and vascular system. Here, we investigate the ADAR2 interactome and uncover a shared interaction network with ADAR1, including multiple components of the RNA exosome complex, a multi-subunit RNase involved in RNA processing, turnover, and surveillance. The interactions between ADARs and RNA exosome components are nuclear, and resistance to RNase A treatment implies their close proximity. We validated these interactions by immunoprecipitation of both endogenous and epitope-tagged ADAR proteins in multiple cell lines and mapped the interaction interfaces to their dsRNA-binding domains. Exploiting an MS2-MCP tethering system, we show that recruitment of ADAR1 or ADAR2 to the 3' UTR of a reporter transcript decreases its stability. This decrease in RNA levels was reversed when EXOSC3 was depleted, demonstrating that this destabilizing effect of ADARs on RNA is via the RNA exosome complex. Finally, knockdown of ADARs perturbs rRNA processing, a canonical function of the nuclear exosome, demonstrating a cellular consequence of disrupting ADAR-exosome interactions. - Source: PubMed
Vukić DraganaDu QiupeiCherian AnnaAmoruso DamianoBrožinová KvětoslavaWacheul LudivineLacovich ValentinaZorbas ChristianeYadav LeenaSedmík JiříKeskitalo SallaHajji KhadijaStejskal StanislavVarjosalo MarkkuLafontaine Denis L JKeegan Liam PO'Connell Mary A - Fuchs endothelial corneal dystrophy (FECD) is a degenerative disease characterized by progressive loss of corneal endothelial cells, yet the role of adenosine-to-inosine (A-to-I) RNA editing mediated by adenosine deaminases acting on RNA (ADARs) remains unelucidated. Our current study aimed to investigate the A-to-I editome in FECD and its underlying epigenetic mechanisms. - Source: PubMed
Yang Kai-TongPan Jia-QiJin Yun-YunMa Le-TongHe Yu-ShanChen Jian-Huan - Osteosarcoma is a highly malignant bone tumor which primarily affects the juvenile population and is characterized by high rate of recurrence and metastasis. RNA editing has emerged as a key process in cancer progression. Herein, we investigated the role of RNA editing enzyme ADAR2 (Adenosine Deaminase Acting on RNA 2) in osteosarcoma. We demonstrated that ADAR2 expression increases during osteoblast differentiation and inversely correlates with the aggressiveness of osteosarcoma cells. Interestingly, the overexpression of ADAR2 in osteosarcoma cell lines reduces their tumoral properties and promotes their differentiation in osteoblast-like cells, as shown by gene expression analysis and mineralization assays. These results were also confirmed by in vivo experiments; indeed, intratibial injection of ADAR2-overexpressing osteosarcoma cells in NSG mice resulted in less aggressive tumors compared to mice injected with pEmpty or pInactive ADAR2 E/A vector-transfected cells. To elucidate the mechanisms by which ADAR2 overexpression induces osteogenic terminal differentiation of osteosarcoma cells, we performed RNA-seq analysis of Saos-2 cells and identified IGFBP7 (Insulin-like Growth Factor Binding Protein 7) as the most highly edited transcript in ADAR2-overexpressing cells. We showed that the editing activity of ADAR2 on IGFBP7 abolishes its proliferative effect on osteosarcoma cells and triggers terminal differentiation. Overall, our results indicate that ADAR2 acts as a tumor suppressor in osteosarcoma and may represent a novel therapeutic target for this aggressive pediatric tumor. - Source: PubMed
Publication date: 2026/04/03
Rossi MichelaScotto di Carlo FedericaDi Gregorio JacopoRusso SharonDi Giuseppe LauraBattafarano GiuliaTerreri SaraPagliarosi OliviaSilvestris Domenico AlessandroCorona MarcoBarra AdrianoPezzullo MarcoDe Stefanis CristianoPelle SimoneCostici Pier FrancescoMinisola SalvatorePepe JessicaLocatelli FrancoGianfrancesco FernandoGallo AngelaDel Fattore Andrea - Understanding how chromosome 21 gene dosage contributes to neurodevelopmental phenotypes in trisomy 21 (T21) remains a fundamental challenge. Here, we perform transcriptome-wide RNA-sequencing of fetal cortical and hippocampal tissues from T21 cases and euploid controls collected during mid-gestation, a critical window for human brain development. We identify widespread gene expression dysregulation with significant enrichment for chromosome 21 genes and perturbation of neurodevelopmental, synaptic, and immune-related pathways. Among the most strongly dysregulated genes is ADARB1, a chromosome 21-encoded RNA editing enzyme, whose overexpression associates with increased adenosine-to-inosine RNA editing, with consistent over-editing at functionally important recoding sites in glutamate and GABA receptor-related genes, including GRIK2, GRIA2, GRIA3, and GABRA3, across cortex and hippocampus. Meta-analyses across independent transcriptomic datasets validate robust chromosome 21 dosage effects, including ADARB1 overexpression and over-editing at 3'UTRs and GRIA3. These findings implicate dysregulated RNA editing as a post-transcriptional mechanism contributing to fetal neuropathology in T21. - Source: PubMed
Publication date: 2026/03/31
Breen Michael SYang AndyWang XuranRodriguez de Los Santos MiguelTao RanWeinberger Daniel RKleinman Joel EMihova KalinaStancheva GerganaSavova SylviaKaneva RadkaDimitrova VioletaVladimirov VladimirHyde Thomas MBuxbaum Joseph D