ADARB1
- Known as:
- ADARB1
- Catalog number:
- 001181A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADARB1
Related genes to: ADARB1
- 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
ADAP2 Gene ArfGAP with dual PH domains 2ADAR2,ADARB1,Double-stranded RNA-specific editase 1,DRADA2,dsRNA adenosine deaminase,Homo sapiens,Human,RED1,RNA-editing deaminase 1,RNA-editing enzyme 1Adar2,Adarb1,Double-stranded RNA-specific editase 1,dsRNA adenosine deaminase,Mouse,Mus musculus,Red1,RNA-editing deaminase 1,RNA-editing enzyme 1ADARB1 ADAR2 antibody Ab host: RabbitADARB1 ADAR2 antibody Ab host: RabbitADARB1 ADAR2 antibody Ab host: RabbitADARB1 ADAR2 IgG antibody Ab host: SheepADARB1 (Human) Recombinant Protein (Q01)ADARB1 / ADAR2 antibody Host rabbitADARB1 / ADAR2 antibody Host rabbitADARB1 / ADAR2 antibodyADARB1 / ADAR2 antibody Host rabbitADARB1 / ADAR2 antibody Host rabbitADARB1 / ADAR2 antibody Isotype IgG Host SheepADARB1 / ADAR2 antibody Host Rabbit Related articles to: ADARB1
- 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 - The RNA-editing proteins ADAR and ADARB1 regulate gene expression through both editing-dependent and editing-independent mechanisms. RNA-Seq analysis of HepaRG cells after knocking down (KD) either protein caused widespread transcriptomic changes, including nearly 1,000 pharmacogenes that were either differentially expressed or alternatively spliced, with isoform switches observed in HNF4A and CYP2C9. These effects were editing-independent, and the two treatments primarily affected distinct gene sets, with ADAR KD having broader effects than ADARB1 KD. Because ADAR KD triggers a type I interferon response, we compared siADAR and IFNα treatments. Although both activated interferon signaling, their transcriptional profiles differed markedly. Despite this, 70% of siADAR-responsive genes were rescued by BX795, an inhibitor of the interferon pathway. Therefore, many of siADAR’s effects are likely due to the activation of immune pathways. Overall, our findings indicated that the ADARs maintain hepatic homeostasis and regulate numerous pharmacogenes, especially those involved in drug metabolism and disposition. - Source: PubMed
Publication date: 2026/03/11
Collins Joseph MYu FahongZhang YanpingWang Danxin