Ask about this productRelated genes to: ADAR antibody
- Gene:
- ADAR NIH gene
- Name:
- adenosine deaminase RNA specific
- Previous symbol:
- IFI4, G1P1
- Synonyms:
- ADAR1
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-12-12
- Date modifiied:
- 2019-04-23
- 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
- Gene:
- ADARB2 NIH gene
- Name:
- adenosine deaminase RNA specific B2 (inactive)
- Previous symbol:
- -
- Synonyms:
- RED2, hRED2, ADAR3
- Chromosome:
- 10p15.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-02
- Date modifiied:
- 2019-01-18
Related products to: ADAR antibody
Related articles to: ADAR antibody
- ADAR1 (), ADAR2 (), and ADAR3 () are deaminase adenosine RNA-specific enzymes that play a significant role in RNA metabolism. ADAR1 () and ADAR2 () catalyze A-to-I editing and ADAR3 () plays a regulatory role. The role of these three genes still remains unknown in head and neck cancers (HNSCC). The aim of this study is to reveal the role of deaminase adenosine RNA-specific enzymes in pathomechanisms of HNSCC and to investigate their potential utility as diagnostic and/or prognostic biomarkers. The quantitative PCR analysis was conducted using RNA isolated from 22 pairs of matched tumor and adjacent normal tissues, 76 formalin-fixed paraffin-embedded (FFPE) tumor samples, and a panel of HNSCC cell lines (DOK, SCC-25, SCC-40, FaDu, and CAL-27). In parallel, transcriptomic and clinical data from the Cancer Genome Atlas HNSCC cohort were analyzed. Patients were stratified into high- and low-expression groups, and statistical assessments included overall survival and progression-free interval analyses, evaluation of gene expression in relation to clinicopathological parameters, correlation with other genes, and functional pathway exploration using gene set enrichment analysis. ADARB2 was significantly downregulated in HNSCC tumor tissues compared to adjacent normal mucosa ( = 0.044), with discriminatory potential to distinguish malignant from non-malignant tissues (AUC = 0.692, = 0.029). TCGA data confirmed ( < 0.0001) and ( < 0.0001) upregulation in tumors, while was markedly reduced ( = 0.04). Patients with high expression showed significantly longer overall survival (pa = 0.0121; pb = 0.0098), with a trend toward improved progression-free survival (pb = 0.0681). Subsite analysis revealed high expression correlated with poor OS in pharyngeal tumors ( < 0.05), whereas high expression was linked to improved DFS (pa = 0.0023, pb = 0.0047). GSEA indicated that low expression was enriched in oncogenic pathways, including Wnt/β-catenin ( = 0.006), MYC targets ( = 0.009), and TGF-β1 ( = 0.009). expression was significantly reduced in HNSCC tumor tissues compared to normal mucosa and demonstrated strong discriminatory power for distinguishing malignant from non-malignant samples. High expression was associated with markedly improved overall survival, whereas low expression correlated with enrichment of oncogenic pathways, including Wnt/β-catenin, Notch, and Hedgehog, consistent with a poorer clinical prognosis. These findings highlight as a promising diagnostic biomarker and independent prognostic factor in HNSCC. - Source: PubMed
Publication date: 2025/11/02
Kolenda TomaszBiałas PiotrPoter PaulinaJaniczek-Polewska MarlenaZapłata AnnaGuglas KacperMantaj PatrycjaPrzybyła AnnaKazimierczak UrszulaLeporowska EwaCybulski ZefirynTeresiak Anna - Transarterial chemoembolization (TACE) is the commonly used therapy of unresectable hepatocellular carcinoma (HCC), though the prognosis of different TACE-treated HCC patients varies, which may be due to the heterogeneity of HCC tumors caused by genetic variants and epigenetic changes such as RNA editing. There is dysregulated RNA adenosine-to-inosine (A-to-I) editing in HCC and RNA-edited genes are involved in the epigenetic process. It remains unclear how genetic variants of RNA editing genes affect the prognosis of HCC cases treated by TACE. - Source: PubMed
Publication date: 2023/03/18
Zeng JiajiaHan LinyuWang TengHuang LinyingZheng YanxiuZhang NashaLi ZiqiangYang Ming - Papillary thyroid cancer (PTC) is one of the histological subtypes of thyroid cancer which is the most common endocrine malignancy in the world. The disrupted balance of the adenosine-to-inosine (A-to-I) RNA editing due to dysregulation of the editing genes exists in thyroid cancer. However, it is still largely unknown how functional single-nucleotide polymorphisms (SNPs) in the A-to-I RNA editing genes contribute to PTC genetic susceptibility. In this study, we systematically annotated and investigated the role of 28 potential functional SNPs of ADAR, ADARB1, ADARB2 and AIMP2 in PTC. We identified ADARB2 rs904957 and rs1007147 genetic variants which are associated with significantly elevated PTC risk in two case-control sets consisting of 2020 PTC cases and 2021 controls. Further investigations disclosed that ADARB2 could inhibit cell viability and invasion capabilities of PTC cells as a novel tumor suppressor. The ADARB2 rs904957 thymine-to-cytosine (T-to-C) polymorphism in gene 3'-untranslated region enhances miR-1180-3p-binding affinity and represses ADARB2 expression through an allele-specific manner. In line with this, carriers with the rs904957 C allele correlated with decreased tumor suppressor ADARB2 expression in tissue specimens showed notably increased risk of developing PTC compared to the T allele carriers. Our findings highlight that the A-to-I RNA editing gene ADARB2 SNPs confer PTC risk. Importantly, these insights would improve our understanding for the general roles of RNA editing and editing genes during cancer development. - Source: PubMed
Publication date: 2022/12/13
Li WenwenWang TengFu GuobinXu YuanZhang NashaHan LinyuYang Ming - The adenosine-to-inosine (A-to-I) RNA editing controlled by the editing genes are known to diversify transcripts in human. Aberrant A-to-I editing due to dysregulation of the editing genes are involved in cancer development. However, it is still largely unclear how single nucleotide polymorphisms (SNPs) in the A-to-I editing genes confer to recurrence and/or drug resistance of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) therapy in non-small-cell lung cancer (NSCLC). - Source: PubMed
Publication date: 2022/02/22
Hua HuiZeng JiajiaXing HaixinHe YuxinHan LinyuZhang NashaYang Ming - RNA-editing by adenosine deaminases acting on RNA (ADARs) converts adenosines to inosines in structured RNAs. Inosines are read as guanosines by most cellular machineries. A to I editing has two major functions: first, marking endogenous RNAs as "self", therefore helping the innate immune system to distinguish repeat- and endogenous retrovirus-derived RNAs from invading pathogenic RNAs; and second, recoding the information of the coding RNAs, leading to the translation of proteins that differ from their genomically encoded versions. It is obvious that these two important biological functions of ADARs will differ during development, in different tissues, upon altered physiological conditions or after exposure to pathogens. Indeed, different levels of ADAR-mediated editing have been observed in different tissues, as a response to altered physiology or upon pathogen exposure. In this review, we describe the dynamics of A to I editing and summarize the known and likely mechanisms that will lead to global but also substrate-specific regulation of A to I editing. - Source: PubMed
Publication date: 2021/07/01
Vesely CorneliaJantsch Michael F