anti-Adenosine Deaminase, RNA-Specific, B1 (ADARB1) Antibodies

Human Adenosine Deaminase, RNA-Specific, B1 (ADARB1) interaction partners

1. Adenosine-to-inosine editing in human miRNAs is enriched in seed sequence, influenced by sequence contexts and significantly hypoedited in glioblastoma multiforme, which correlated with downregulation of ADAR2.

2. This study investigates the genome-wide binding preferences of the nuclear constitutive isoforms ADAR1-p110 and ADAR2 on human miRNA species by RNA immunoprecipitation of ADAR-bound small RNAs .

3. The deaminase domain-RNA contact surfaces are reviewed and models of how full length ADARs, bearing double stranded RNA-binding domains (dsRBDs) and deaminase domains, could process naturally occurring substrate RNAs are presented.

4. 2-way interaction between TPH2 rs4290270 and general traumas revealed that TT homozygotes with history of general traumas had an increased risk for suicide attempt. 3-way interaction of general traumas, TPH2 rs4290270 and ADARB1 rs4819035 indicated that highest predisposition to suicide attempt was observed in individuals who experienced general traumas and were TT homozygote for rs4290270 and TT homozygote for rs4819035.

5. The range of human disease associated with ADAR1 mutations may extend further to include other inflammatory conditions while ADAR2 mutations may affect psychiatric conditions.

6. Four crystal structures of the human ADAR2 deaminase domain bound to RNA duplexes bearing a mimic of the deamination reaction intermediate.

7. we determined the importance of specific amino acids at 19 different positions in the ADAR2 5' binding loop and revealed six residues that provide essential structural elements supporting the fold of the loop and key RNA-binding functional groups. This work provided new insight into RNA recognition by ADAR2 and established a new tool for defining structure-function relationships in ADAR reactions.

8. Data indicate that ADAR2 suppresses tumor growth and induces apoptosis by editing and stabilizing IGFBP7 in esophageal squamous cell carcinoma.

9. These findings suggest that adenosine deaminase acting on RNA 2 is subject to different regulations by DNA methyltransferase and histone deacetylase enzymes in neuronal SH-SY5Y cells.

10. These data suggest that, like ADAR2, underlying sequences in dsRNA may influence how NF90 recognizes its target RNAs

11. Detailed structural analysis indicates that the minor groove width of dsRNA and global shape of RNA may play an important role in the specific reading mechanism of ADAR2.

12. A-to-I RNA editing levels catalyzed by ADAR1 and ADARB1 decreased in Alzheimer's disease patients' brain tissues, mainly in the hippocampus and to a lesser degree in the temporal and frontal lobes.

13. we conclude that this aberrant alternative splicing pattern of ADAR2 downregulates A-to-I editing in glioma

14. ADARB1 rs9983925 and rs4819035 and HTR2C rs6318 were associated with suicide attempt risk.

15. Therefore, the expression of ADAR1 and ADAR2 was analyzed in chordoma tissues. It was found that ADAR1 was significantly overexpressed, which was accompanied by enhanced pre-miR-10a and pri-miR-125a A-to-I editing

16. ADAR2 is a key factor for maintaining edited-miRNA population and balancing the expression of several essential miRNAs involved in cancer.

17. Data show that a large fraction of the edited genes are positively correlated ADAR (ADAR1) and ADARB1 (ADAR2).

18. The ADAR2 alternative splicing variants may be correlated with the invasiveness of gliomas.

19. Characterization of the ADAR2 catalytic domain-RNA interaction.

20. ADAR2-mediated editing of the complementary antisense transcripts is a novel mechanism for regulating the biogenesis of specific miRNAs during hepatocarcinogenesis.

Mouse (Murine) Adenosine Deaminase, RNA-Specific, B1 (ADARB1) interaction partners

1. FMRP inhibits ADAR2 activity, absence of FMRP results in defects of RNA editing of neuronal mRNAs in the mouse model of Fragile X Syndrome.

2. ADARB1 mediates adenosine to inosine RNA editing in the testis, and these editing events are dispensable for male fertility in an inbred mouse strain in the lab.

3. that ADAR2 is a mediator of injury-induced tactile allodynia and thus a potential therapeutic target for the treatment of neuropathic pain

4. Results show that ADAR2 is important in site-specific changes of protein coding sequences but has relatively modest effects on gene expression and splicing in the adult mouse frontal cortex.

5. Thus, Adarb1 and Adarb2 have nearly exclusive expression within brain tissue, while Adar has more appreciable expression across multiple tissues.

6. After fear conditioning protocol, mRNA expression of ADAR2 increased in amygdala and hippocampus, and those mice had a learning-dependent increase in the alternatively spliced inactive form of ADAR2 in the amygdala.

7. ADAR2 is a key factor for maintaining edited-miRNA population and balancing the expression of several essential miRNAs involved in cancer.

8. This study clearly demonstrates that ADAR2 influences miRNA abundance and targeting at several levels in the mouse brain.

9. chronically elevated intraocular pressure in adult mice reduces expression of the ADAR2 enzyme.

10. Analysis of editing in the filamin A encoding mRNA shows very high editing levels outside the nervous system; further shows FLNA editing is mainly achieved by ADAR2 but that in some cases ADAR1 can efficiently compensate for ADAR2.

11. Results suggest that ADAR2-reduction is associated with progressive deterioration of nuclear architecture, resulting in vacuolated nuclei due to a Ca2+-permeable AMPA receptor-mediated mechanism

12. altered RNA editing efficiency of AMPA receptors due to down-regulation of ADAR2 has a possible role in the pathophysiology of mental disorders.

13. Goal-oriented overeating behavior of ADAR2 transgenic mice is associated with altered feeding, reward-related mRNAs and hyperactive brain mesolimbic region.

14. The JNK1 pathway may be functionally linked to the nutrient-sensing actions of ADAR2-mediated RNA editing in professional secretory cells.

15. Study show co-occurrence of TDP-43 mislocalization with reduced activity of an RNA editing enzyme, ADAR2, in aged mouse motor neurons.

16. miRNA abundance and miRNA processing are mainly influenced by ADARB1; an additional loss of ADAR has only a minor effect on expression of mature miRNAs.

17. Through these gene knockout animal models we demonstrated for the first time that ADAR1 is an essential molecule for skin integrity.

18. These results altogether suggest that altered 5HT(2C) R function could be contributing to enhanced depression-like behavior of ADAR2 transgenic mice and further implicate ADAR2 as a contributing factor in cases of affective disorder.

19. ADAR2 protein levels and catalytic activity are coordinately regulated in a positive manner by Pin1 and negatively by WWP2 and this may have downstream effects on the function of glutamate receptor 2.

20. These results provide evidence that ADAR1, and not ADAR2, is the deaminase responsible for protection against virus-induced cytopathic effects, and that ADAR de fi ciency does not adversely affect PyV growth.

Zebrafish Adenosine Deaminase, RNA-Specific, B1 (ADARB1) interaction partners

1. Adar2 Edits the Q/R site of AMPA receptor Subunit gria2alpha transcript to ensure normal development of nervous system and cranial neural crest cells