ADAR1 geeneistä GeneCards lähteessä ADAR1 ( Kr.1q21.3)

ADAR1 geeni Covid-19 taudissa 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8774467/

YLEISTIETOA  ADAR geenistä ja  sen kaikista nimistä:

https://www.genecards.org/cgi-bin/carddisp.pl?gene=ADAR&keywords=ADAR

Aliases for ADAR Gene

• GeneCards Symbol: ADAR ²
• Adenosine Deaminase RNA Specific ^{2 3 5}
• ADAR1 ^{2 3 4 5}
• Double-Stranded RNA-Specific Adenosine Deaminase ^{2 3 4}
• DRADA ^{2 3 4}
• G1P1 ^{3 4 5}
• IFI4 ^{3 4 5}
• 136 KDa Double-Stranded RNA-Binding Protein ^{3 4}
• Interferon-Inducible Protein 4 ^{3 4}
• Interferon-Induced Protein 4 ^{2 3}
• K88DSRBP ^{3 4}

• DSRAD ^{3 4}
• IFI-4 ^{3 4}
• P136 ^{3 4}
• Adenosine Deaminase Acting On RNA 1-A ³
• DsRNA Adeonosine Deaminase ³
• DsRNA Adenosine Deaminase ³
• EC 3.5.4.37 ⁴
• EC 3.5.4 ⁴⁸
• AGS6 ³
• DSH ³

Entrez Gene Summary for ADAR Gene

• This gene encodes the enzyme responsible for RNA editing by site-specific deamination of adenosines. This enzyme destabilizes double-stranded RNA through conversion of adenosine to inosine. Mutations in this gene have been associated with dyschromatosis symmetrica hereditaria. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jul 2010]

GeneCards Summary for ADAR Gene

ADAR (Adenosine Deaminase RNA Specific) is a Protein Coding gene. Diseases associated with ADAR include Dyschromatosis Symmetrica Hereditaria and Aicardi-Goutieres Syndrome 6. Among its related pathways are Formation of editosomes by ADAR proteins and mRNA Editing: C to U Conversion. Gene Ontology (GO) annotations related to this gene include RNA binding and adenosine deaminase activity. An important paralog of this gene is ADARB2.

UniProtKB/Swiss-Prot Summary for ADAR Gene

Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing (PubMed:7972084, 7565688, 12618436). This may affect gene expression and function in a number of ways that include mRNA translation by changing codons and hence the amino acid sequence of proteins since the translational machinery read the inosine as a guanosine; pre-mRNA splicing by altering splice site recognition sequences; RNA stability by changing sequences involved in nuclease recognition; genetic stability in the case of RNA virus genomes by changing sequences during viral RNA replication; and RNA structure-dependent activities such as microRNA production or targeting or protein-RNA interactions. Can edit both viral and cellular RNAs and can edit RNAs at multiple sites (hyper-editing) or at specific sites (site-specific editing). Its cellular RNA substrates include: bladder cancer-associated protein (BLCAP), neurotransmitter receptors for glutamate (GRIA2) and serotonin (HTR2C) and GABA receptor (GABRA3). Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alters their functional activities. Exhibits low-level editing at the GRIA2 Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Its viral RNA substrates include: hepatitis C virus (HCV), vesicular stomatitis virus (VSV), measles virus (MV), hepatitis delta virus (HDV), and human immunodeficiency virus type 1 (HIV-1). Exhibits either a proviral (HDV, MV, VSV and HIV-1) or an antiviral effect (HCV) and this can be editing-dependent (HDV and HCV), editing-independent (VSV and MV) or both (HIV-1). Impairs HCV replication via RNA editing at multiple sites. Enhances the replication of MV, VSV and HIV-1 through an editing-independent mechanism via suppression of EIF2AK2/PKR activation and function. Stimulates both the release and infectivity of HIV-1 viral particles by an editing-dependent mechanism where it associates with viral RNAs and edits adenosines in the 5'UTR and the Rev and Tat coding sequence. Can enhance viral replication of HDV via A-to-I editing at a site designated as amber/W, thereby changing an UAG amber stop codon to an UIG tryptophan (W) codon that permits synthesis of the large delta antigen (L-HDAg) which has a key role in the assembly of viral particles. However, high levels of ADAR1 inhibit HDV replication. ( DSRAD_HUMAN,P55265 )

1. A Comprehensive and Systematic Analysis Revealed the Role of ADAR1 in Pan-Cancer Prognosis and Immune Implications.
2. ADAR1 and ZBP1 in innate immunity, cell death, and disease.
3. ADAR1 is a promising risk stratification biomarker of remnant liver recurrence after hepatic metastasectomy for colorectal cancer.
4. ADAR1 improved Treg cell function through the miR-21b/Foxp3 axis and inhibits the progression of acute graft-versus-host disease after allogeneic hematopoietic stem cell transplantation.
5. ADAR1-dependent editing regulates human beta cell transcriptome diversity during inflammation.
6. ADAR activation by inducing a syn conformation at guanosine adjacent to an editing site.
7. Immunosuppressive lncRNA LINC00624 promotes tumor progression and therapy resistance through ADAR1 stabilization.
8. RNA Editing Enzyme ADAR1 Regulates METTL3 in an Editing Dependent Manner to Promote Breast Cancer Progression via METTL3/ARHGAP5/YTHDF1 Axis.
9. Adenosine-Deaminase-Acting-on-RNA-1 Facilitates T-cell Migration toward Human Melanoma Cells.
10. RNA editing enzyme ADAR1 controls miR-381-3p-mediated expression of multidrug resistance protein MRP4 via regulation of circRNA in human renal cells.