2l54: Difference between revisions

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[[Image:2l54.png|left|200px]]


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==Solution structure of the Zalpha domain mutant of ADAR1 (N43A,Y47A)==
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== Structural highlights ==
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<table><tr><td colspan='2'>[[2l54]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2L54 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2L54 FirstGlance]. <br>
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</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR</td></tr>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=2l54 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2l54 OCA], [https://pdbe.org/2l54 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2l54 RCSB], [https://www.ebi.ac.uk/pdbsum/2l54 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2l54 ProSAT]</span></td></tr>
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== Disease ==
[https://www.uniprot.org/uniprot/DSRAD_HUMAN DSRAD_HUMAN] Defects in ADAR are a cause of dyschromatosis symmetrical hereditaria (DSH) [MIM:[https://omim.org/entry/127400 127400]; also known as reticulate acropigmentation of Dohi. DSH is a pigmentary genodermatosis of autosomal dominant inheritance characterized by a mixture of hyperpigmented and hypopigmented macules distributed on the dorsal parts of the hands and feet.<ref>PMID:12916015</ref> <ref>PMID:15146470</ref> <ref>PMID:15659327</ref>
== Function ==
[https://www.uniprot.org/uniprot/DSRAD_HUMAN DSRAD_HUMAN] Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing. 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; 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.<ref>PMID:15556947</ref> <ref>PMID:15858013</ref> <ref>PMID:16475990</ref> <ref>PMID:17079286</ref> <ref>PMID:19710021</ref> <ref>PMID:19605474</ref> <ref>PMID:19651874</ref> <ref>PMID:19908260</ref> <ref>PMID:21289159</ref> <ref>PMID:22278222</ref>  


===Solution structure of the Zalpha domain mutant of ADAR1 (N43A,Y47A)===
==See Also==
 
*[[Adenosine deaminase 3D structures|Adenosine deaminase 3D structures]]
 
== References ==
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{{ABSTRACT_PUBMED_21217697}}
 
==About this Structure==
[[2l54]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2L54 OCA].
 
==Reference==
<ref group="xtra">PMID:21217697</ref><references group="xtra"/>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Droge, P.]]
[[Category: Large Structures]]
[[Category: Feng, S.]]
[[Category: Droge P]]
[[Category: Pervushin, K.]]
[[Category: Feng S]]
[[Category: Zhao, J.]]
[[Category: Pervushin K]]
[[Category: Zhao J]]