2z0a: Difference between revisions

From Proteopedia
Jump to navigation Jump to search
No edit summary
No edit summary
 
Line 3: Line 3:
<StructureSection load='2z0a' size='340' side='right'caption='[[2z0a]], [[Resolution|resolution]] 1.85&Aring;' scene=''>
<StructureSection load='2z0a' size='340' side='right'caption='[[2z0a]], [[Resolution|resolution]] 1.85&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[2z0a]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/9infa 9infa]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2Z0A OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2Z0A FirstGlance]. <br>
<table><tr><td colspan='2'>[[2z0a]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/Influenza_A_virus Influenza A virus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2Z0A OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2Z0A FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GLY:GLYCINE'>GLY</scene>, <scene name='pdbligand=SIN:SUCCINIC+ACID'>SIN</scene></td></tr>
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.85&#8491;</td></tr>
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">NS1 ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=11320 9INFA])</td></tr>
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GLY:GLYCINE'>GLY</scene>, <scene name='pdbligand=SIN:SUCCINIC+ACID'>SIN</scene></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=2z0a FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2z0a OCA], [https://pdbe.org/2z0a PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2z0a RCSB], [https://www.ebi.ac.uk/pdbsum/2z0a PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2z0a ProSAT], [https://www.topsan.org/Proteins/RSGI/2z0a TOPSAN]</span></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=2z0a FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2z0a OCA], [https://pdbe.org/2z0a PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2z0a RCSB], [https://www.ebi.ac.uk/pdbsum/2z0a PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2z0a ProSAT], [https://www.topsan.org/Proteins/RSGI/2z0a TOPSAN]</span></td></tr>
</table>
</table>
== Function ==
== Function ==
[[https://www.uniprot.org/uniprot/Q5H7I4_9INFA Q5H7I4_9INFA]] Inhibits post-transcriptional processing of cellular pre-mRNA, by binding and inhibiting two cellular proteins that are required for the 3'-end processing of cellular pre-mRNAs: the 30 kDa cleavage and polyadenylation specificity factor (CPSF4) and the poly(A)-binding protein 2 (PABPN1). This results in the accumulation of unprocessed 3' end pre-mRNAs which can't be exported from the nucleus. Cellular protein synthesis is thereby shut off very early after virus infection. Viral protein synthesis is not affected by the inhibition of the cellular 3' end processing machinery because the poly(A) tails of viral mRNAs are produced by the viral polymerase through a stuttering mechanism.[SAAS:SAAS00141143]  Prevents the establishment of the cellular antiviral state by inhibiting TRIM25-mediated DDX58 ubiquitination, which normally triggers the antiviral transduction signal that leads to the activation of type I IFN genes by transcription factors like IRF3 and IRF7. Prevents human EIF2AK2/PKR activation, either by binding double-strand RNA, or by interacting directly with EIF2AK2/PKR. This function may be important at the very beginning of the infection, when NS1 is mainly present in the cytoplasm. Also binds poly(A) and U6 snRNA. Suppresses the RNA silencing-based antiviral response in Drosophila cells.[SAAS:SAAS00141179]  
[https://www.uniprot.org/uniprot/Q5H7J4_9INFA Q5H7J4_9INFA] Inhibits post-transcriptional processing of cellular pre-mRNA, by binding and inhibiting two cellular proteins that are required for the 3'-end processing of cellular pre-mRNAs: the 30 kDa cleavage and polyadenylation specificity factor/CPSF4 and the poly(A)-binding protein 2/PABPN1. In turn, unprocessed 3' end pre-mRNAs accumulate in the host nucleus and are no longer exported to the cytoplasm. Cellular protein synthesis is thereby shut off very early after virus infection. Viral protein synthesis is not affected by the inhibition of the cellular 3' end processing machinery because the poly(A) tails of viral mRNAs are produced by the viral polymerase through a stuttering mechanism.[RuleBase:RU362113]  Prevents the establishment of the cellular antiviral state by inhibiting TRIM25-mediated RIGI ubiquitination, which normally triggers the antiviral transduction signal that leads to the activation of type I IFN genes by transcription factors IRF3 and IRF7. Prevents human EIF2AK2/PKR activation, either by binding double-strand RNA, or by interacting directly with EIF2AK2/PKR. This function may be important at the very beginning of the infection, when NS1 is mainly present in the cytoplasm. Also binds poly(A) and U6 snRNA.[RuleBase:RU362113]


==See Also==
==See Also==
Line 15: Line 15:
__TOC__
__TOC__
</StructureSection>
</StructureSection>
[[Category: Influenza A virus]]
[[Category: Large Structures]]
[[Category: Large Structures]]
[[Category: Ito, H]]
[[Category: Ito H]]
[[Category: Ito, T]]
[[Category: Ito T]]
[[Category: Kamo-Uchikubo, T]]
[[Category: Kamo-Uchikubo T]]
[[Category: Kishishita, S]]
[[Category: Kishishita S]]
[[Category: Structural genomic]]
[[Category: Saijo S]]
[[Category: Saijo, S]]
[[Category: Shirouzu M]]
[[Category: Shirouzu, M]]
[[Category: Terada T]]
[[Category: Terada, T]]
[[Category: Yokoyama S]]
[[Category: Yokoyama, S]]
[[Category: Avian influenza]]
[[Category: H5n1]]
[[Category: National project on protein structural and functional analyse]]
[[Category: Nppsfa]]
[[Category: Ns1]]
[[Category: Rna-binding]]
[[Category: Rsgi]]
[[Category: Viral protein]]

Latest revision as of 21:45, 20 September 2023

Crystal structure of RNA-binding domain of NS1 from influenza A virus A/crow/Kyoto/T1/2004(H5N1)Crystal structure of RNA-binding domain of NS1 from influenza A virus A/crow/Kyoto/T1/2004(H5N1)

Structural highlights

2z0a is a 4 chain structure with sequence from Influenza A virus. Full crystallographic information is available from OCA. For a guided tour on the structure components use FirstGlance.
Method:X-ray diffraction, Resolution 1.85Å
Ligands:,
Resources:FirstGlance, OCA, PDBe, RCSB, PDBsum, ProSAT, TOPSAN

Function

Q5H7J4_9INFA Inhibits post-transcriptional processing of cellular pre-mRNA, by binding and inhibiting two cellular proteins that are required for the 3'-end processing of cellular pre-mRNAs: the 30 kDa cleavage and polyadenylation specificity factor/CPSF4 and the poly(A)-binding protein 2/PABPN1. In turn, unprocessed 3' end pre-mRNAs accumulate in the host nucleus and are no longer exported to the cytoplasm. Cellular protein synthesis is thereby shut off very early after virus infection. Viral protein synthesis is not affected by the inhibition of the cellular 3' end processing machinery because the poly(A) tails of viral mRNAs are produced by the viral polymerase through a stuttering mechanism.[RuleBase:RU362113] Prevents the establishment of the cellular antiviral state by inhibiting TRIM25-mediated RIGI ubiquitination, which normally triggers the antiviral transduction signal that leads to the activation of type I IFN genes by transcription factors IRF3 and IRF7. Prevents human EIF2AK2/PKR activation, either by binding double-strand RNA, or by interacting directly with EIF2AK2/PKR. This function may be important at the very beginning of the infection, when NS1 is mainly present in the cytoplasm. Also binds poly(A) and U6 snRNA.[RuleBase:RU362113]

See Also

2z0a, resolution 1.85Å

Drag the structure with the mouse to rotate

Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)

OCA