4rwq: Difference between revisions
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New page: '''Unreleased structure''' The entry 4rwq is ON HOLD Authors: Lohoefener, J., Steinke, N., Kay-Fedorov, P., Baruch, P., Nikulin, A., Tishchenko, S., Manstein, D.J., Fedorov, R. Descrip... |
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==Crystal structure of the apo-state of porcine OAS1== | |||
<StructureSection load='4rwq' size='340' side='right'caption='[[4rwq]], [[Resolution|resolution]] 3.10Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[4rwq]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Sus_scrofa Sus scrofa]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4RWQ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4RWQ FirstGlance]. <br> | |||
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 3.1Å</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=4rwq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4rwq OCA], [https://pdbe.org/4rwq PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4rwq RCSB], [https://www.ebi.ac.uk/pdbsum/4rwq PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4rwq ProSAT]</span></td></tr> | |||
</table> | |||
== Function == | |||
[https://www.uniprot.org/uniprot/OAS1_PIG OAS1_PIG] Interferon-induced, dsRNA-activated antiviral enzyme which plays a critical role in cellular innate antiviral response. In addition, it may also play a role in other cellular processes such as apoptosis, cell growth, differentiation and gene regulation. Synthesizes higher oligomers of 2'-5'-oligoadenylates (2-5A) from ATP which then bind to the inactive monomeric form of ribonuclease L (RNase L) leading to its dimerization and subsequent activation. Activation of RNase L leads to degradation of cellular as well as viral RNA, resulting in the inhibition of protein synthesis, thus terminating viral replication. Can mediate the antiviral effect via the classical RNase L-dependent pathway or an alternative antiviral pathway independent of RNase L. The secreted form displays antiviral effect against vesicular stomatitis virus (VSV), herpes simplex virus type 2 (HSV-2), and encephalomyocarditis virus (EMCV) and stimulates the alternative antiviral pathway independent of RNase L.<ref>PMID:20844035</ref> | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Large Structures]] | |||
[[Category: Sus scrofa]] | |||
[[Category: Baruch P]] | |||
[[Category: Fedorov R]] | |||
[[Category: Kay-Fedorov P]] | |||
[[Category: Lohoefener J]] | |||
[[Category: Manstein DJ]] | |||
[[Category: Nikulin A]] | |||
[[Category: Steinke N]] | |||
[[Category: Tishchenko S]] | |||
Latest revision as of 15:56, 1 March 2024
Crystal structure of the apo-state of porcine OAS1Crystal structure of the apo-state of porcine OAS1
Structural highlights
FunctionOAS1_PIG Interferon-induced, dsRNA-activated antiviral enzyme which plays a critical role in cellular innate antiviral response. In addition, it may also play a role in other cellular processes such as apoptosis, cell growth, differentiation and gene regulation. Synthesizes higher oligomers of 2'-5'-oligoadenylates (2-5A) from ATP which then bind to the inactive monomeric form of ribonuclease L (RNase L) leading to its dimerization and subsequent activation. Activation of RNase L leads to degradation of cellular as well as viral RNA, resulting in the inhibition of protein synthesis, thus terminating viral replication. Can mediate the antiviral effect via the classical RNase L-dependent pathway or an alternative antiviral pathway independent of RNase L. The secreted form displays antiviral effect against vesicular stomatitis virus (VSV), herpes simplex virus type 2 (HSV-2), and encephalomyocarditis virus (EMCV) and stimulates the alternative antiviral pathway independent of RNase L.[1] References
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