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A co-opted ISG15-USP18 binding mechanism normally reserved for deISGylation controls type I IFN signalling

2021-06-03

Abstract excerpt

Type I interferon (IFN) signalling induces the expression of several hundred IFN-stimulated genes (ISGs) that provide an unfavourable environment for viral replication. To prevent an overexuberant response and autoinflammatory disease, IFN signalling requires tight control. One critical regulator is the ubiquitin-like protein ISG15, evidenced by autoinflammatory disease in patients with inherited ISG15 deficiencie...

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Literature Corpus work
718feb6b-7f63-5625-b37a-022228f55170
DOI
10.1101/2021.06.01.446527
Open publication

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A co-opted ISG15-USP18 binding mechanism normally reserved for deISGylation controls type I IFN signallingDOI 10.1101/2021.06.01.446527
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