# cache

engine: gpt-3.5-turbo
prompt:
From the text below, extract the following entities in the following format:

genes: <semicolon-separated list of genes>
organisms: <semicolon-separated list of organism taxons>
gene_organisms: <semicolon-separated list of asterisk separated gene to organism relationships>
activities: <semicolon-separated list of molecular activities>
gene_functions: <semicolon-separated list of gene to molecular activity relationships>
cellular_processes: <semicolon-separated list of cellular processes>
pathways: <semicolon-separated list of pathways>
gene_gene_interactions: <semicolon-separated list of gene to gene interactions>
gene_localizations: <semicolon-separated list of genes plus their location in the cell; for example, "gene1 / cytoplasm; gene2 / mitochondrion">


Text:
Title: β-Catenin Is Required for the cGAS/STING Signaling Pathway but Antagonized by the Herpes Simplex Virus 1 US3 Protein
Text:
The cGAS/STING-mediated DNA-sensing signaling pathway is crucial
for interferon (IFN) production and host antiviral
responses. Herpes simplex virus I (HSV-1) is a DNA virus that has
evolved multiple strategies to evade host immune responses. Here,
we demonstrate that the highly conserved β-catenin protein in the
Wnt signaling pathway is an important factor to enhance the
transcription of type I interferon (IFN-I) in the cGAS/STING
signaling pathway, and the production of IFN-I mediated by
β-catenin was antagonized by HSV-1 US3 protein via its kinase
activity. Infection by US3-deficienct HSV-1 and its kinase-dead
variants failed to downregulate IFN-I and IFN-stimulated
gene (ISG) production induced by β-catenin. Consistent with this,
absence of β-catenin enhanced the replication of US3-deficienct
HSV-1, but not wild-type HSV-1. The underlying mechanism was the
interaction of US3 with β-catenin and its hyperphosphorylation of
β-catenin at Thr556 to block its nuclear translocation. For the
first time, HSV-1 US3 has been shown to inhibit IFN-I production
through hyperphosphorylation of β-catenin and to subvert host
antiviral innate immunity.IMPORTANCE Although increasing evidence
has demonstrated that HSV-1 subverts host immune responses and
establishes lifelong latent infection, the molecular mechanisms
by which HSV-1 interrupts antiviral innate immunity, especially
the cGAS/STING-mediated cellular DNA-sensing signaling pathway,
have not been fully explored. Here, we show that β-catenin
promotes cGAS/STING-mediated activation of the IFN pathway, which
is important for cellular innate immune responses and intrinsic
resistance to DNA virus infection. The protein kinase US3
antagonizes the production of IFN by targeting β-catenin via its
kinase activity. The findings in this study reveal a novel
mechanism for HSV-1 to evade host antiviral immunity and add new
knowledge to help in understanding the interaction between the
host and HSV-1 infection.

Keywords: HSV-1; US3; type I IFN; β-catenin.

===

payload:
genes: β-catenin; cGAS; STING; IFN; ISG; US3; Wnt signaling pathway
organisms: Herpes simplex virus 1 (HSV-1)
gene_organisms: β-catenin * Wnt signaling pathway; β-catenin * cGAS/STING; HSV-1 US3 protein * β-catenin
activities: transcription; kinase activity; replication; hyperphosphorylation; nuclear translocation; inhibit IFN-I production
gene_functions: β-catenin * enhance transcription of IFN-I; US3 protein * antagonize production of IFN-I
cellular_processes: interferon (IFN) production; host antiviral responses; IFN-stimulated gene (ISG) production; innate immunity; DNA virus infection
pathways: cGAS/STING signaling pathway; Wnt signaling pathway; IFN pathway; antiviral immunity
gene_gene_interactions: No gene to gene interactions mentioned
gene_localizations: No gene localizations mentioned


engine: gpt-3.5-turbo
payload: gene: β-catenin organism: Wnt signaling pathway
prompt:
Split the following piece of text into fields in the following format:

gene: <the value for gene>
organism: <the value for organism>


Text:
β-catenin * Wnt signaling pathway

===


engine: gpt-3.5-turbo
payload: gene: β-catenin organism: cGAS/STING
prompt:
Split the following piece of text into fields in the following format:

gene: <the value for gene>
organism: <the value for organism>


Text:
β-catenin * cGAS/STING

===


engine: gpt-3.5-turbo
payload: gene: US3 protein organism: HSV-1
prompt:
Split the following piece of text into fields in the following format:

gene: <the value for gene>
organism: <the value for organism>


Text:
HSV-1 US3 protein * β-catenin

===


engine: gpt-3.5-turbo
payload: gene: β-catenin molecular_activity: enhance transcription of IFN-I
prompt:
Split the following piece of text into fields in the following format:

gene: <the name of the gene in the pair. This comes first.>
molecular_activity: <the name of the molecular function in the pair. This comes second. May be a GO term.>


Text:
β-catenin * enhance transcription of IFN-I

===


engine: gpt-3.5-turbo
payload: gene: US3 protein molecular_activity: antagonize production of IFN-I
prompt:
Split the following piece of text into fields in the following format:

gene: <the name of the gene in the pair. This comes first.>
molecular_activity: <the name of the molecular function in the pair. This comes second. May be a GO term.>


Text:
US3 protein * antagonize production of IFN-I

===


engine: gpt-3.5-turbo
payload: No gene to gene interactions mentioned
prompt:
Split the following piece of text into fields in the following format:

gene1: <the value for gene1>
gene2: <the value for gene2>


Text:
No gene to gene interactions mentioned

===


engine: gpt-3.5-turbo
payload: gene: None location: None
prompt:
Split the following piece of text into fields in the following format:

gene: <the value for gene>
location: <the value for location>


Text:
No gene localizations mentioned

===


