add requiretment

abstract.txt

@@ -0,0 +1,36 @@
+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.

app.py

@@ -22,12 +22,13 @@ def greet(name1, name2, name3, name4):
     output_string2, error_string2= run_command(f"poetry run runoak set-apikey -e openai {str1}")
     run_command(f"poetry run runoak set-apikey -e bioportal {str2}")
     run_command(f"poetry run runoak set-apikey -e hfhub-key {str3}")
+    output = run_command(f"ontogpt extract -t gocam.GoCamAnnotations -i ./abstract.txt")
 
 
 #     output_string1, error_string1=run_command("poetry")# ontogpt")
 
     # For the purpose of this example, I'm just returning the values concatenated
-    return f"Inputs received: {str1}, {str2}, {str3}, {str4},  {output_string1},{error_string1},{output_string2},{error_string2}"
+    return f"Inputs received: {str1}, {str2}, {str3}, {str4},  {output_string1},{error_string1},{output_string2},{error_string2},{output}"
 
 # Define 5 text input boxes with labels
 input_boxes = [