Project description:To investigate the function LGP2 in the regulation of tumor progression and development, we established 2 T98G cell lines in which LGP2 gene has been overexpressed.
Project description:To investigate the function LGP2 in the regulation of tumor progression and development, we established 2 T98G cell lines in which LGP2 gene has been overexpressed.
Project description:mRNA expression profiles were compared between wild-type LGP2 and four amino acid replacement LGP2 (LGP2-4KR) cells in the presence or absence of a RIG-I ligand, short poly I:C.
Project description:The RIG-I-like receptors (RLRs: RIG-I, MDA5 and LGP2) trigger inflammatory and antiviral responses by sensing non-self RNA molecules produced during viral replication. LGP2 regulation of RIG-I and MDA5-dependant type-I interferon signaling is a matter of controversy. Here we show that LGP2 interacts with different components of the RNA silencing machinery. Particularly, we identified a direct protein-protein interaction between LGP2 and interferon-inducible double-stranded RNA-dependent protein kinase activator A (PACT). The LGP2-PACT interaction is mediated by the regulatory C-terminal domain of LGP2 and is necessary for inhibiting the RIG-I- and amplifying the MDA5-responses. We describe a point mutation within LGP2 that disrupts LGP2-PACT interaction and leads to the loss of LGP2 regulatory activity over RIG-I and MDA5. These results provide a model in which PACT-LGP2 interaction regulates RIG-I and MDA5 inflammatory response and allows cellular RNA silencing machinery to coordinate the innate immune response.
Project description:To reveal the fuction of cytoplasmic virus sensor protein, LGP2, on RNA silencing, we analyzed gene expression profiles on HeLa WT and LGP2 knockout cells, which were generated with CRISPR/Cas system.
Project description:We performed RNAseq analysis on WT and LGP2-/- BM-DCs treated with a RIG-I agonist (HCV Poly-U/C RNA) to understand how LGP2 impacts global transcriptional changes following activation of the RIG-I pathway. Analysis of the transcriptional profiles revealed that LGP2 functions as a negative regulator of RIG-I signaling as early as 1 hours post-RIG-I agonist treatment. This finding led us to study how LGP2 negatively influences RIG-I activation through post-translational modification.
Project description:To reveal the fuction of cytoplasmic virus sensor protein, LGP2, on RNA silencing, we analyzed gene expression profiles on HeLa WT and LGP2 knockout cells during SeV infection, which were generated with CRISPR/Cas system.