Description
Key facts
Cell type:A549,
Species or organism:Human,
Tissue:Lung,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 2 bp deletion in exon 2 and 5 bp deletion in exon 2,
Disease:Carcinoma
Product details:
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-DDX58, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
RIG-I also known as DDX58 is an important protein with mass of approximately 102 kDa. This protein acts as a cytosolic sensor for viral double-stranded RNA playing an essential role in the detection of viral infections. It is expressed in many cell types including immune and epithelial cells. RIG-I consists of two N-terminal caspase activation and recruitment domains (CARDs) a DExD/H box helicase domain and a C-terminal regulatory domain. These domains enable RIG-I to recognize and bind viral RNA initiating downstream signaling for immune responses.
Biological function summary
RIG-I contributes significantly to the innate immune response. It acts to sense viral RNA and triggers the production of type I interferons and other pro-inflammatory cytokines. This protein functions as part of a complex that includes MAVS (mitochondrial antiviral signaling protein) and other signaling adapters. Upon activation RIG-I undergoes a conformational change leading to the exposure of its CARDs which interact with CARDs of MAVS facilitating downstream signaling to induce an antiviral state in host cells.
Pathways
RIG-I plays a central role in the RNA sensing pathway critical for antiviral immunity. This pathway involves several steps beginning with the recognition of viral RNA leading to the activation of interferon regulatory factors like IRF3 and IRF7 as well as nuclear factor kappa B (NF-κB). These factors then promote the expression of interferon-stimulated genes (ISGs). RIG-I also relates closely to the Jak-STAT signaling pathway which is activated by interferons and enhances the transcription of ISGs further amplifying the antiviral response.
RIG-I is often associated with viral infections such as hepatitis C and influenza. By detecting viral RNA RIG-I activates immune responses that help to control these infections. However dysfunction or aberrations in RIG-I signaling can lead to autoimmune disorders such as Aicardi-Goutières syndrome where there is an inappropriate response to self nucleic acids. In these disease contexts RIG-I interacts with MAVS and indirectly with proteins involved in regulating immune responses such as STING which plays a role in the innate immune response against DNA viruses.
