Publications by authors named "Jackson R Pierce"
Article Synopsis
- Recognition of viral infection often involves detecting double-stranded RNA (dsRNA) using proteins like MDA5 and RIG-I, but these proteins can have trouble telling viral dsRNA apart from the body's own.
- A study shows that using shRNA to knock down DDX54 can activate PKR, a crucial immune response protein, even when DDX54 levels are high, pointing to a possible off-target effect.
- The activation of PKR by the shRNA was further boosted by reducing ADAR1, a protein that normally inhibits PKR, suggesting that this activation happens through a dsRNA-dependent mechanism.
Immunotherapy has emerged as a therapeutic option for many cancers. For some tumors, immune checkpoint inhibitors show great efficacy in promoting anti-tumor immunity. However, not all tumors respond to immunotherapies.
View Article and Find Full Text PDFRecognition of viral infection often relies on the detection of double-stranded RNA (dsRNA), a process that is conserved in many different organisms. In mammals, proteins such as MDA5, RIG-I, OAS, and PKR detect viral dsRNA, but struggle to differentiate between viral and endogenous dsRNA. This study investigates an shRNA targeting DDX54's potential to activate PKR, a key player in the immune response to dsRNA.
View Article and Find Full Text PDFUnlabelled: Detection of viral double-stranded RNA (dsRNA) is an important component of innate immunity. However, many endogenous RNAs containing double-stranded regions can be misrecognized and activate innate immunity. The IFN-inducible ADAR1-p150 suppresses dsRNA sensing, an essential function for adenosine deaminase acting on RNA 1 (ADAR1) in many cancers, including breast.
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