The aim of this research is to uncover the molecular mechanisms of how Regnase-1 degrades cytokine mRNAs. Inflammation is mediated by proinflammatory cytokines and cytokine expression is tightly regulated in innate immune cells such as macrophages and dendritic cells controlling their activation and maturation. Cytokine mRNA expression is controlled at both transcriptional and post-transcriptional levels, and post-transcriptional damping of cytokine expression is a critical step for resolution of inflammation and prevention of unintended tissue damage. However, the mechanisms of RNA metabolism in immune system is not clear. Thus, the aim of this research project is to investigate the molecular mechanisms of RNA metabolism by Regnase-1 in immune system.
Translation-dependent unwinding of stem-loops by UPF1 licenses Regnase-1 to degrade inflammatory mRNAs.
Cell line
View SamplesKaposi sarcoma is the most common cancer in AIDS patients and is typified by red skin lesions. The disease is caused by the KSHV virus (HHV8) and is recognizable by its distinctive red skin lesions. The lesions are KSHV infected spindle cells, most commonly the lymphatic endothelial and blood vessel endothelial cells (LEC and BEC), plus surrounding stroma. Here we examine KSHVs modulation of Notch signaling using wild-type LEC cells co-cultured with DLL4 and JAG1 expressing LEC cells.
KSHV manipulates Notch signaling by DLL4 and JAG1 to alter cell cycle genes in lymphatic endothelia.
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