Samir lab studies crosstalk between stress, innate immune, and programmed cell death signaling in response to pathogenic challenges. We are using, or willing to use, any tool and the kitchen sink if it can help. The innate immune system is the first line of defense against pathogenic challenges including microbial pathogens. Innate immune activation can lead to programmed cell death. Uncontrolled programmed cell death can cause severe disease, and even death. Pathogenic challenges also activate stress signaling pathways which can lead to assembly of a membraneless cytoplasmic component called stress granules. Stress granules have been reported to inhibit programmed cell death and in the context of viral infections amplify the type I interferon signaling. Therefore, stress granule assembly could be a mechanism to restrict uncontrolled programmed cell while maintaining antiviral state. Interestingly, Toll-like Receptor (TLR) mediated innate immune signaling compromises stress granules through the inhibitor of kappa b kinase complex (IKK complex). This suggests another layer of interplay between the stress, innate immune and programmed cell signaling pathways. Our goal is to elucidate molecular mechanisms that govern this cross regulation and ultimately build quantitative models that would allow us to design precision therapeutic interventions.
Publications/Creative Works
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Affiliations
Research Consortia
Junior Faculty Network
Gulf Coast Consortia Immunology Cluster
Gulf Coast Cluster for Single Cell Omics
John S. Dunn Gulf Coast Consortium for Innovative Drug Discovery and Development
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