The Fukunaga Lab uses multidisciplinary approaches to understand the cell biology, biogenesis and function of RNA-binding proteins and small silencing RNAs from the atomic to the organismal level. The lab studies (1) biology and molecular functions and mechanisms of uncharacterized RNA-binding proteins, and (2) how small silencing RNAs, including microRNAs (miRNAs), small interfering RNAs (siRNAs) and piwi-interacting RNAs (piRNAs), are produced and function. Mutations in the RNA-binding protein and small RNA genes cause many diseases, including cancers. We use a combination of biochemistry, Drosophila genetics, molecular biology, cell culture, and next-generation sequencing, to answer fundamental biological questions and also potentially lead to therapeutic applications to human diseases.

Work in the Rachel Damico Lab explores topics within the fields of vascular biology and pulmonary medicine, with a focus on acute lung injury and apoptosis in lung diseases. Our studies have included examining idiopathic and scleroderma-associated pulmonary arterial hypertension, vascular receptor autoantibodies, and the link between inflammation and the Warburg phenomenon in patients with pulmonary arterial hypertension. We have also researched the inhibitory factor of macrophage migration and its governing of endothelial cell sensitivity to LPS-induced apoptosis.

The Shanthini Sockanathan Laboratory uses the developing spinal cord as our major paradigm to define the mechanisms that maintain an undifferentiated progenitor state and the molecular pathways that trigger their differentiation into neurons and glia. The major focus of the lab is the study of a new family of six-transmembrane proteins (6-TM GDEs) that play key roles in regulating neuronal and glial differentiation in the spinal cord. We recently discovered that the 6-TM GDEs release GPI-anchored proteins from the cell surface through cleavage of the GPI-anchor. This discovery identifies 6-TM GDEs as the first vertebrate membrane bound GPI-cleaving enzymes that work at the cell surface to regulate GPI-anchored protein function. Current work in the lab involves defining how the 6-TM GDEs regulate cellular signaling events that control neuronal and glial differentiation and function, with a major focus on how GDE dysfunction relates to the onset and progression of disease. To solve these questions, we use an integrated approach that includes in vivo models, imaging, molecular biology, biochemistry, developmental biology, genetics and behavior.

The Taverna Laboratory studies histone marks, such as lysine methylation and acetylation, and how they contribute to an epigenetic/histone code that dictates chromatin-templated functions like transcriptional activation and gene silencing. Our lab uses biochemistry and cell biology in a variety of model organisms to explore connections between gene regulation and proteins that write and read histone marks, many of which have clear links to human diseases like leukemia and other cancers. We also investigate links between small RNAs and histone marks involved in gene silencing.

Chronic viral hepatitis (due to HBV and HCV) is a major cause of liver disease worldwide, and an increasing cause of death in persons living with HIV/AIDS. Our laboratory studies are aimed at better defining the host-pathogen interactions in these infections, with particular focus on humoral and cellular immune responses, viral evasion, inflammation, fibrosis progression, and drug resistance. We are engaged in synthetic biology approaches to rational vaccine development and understanding the limits on the extraordinary genetic variability of HCV.

The Michaelis Laboratory's research goal is to dissect fundamental cellular processes relevant to human health and disease, using yeast and mammalian cell biology, biochemistry and high-throughput genomic approaches. Our team studies the cell biology of lamin A and its role in the premature aging disease Hutchinson-Gilford progeria syndrome (HGPS). Other research focuses on the core cellular machinery involved in recognition of misfolded proteins. Understanding cellular protein quality control machinery will ultimately help researchers devise treatments for protein misfolding diseases in which degradation is too efficient or not enough.

Current research in the Sean T. Prigge Lab explores the biochemical pathways found in the apicoplast, an essential organelle found in malaria parasites, using a combination of cell biology and genetic, biophysical and biochemical techniques. We are particularly focused on the pathways used for the biosynthesis and modification of fatty acids and associated enzyme cofactors, including pantothenate, lipoic acid, biotin and iron-sulfur clusters. We want to better understand how the cofactors are acquired and used, and whether they are essential for the growth of blood-stage malaria parasites.

The research in the Sarbjit Saini Laboratory focuses on IgE receptor biology and IgE receptor-mediated activation of blood basophils and mast cells. We have examined the role of IgE receptor expression and activation in allergic airways disease, anaphylaxis and chronic urticaria. Our research has been supported by the NIH, American Lung Association and the AAAAI. Our current research interests have focused mechanisms of diease in allergic asthma, allergic rhinitis and also translational studies in chronic idiopathic urticaria.

Investigators in the Pablo Iglesias Lab use analytic tools from control systems and dynamical systems to study cell biology, including biological signal transduction pathways. Our research interests include the ways cells interpret directional cues to guide their motion, regulatory mechanisms that control cell division, and the sensing and actuation that enable cells to maintain lipid homeostasis.

The Arturo Casadevall Lab uses a multidisciplinary approach to explore two key topics within microbiology and immunology: how microbes cause disease and how hosts can protect themselves against those microbes. Much of our research focuses on the fungus Cryptococcus neoformans, which frequently causes lung infections in people with impaired immunity. We also work with the microorganism Bacillus anthracis, a bacterium that causes anthrax and is frequently used in biological warfare. Our goal is to devise antibody-based countermeasures to protect against this and other similar threats.