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Join the Casper lab and dive into genetics! Our lab studies a repair process called break-induced replication (BIR). BIR is often used to repair breaks that result from collapse of DNA replication forks. In human cells, DNA repair by BIR can be stimulated by oncogene expression in cancer, and the process leads to genetic rearrangements. We study BIR in yeast cells, a model organism that is easy to manipulate and fun to work with. Since the process of BIR is similar in human and yeast cells, our research helps explain how genetic changes happen in cancer cells.
The Backues lab studies autophagy – a process of cellular “self-eating” that helps cells survive starvation as well as getting rid of damaged or malfunctioning subcellular components that would otherwise be toxic to the cell. In humans, autophagy is part of our defense against pathogens and cancer, as well as helping to prevent neurodegenerative diseases like Alzheimer’s and Parkinson’s. Autophagy is carried out by a suite of 30+ “Atg” proteins that create the autophagosome – a double-membrane vesicle that surrounds cargo in the cytoplasm (the body of the cell) and then delivers it to the vacuole/lysosome (the stomach of the cell) where it is broken down and the nutrients are recycled. We seek to understand how this process works by studying the functions of key Atg proteins in baker’s yeast, an easy-to-work with model system that has most of the same autophagy proteins as humans. Current projects are focused on understanding which Atg proteins control the size of the autophagosomes formed, vs which ones control their number.
Conotoxins are antimicrobial and anticancer peptides isolated from cone snails that have a dual mechanism; they work both by destroying cell membranes and by binding at nicotinic acetylcholine receptors (nAchRs). Molecules like acetylcholine and nicotine that bind to nAchRs and activate them are associated with aggressive and metastatic cancers, particularly in lung tissue. Conotoxins, however, do not activate nAchRs when they bind and therefore have the opposite effect. They consequently have potential as anticancer therapeutics. The problem with these peptides is that they are difficult to synthesize because they contain several cysteine (C) amino acid residues, which naturally cyclize in cells to form ring structures, a process that is hard to mimic in the laboratory. Previously, we developed an active antimicrobial and anticancer peptide called cysteine-deleted tachyplesin (CDT), which is linear because it lacks the cysteine residues. Our current objective is to use a similar strategy to determine if linear versions of conotoxins will also retain antitumor activity in lung cancer cells.
EMU APEX students design and build payloads that make measurements of Earth's atmosphere and are launched with a high altitude weather balloon. In the past, we have made observations of different weather phenomena, launched balloons during solar eclipses and collected cosmic ray data during interesting space weather events. This summer, our focus is on improving our atmosphere observation payload while also trying to build an instrument that is capable of measuring the flow of helium from a balloon that is actively venting. Summer Science Program participants will learn how to build a scientific payload, analyze observations and participate in a balloon launch!
Our research project will investigate how Vascular Endothelial Growth Factor (VEGF), an angiogenic signaling protein that regulates cell survival, growth, and proliferation influences cellular behavior. VEGF plays a critical role in physiological processes such as wound healing and blood vessel formation; however, its dysregulation is strongly
associated with pathological conditions, including cancer. In this research project, we will examine the responses of Non-Small Cell Lung Cancer (NSCLC) cells to VEGF stimulation, VEGF inhibition, and the combination of both treatments. By analyzing changes in protein expression and cell viability, we aim to better understand the role of VEGF in promoting cancer cell survival and to evaluate how inhibition of this pathway may suppress abnormal cell growth. These findings may provide insight into the potential of targeting VEGF signaling as a therapeutic strategy.
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