Alexander Cartagena-Rivera, PhD
Investigator (Tenure-Track)
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National Institute of Biomedical Imaging and Bioengineering
IMB Seminar Series
Jan 27, 2026 | 12:00 pm | Knight Campus Beetham Family Seminar Room
The cellular glycocalyx plays a crucial role in making pancreatic cancer one of the deadliest malignancies globally. It complicates early detection and reduces the effectiveness of conventional therapies. In pancreatic cancer, the components of the glycocalyx are often upregulated or abnormally glycosylated, promoting tumor progression through immune evasion, enhanced metastasis, and drug resistance. While these biochemical effects are known, the biophysical impact of the glycocalyx on cancer cells is less understood. In our study, we explored the structural and biomechanical effects of modifying the glycocalyx architecture in pancreatic cancer cells using various chemical compounds. We employed a recently developed Atomic Force Microscopy nanomechanical mapping method to visualize cellular mechanical heterogeneities in a high spatiotemporal context. Our new approach allows for the viscoelastic inversion of high-resolution spatiotemporal data at rates which are orders of magnitude faster (more than 37,386-fold) than optimizing a traditional rheological model for each pixel. Then, we investigated the architectural and biophysical effects of glycocalyx architectural modulation in pancreatic cancer cells. Perturbations of hyaluronic acid (HA), sialic acid (SA), mucins, and N-glycans through enzymatic treatments led to significant architectural remodeling of the cell surface. Interestingly, removal of SA and mucins resulted in a softer and more fluid cell surface, while removal of HA softened and increased viscosity. In addition, preliminary cytokine expression results suggested that SA removal leads to a pronounced pro-inflammatory response (IL-2, IL-8, INF-γ among others) of human cytotoxic CD8+ T Lymphocytes, greater than removing other glycocalyx components. Lastly, a glycomics study also revealed unique changes in the structure of N- and O-glycans, with significantly more heterogeneity in the structure of N-glycans on pancreatic cancer cells, and O-glycans showing a particularly higher degree of SA deposition. Our findings suggest that the glycocalyx of human pancreatic ductal adenocarcinoma cells fundamentally regulate extracellular surface architecture, mechanical properties, composition, and function, thereby promoting tumor progression and metastasis by acting as a physical barrier to antitumor responses.
Dr. Rebecca Abergel
Associate Professor, UC Berkeley and Senior Faculty Scientist
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Lawrence Berkeley National Laboratory
Career Exploration Speaker Series
Feb 4, 2026 | 4:00 pm | Novick Room - Streisinger 225
Dr. Berton Earnshaw
AI Founding Fellow, Recursion, and Scientific Director
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Valence Labs
Career Exploration Speaker Series
May 6, 2026 | 4:00 pm | Novick Room - Streisinger 225
Past Events
POSTPONED - Kim McKim, PhD
Professor
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Rutgers University
IMB Seminar Series
Nov 18, 2025 | 4:00 pm | Willamette 110
Meiosis is characterized by the first, or reductional, division. We use Drosophila melanogaster females as a model to understand the mechanisms that promote accurate chromosome segregation on the acentrosomal spindle of oocytes. Furthermore, we are interested in understanding the features of the oocyte spindle that make it susceptible to chromosome segregation errors. An important part of this process is how the kinetochores on the chromosomes interact with the microtubules of the spindle. The kinetochore interacts with the microtubules in two ways. First, lateral attachments, where the kinetochores move along the sides of microtubules. Second, end-on attachments, where the kinetochores make a stable attachment to the ends of microtubules, maintain connections to a pole and segregate the homologs. The lateral interactions occur between the kinetochores and central spindle, which is composed of overlapping antiparallel microtubules and may be particularly important for acentrosomal oocytes. We hypothesize that the transition between lateral and end-on attachments is regulated to avoid errors in chromosome segregation.
Nick Pokorzynski, PhD
Assistant Professor
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Oregon State University
IMB Seminar Series
Nov 4, 2025 | 12:00 pm | Knight Campus Beetham Family Seminar Room
Most antibiotics only kill growing bacteria. Thus, slower bacterial growth leads to antibiotic tolerance. During infection, Salmonella enterica serovar Typhimurium faces low cytoplasmic Mg2+, which slows growth and increases tolerance to antibiotics targeting cell wall synthesis and DNA gyrase. We now report that this same condition renders S. Typhimurium vulnerable to the RNA polymerase (RNAP) inhibitor rifampicin. This specific vulnerability results from a reduction in the amounts of RNAP subunits RpoB and RpoC that is dependent on the protease Lon and master virulence regulator PhoP. By decreasing RNAP amounts, S. Typhimurium advances specific transcription of virulence determinants. Our results uncover a pathogen vulnerability concealed by clinical microbiology conditions that emerges from the activation of bacterial virulence.
Mike Harms, PhD
Associate Professor
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University of Oregon
IMB Seminar Series
Oct 28, 2025 | 12:00 pm | Knight Campus Beetham Family Seminar Room
Claire Richardson, PhD
Assistant Professor
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University of Wisconsin
IMB Seminar Series
Oct 21, 2025 | 12:00 pm | Knight Campus Beetham Family Seminar Room
Neurons have exceptionally long lifespans. By contrast, the proteins and organelles within neurons are continuously being degraded, largely by lysosomes, and replaced to ensure their quality and proper abundance. Illustrating this importance of this continuous turnover for neuron maintenance, dysfunctional degradation of neuronal subcellular components leads to neurodegenerative diseases including Alzheimer’s disease, and it contributes to aging and diseases of aging, wherein degradative cargoes accumulate. I will discuss two ongoing projects in my lab that use Caenorhabditis elegans to investigate aspects of lysosome-mediated turnover within neurons. First, we ask how neuronal lysosomal capacity is regulated. We show that Transcription Factor EB (TFEB)/HLH-30 has a basal role of expanding neuronal lysosomal capacity in early adulthood, which is required to maintain neuron morphological integrity during aging. Second, we ask how synaptic vesicle protein turnover is controlled, as the proper abundance and composition of synaptic vesicles is important for neurotransmission. To address this, we developed a fully genetically encoded, fluorescence microscopy method to visualize protein turnover with subcellular resolution in vivo, called ARGO (Analysis of Red Green Offset). I will show how we used ARGO to begin to understand the turnover of Synpatogyrin/SNG-1.
RNA Club Film Screening
"Cracking the Code: Phil Sharp and the Biotech Revolution"
RNA Club
Oct 20, 2025 | 4:00 pm | EMU, Redwood Auditorium 214
Host:
Oregon RNA Club
"Cracking the Code: Phil Sharp and the Biotech Revolution"
Cracking the Code, narrated by Mark Ruffalo, is an inspiring story of vision, perseverance, and the power of science to change the world. Phil Sharp’s journey from a Kentucky farm boy to Nobel laureate embodies the American Dream and the triumph of entrepreneurial spirit. His 1977 groundbreaking discovery of RNA splicing rewrote the rules of molecular biology and ignited a life-saving scientific revolution, laying the foundation for an industry that has become a cornerstone of global innovation and economic growth – and transformed the health of billions of patients worldwide.
Cracking the Code, narrated by Mark Ruffalo, is an inspiring story of vision, perseverance, and the power of science to change the world. Phil Sharp’s journey from a Kentucky farm boy to Nobel laureate embodies the American Dream and the triumph of entrepreneurial spirit. His 1977 groundbreaking discovery of RNA splicing rewrote the rules of molecular biology and ignited a life-saving scientific revolution, laying the foundation for an industry that has become a cornerstone of global innovation and economic growth – and transformed the health of billions of patients worldwide.
Carole LaBonne, PhD
Professor and Chair, Department of Molecular Biosciences, Erastus O. Haven Professor of Life Sciences
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Northwestern
IMB Seminar Series
Oct 14, 2025 | 12:00 pm | Knight Campus Beetham Family Seminar Room
The neural crest is a vertebrate-specific stem cell population that helped drive the origin and evolution of vertebrates. A distinguishing feature of these cells is their multi-germ layer potential, which has parallels to another stem cell population—pluripotent stem cells of the vertebrate blastula. Our recent studies have shown that neural crest potency derives in part from the deployment of pluripotency gene regulatory network (GRN) components. We have shown that soxB1 factors, krüppel-like factors (klfs), and the pluripotency regulator pou5f cooperate with neural play border genes such as pax3 and zic1 to establish neural plate border identity, but soxB1 expression must be extinguished for neural crest progression to occur. soxb1 factors are replaced in the neural crest GRN by soxE factors and studies of this change of sox provides novel insights into how GRNs evolve. Moreover our recent work suggests that pluripotent blastula (inner cell mass) cells evolved from an ancient neural progentor cell population, and that this was driven in part by duplication and divergence of an ancestral pou3f like protein leading to the pou5f proteins of extant vertebrates.
POSTPONED Kamena Kostova, PhD
Assistant Investigator
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Stower's Institute for Medical Research
IMB Seminar Series
Oct 7, 2025 | 12:00 pm | Knight Campus Beetham Family Seminar Room
The ribosome is the essential molecular machine responsible for translation of mRNA to protein. Its composition is complex; it comprises four ribosomal RNAs (rRNAs) and approximately 80 ribosomal proteins that form two subunits: the small 40S and the large 60S. For decades, the composition of the ribosome has been deemed static; ribosomes are assembled and they do not change in response to environmental stimuli, in different tissues or organs, or during disease initiation and progression. Now we know that this notion is simply not true, as changes in both rRNA and proteins have been documented. In general, there are two ways in which the ribosome composition can change: as a result of damage or due to programmed changes in ribosomal components. Indeed, mutations, environmental stress, or mistakes during assembly can lead to defective ribosomes. Accumulation of such faulty ribosomes is associated with diseases such as neurodegeneration, cancer and ribosomopathies, further emphasizing the importance of these pathological changes for human health. Alterations in the ribosomal RNA and proteins have also been associated with normal physiological processes, such as development, differentiation, and adaptation. For example, zebrafish larvae assemble two structurally distinct types of ribosomes, maternal and somatic, during early development. Although we now know that the composition of the ribosome is dynamic, we have a limited understanding of how changes in the ribosome impact protein production and facilitate complex physiological processes. In my laboratory, we have developed unique tools and biological systems to answer two outstanding questions in the translation field: 1) What are the quality control factors that cope with defective ribosomes? and 2) How do programmed changes in the ribosome composition regulate translation to facilitate development?