Cell, Developmental & Microbiology Research Area

Oncolytic viruses are an emerging form of cancer therapy with the ability to selectively lyse and kill tumor cells. My research program seeks to investigate the mechanisms by which a negative-sense RNA virus, vesicular stomatitis virus (VSV), manipulates immune components of the tumor microenvironment.

The unifying theme of my scholarly work is obesity. The majority of my scholarly efforts are to assess the nutritional and hormonal factors that impact adipose (fat) tissue and influence risk of obesity as well as its associated diseases.

Research in my laboratory explores the mechanisms that allow Staphylococcus aureus to cause disease in humans, particularly those caused by the highly drug resistant form, methicillin resistant S. aureus (MRSA), a growing problem in the United States.

Dr. Kopchick is an expert on growth hormone (GH). With over 20 years of research experience on human and animal GH, Kopchick and colleagues have focused on the molecular biology of GH in relation to growth, obesity, insulin resistance, diabetes and aging.

My laboratory has found that adipose tissue is comprised of developmentally and functionally distinct subpopulations of adipocytes.  We are examining the molecular biology of these adipocyte subpopulations and determining their effects on systemic metabolism and physiology.

I study molecular pathways involved in autoimmune/inflammatory diseases (AIDs) & utilize this knowledge to develop novel therapeutics. My work established aberrant toll-like receptor (TLR) expression & signaling in non-immune cells is a key mediator of AIDs; work that initiated a paradigm shift.

Our research focuses on understanding how disease-causing bacteria regulate gene expression in response to specific environmental conditions encountered within the infected host. Focus is placed on the study of RNA-mediated gene regulation that impact the ability of bacteria to survive within the host and cause disease.

The brain vasculature provides a critical and expansive blood supply to support neuronal metabolism and function, and vascular lesions within the brain are often accompanied by neurological dysfunction. Our lab is interested in understanding how these systems influence one another.

I study beta-cell decline in early diabetes. I showed that circulating levels of cytokines caused by obesity are sufficient to trigger beta-cell failure in diabetes-prone mice. We are also develop novel dual-action compounds that stimulate insulin secretion and block immune-mediated beta-cell death.

The majority of most eukaryotic genomes is comprised of DNA that is annotated as being non-protein-coding in nature. However, much of this non-coding DNA is transcribed into RNA by RNA polymerase II. My research is driven by a desire to better understand the roles of these genes and how they are shaped by evolution.

Recent work focuses on prostate, breast, head and neck cancer, thyroid cancer, lymphoma, and automated pathology using image analysis and artificial intelligence algorithms. 

We are studying molecular mechanisms of DNA repair and mutagenesis. By using biochemical methods and next-generations sequencing technology, we are analyzing the details of mutational processes that cause various types of cancer.

We focus largely on the bacterial pathogen studies especially Clostridioides difficile (C. difficile). C. difficile is the most common hospital acquired infections, with high rate of antibiotic resistance and recurrence incidences, became a debilitating public health threat, with no successful preventive and treatment options. 

One bacterial pathogen capable of high levels of asymptomatic carriage in humans is Neisseria gonorrhoeae. N. gonorrhoeae recruits human proteins on the surface of infected cells to the site bacterial adhesion. I am working to understand the functional consequences of protein recruitment.