Investigating CK2 In Alveolar Interferon Regulation
Nandhini Sundar (she/her) (2027) | Molecular and Cell Biology and Minor in Data Science.
Nandhini is a SURF L&S scholarship recipient majoring in Molecular and Cell Biology with a minor in Data Science. For her SURF project this summer, Nandhini is studying how interferon signaling can be regulated in the lung without disrupting the growth of alveolar type II (AT2) cells, which are essential for lung repair and gas exchange. Using precision-cut lung slice models, she is testing whether inhibiting Casein Kinase 2 (CK2) can enhance immune signaling while preserving AT2 cell function, with potential implications for developing safer cancer immunotherapies that maintain healthy lung tissue.
What made you choose this research project? How did your interest in your research topic emerge?
I’ve always been drawn to cellular signaling, the way cells inter-communicate and respond to their environments at a molecular level. When I joined the Nabhan Lab, I got especially immersed in studying the lung as a model of stem cell-niche communication, exploring the different pathways that regulate repair of the alveoli. This specific project grew out of a screen my PI had previously conducted, which flagged Casein Kinase 2 (CK2) as a potentially interesting signaling molecule. Once I understood the question, I was deeply invested. It is relevant to immunology, cell signaling, and therapeutic development, which is exactly the kind of multi-layered research I like to explore.
What is your project about (in simple terms)?
Interferons are signaling molecules that help the immune system detect and destroy cancer cells and viruses, so they’re a strong target for developing lung cancer immunotherapy. The problem is that boosting interferon activity also tends to suppress regeneration of the stem cells that repair lung tissue, called Alveolar Type 2 (AT2) cells. Previous work in my lab showed that knocking out a protein CK2 increased interferon signaling without harming those AT2 cells, which is really exciting. But there’s a confound: the tool used for knock-out, CRISPR-Cas9, can also trigger interferon signaling, so we can’t be sure if CK2 was truly responsible. My project uses a small-molecule inhibitor instead to test whether blocking CK2 can boost immune signaling while keeping lung repair intact, potentially opening a new avenue for immunotherapy that doesn’t compromise lung function. My MCB coursework has given me a strong foundation in cellular signaling networks and how biochemical interactions regulate cell behavior. Understanding how kinases like CK2 fit into broader signaling cascades, and how disruptions in those pathways can drive disease, is something I’ve studied in the classroom and now get to investigate directly in the lab. It’s been really fulfilling to see those concepts manifest in my research, and it also reinforces my learning.
What are you most excited about this summer? Will your research entail travel, access to special collections, or experiments?
For one, I’m excited to get real results and to see whether the data supports what we’re hypothesizing. I’m also looking forward to developing my scientific communication and presentation skills, which I know will be essential as I start thinking about PhD programs. I’m excited to connect with other undergraduate researchers and scientists through the SURF cohort. Hearing about the work other people are passionate about across different fields is inspiring. My research is fully experimental and takes place in the Nabhan Lab at UC Berkeley. I’ll be working with precision-cut lung slices derived from laboratory mice and utilizing various protein and RNA expression assays to quantify and visualize my results.
What do you hope to learn from this experience? What would success look like for you? What challenges do you anticipate confronting?
I hope to grow into a more independent researcher. I’ve always had strong support from mentors and lab teams, and this summer is an opportunity to take more ownership over my own project, troubleshoot on my own, and push through uncertainty without always having a clear answer. Success for me is fulfillment with my learning experience and education, and generating meaningful data that either confirms or challenges our hypothesis. The biggest challenge will probably be navigating my own project. There’s a lot of problem-solving and depth that’s needed, and I’m excited to develop the organization and time-management skills that are required. The PCLS model I’m using also introduces some natural variability given how many cell types are present, so designing experiments that account for that will be important.
What do you hope comes out of this research? What impact do you hope your research will have?
I hope this project contributes to a deeper understanding of the many signaling molecules involved in alveolar cell communication. The lung is a very complex environment, and a lot is left to be known about how immune and regenerative signals interact within it. Studies such as mine add to our collective knowledge of viral infections, lung injury recovery, and disease.