As a Translational Investigator and Senior Research Fellow at the Institute for Protein Design, I am working on developing an oral therapeutic for celiac disease called KumaMax. Celiac disease is characterized by an inflammatory intestinal immune response directed against gluten, which is a protein found in any food containing wheat, rye, or barley. This disease is a serious health problem in the U.S., afflicting approximately 2.4 million people, and costing $15-35 billion in health care costs annually. The basis for this disease is that human digestive enzymes cannot completely break down gliadin, the major protein component of gluten, because gliadin is highly enriched in the difficult-to-digest amino acids proline and glutamine. By using the Rosetta Molecular Modeling Suite and Foldit, we have designed an enzyme called KumaMax that is meant to break down gluten in the stomach before the gluten can reach the intestine and elicit an immune response.
This project has been the recipient of several awards including Commercialization Gap Funding awards in 2012 and 2013 from the UW Center for Commercialization, and the recipient of the “People’s Choice” award at the C4C Innovation Recognition Event in December 2013 (read more here).
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I began my career path with a BA in Biology from Wellesley College in 2003. During this time I studied learning and memory in a mouse model in Susumu Tonegawa’s lab at MIT. After graduation, I spent two years studying the mechanisms of tumorigenesis of a mouse retrovirus called Mouse Mammary Tumor Virus (MMTV) in the lab of Dr. Tanya Golovkina, who was then at the Jackson Labs in Bar Harbor, Maine, which resulted in a first-author publication in the Journal of Virology. After this work, I entered graduate school in the Department of Microbiology at the University of Washington (UW). My thesis work was performed in the lab of Dr. Sam Miller, on how the bacterial second messenger c-di-GMP regulates many different cellular processes in response to environmental stimuli. During my time in graduate school, I founded the UW International Genetically Engineered Machine (iGEM) team (www.igem.org), and acted as an advisor from 2008-2011. KumaMax actually began as an undergraduate student project for the iGEM competition in the summer of 2011, and has since shown great promise as an oral therapeutic to treat celiac disease.Ingrid Swanson Pultz, Ph.D.
 Harger M., Zheng L., Zheng L., Moon A., Ager C, An J.H., Choe C., Lai Y., Mo B., Zong D., Smith M.D., Egbert R. G., Mills J.H.,Baker D., Pultz I.S., Siegel J.B. (2013). Expanding the product profile of a microbial alkane biosynthetic pathway. ACS Synth. Biol.2(1):59-62.
 Pultz I.S., Christen M., Kulasekara H.D., Kennard A., Kulasekara B., Miller S.I. (2012). The response threshold of Salmonella PilZ domain proteins is determined by their binding affinities for c-di-GMP. Mol Microbiol. 86(6):1424-40.
 Gordon S.R., Stanley E.J., Wolf S., Toland A., Wu S.J., Hadidi D., Mills J.H., Baker D., Pultz I.S.*, Siegel J.B*. (2012). Computational design of an a-gliadin peptidase. JACS. 134(50):20513-20. *Both authors are corresponding authors.
 Beyer A.R., Bann D.V., Rice B., Pultz I.S., Kane M., Goff S.P., Golovkina T.V., Parent L.J. (2012). Nucleolar trafficking of the Mouse Mammary Tumor Virus Gag protein induced by interaction with ribosomal protein L9. J Virol. 87(2):1069-82.
 Pultz I.S.*, Mills E.*, Kulasekara H.D., Miller S.I. (2011). The bacterial second messenger c-di-GMP: mechanisms of signaling. Cell Microbiol. *These authors contributed equally to this work. 13(8):1122-9.
 Costa K.C., Wong P.M., Wang T., Lie T.J., Dodsworth J.A., Swanson I., Burn J.A., Hackett M., Leigh J.A. (2010). Protein complexing in a methanogen suggests electron bifurcation and electron delivery from formate to heterodisulfide reductase. PNAS.107(24):11050-5.
 Swanson I., Jude B.A., Zhang A.R., Pucker A., Smith Z.E., Golovkina T.V. (2006). Sequences within the gag gene of Mouse Mammary Tumor Virus needed for mammary gland cell transformation. J Virol. 80(7):3215-24.