I am broadly interested in how mutations in proteins alter its structre and function, ultimately leading to a diseased state. Currently, using various molecular biophysics and biochemistry techniques, I investigate the effect of point muatations in human cardiac myosin that cause hypertrophic cardiomyopathy, a leading genetic heart disease where the heart becomes hypercontractile.

1. Nandwani, N.*, Bhowmik, D.*, Childers, M.C., Goluguri, R.R., Dawood, A., Regnier, M.,Spudich, J.A, and Ruppel, K.M.  Hypertrophic cardiomyopathy mutations Y115H and E497D disrupt the folded-back state of human b-cardiac myosin allosterically. (2024) bioRxiv; https://doi.org/10.1101/2024.02.29.582851 (* equal contribution)

2. Grinzato, A.#, Auguin, D.#, Kikuti, C., Nandwani, N., Moussaoui, D., Pathak, D., Kandiah, E., Ruppel, K.M.*, Spudich, J.A., Houdusse, A.*, and Robert-Paganin, J.* Cryo-EM structure of the folded-back state of human β-cardiac myosin. (2023) Nature Communications; 14(1):3166

3. Nandwani, N., Surana, P., Negi, H., Mascarenhas, N.M., Udgaonkar, J.B., Das, R., and Gosavi, S. A five-residue motif for the design of domain swapping in proteins. (2019) Nature Communications; 28;10(1):452

4. Nandwani, N.*, Surana, P.*, Udgaonkar, J.B., Das, R., and Gosavi, S. Amino-acid composition after loop deletion drives domain swapping. (2017) Protein Science; 26(10):1994-2002 (* equal contribution)

5. Naramura, M., Nandwani, N., Gu, H., Band, V., and Band, H. Rapidly fatal myeloproliferative disorders in mice with deletion of Casitas B-cell lymphoma (Cbl) and Cbl-b in hematopoietic stem cells. (2010) Proc Natl Acad Sci USA; 107(37):16274-9