Recent Publications

Nag, S., Trivedi, D.V., Sarkar, S.S., Adhikari, A.S., Sunitha, M.S., Sutton, S., Ruppel, K.M. and Spudich, J.A. (2017). The myosin mesa and the basis of hypercontractility caused by hypertrophic cardiomyopathy mutations. Nat. Struct. Mol. Biol., Advance Online Publication. DOI: 10.1038/nsmb.3408 (2017).

Kawana, M. Sarkar, S.S., Sutton, S., Ruppel, K.M. and Spudich, J.A. (2017). Biophysical Properties of Human β-cardiac Myosin with Converter Mutations that Cause Hypertrophic Cardiomyopathy. Sci. Adv. 3, e1601959.

Adhikari, A.S., Kooiker, K.B., Sarkar, S.S., Liu, C., Bernstein, D., Spudich, J.A. and Ruppel, K.M. (2016). Early Onset HCM Mutations H251N and D239N Significantly Increase the Velocity, Force, and Actin-activated ATPase activity of human β-cardiac Myosin.  Cell Rep. 17:2857-2864. doi: 10.1016/j.celrep.2016.11.040.  PMID:27974200.

Homburger, J.R., Green, E.M., Caleshu, C., Sunitha, M.S., Taylor, R.E., Ruppel, K.M., Metpally, R.P., Colan, S.D., Michels, M., Day, S.M., Olivotto, I., Bustamante, C.D., Dewey, F.E., Ho, C.Y., Spudich, J.A. and Ashley, E.A. (2016). Multidimensional Structure-function Relationships in Human β-cardiac Myosin from Population-scale Genetic Variation. Proc Natl Acad Sci U.S.A. 113:6701-6706. doi: 10.1073/pnas.1606950113.  PMID:27247418.

Green, E.M., Wakimoto, H., Anderson, R.L., Evanchik, M.J., Gorham, J.M., Harrison, B.C., Henze, M., Kawas, R., Oslob, J.D., Rodriguez, H.M., Song, Y., Wan, W., Leinwand, L.A., James A. Spudich, J.A., McDowell, R.S., Seidman, J.G. and Seidman, C.E. (2016). A Small-molecule Inhibitor of Sarcomere Contractility Suppresses Hypertrophic Cardiomyopathy in Mice. Science 351:617-621. PMID:26912705.

Spudich, J.A., Aksel, T., Bartholomew, S.R., Nag, S., Kawana, M., Choe Yu, E., Sarkar, S.S., Sung, J., Sommese, R.F., Sutton, S., Cho, C., Adhikari, A.S., Taylor, R., Liu, C., Trivedi, D. and Ruppel, K.M. (2015).  Effects of hypertrophic and dilated cardiomyopathy mutations on power output by human b-cardiac myosin. J Exp Biol 219:161-167. PMID: 26792326.

Manor, U., Bartholomew, S., Golani, G., Christenson, E., Kozlov, M., Higgs, H., Spudich, J.A. and Lippincott-Schwartz J. (2015). A Mitochondria-anchored Isoform of the Actin-nucleating Spire Protein Regulates Mitochondrial Division. Elife. Aug 25;4. doi: 10.7554/eLife.08828.  PMID: 26305500.

Pan, S., Sommese, R.F., Sallam, K.I., Nag, S., Sutton, S., Miller, S.M., Spudich, J.A., Ruppel, K.M. and Ashley, E.A. (2015).  Establishing Disease Causality for a Novel Gene Variant in Familial Dilated Cardiomyopathy using a Functional In-vitro Assay of Regulated Thin Filaments and Human Cardiac Myosin.  BMC Med Genet 16: 97-103. PMID: 26498512.

Mortensen, K.I., Sung, J., Flyvbjerg, H. and Spudich, J.A. (2015). Optimized Measurements of Separations and Angles between Intra-molecular Fluorescent Markers. Nature Commun 6:8621-8629.  PMID: 26509412.

Sung, J., Nag, S., Mortensen, K.I., Vestergaard, C.L., Sutton, S., Ruppel, K., Flyvbjerg, H. and Spudich, J.A. (2015). Harmonic force spectroscopy measures load-dependent kinetics of individual human β-cardiac myosin molecules. Nat Commun6:  Article number: 7931. doi:10.1038/ncomms8931. PMID: 26239258.

Nag, S., Sommese, R.F., Ujfalusi, Z., Combs, A., Langer, S., Sutton, S., Leinwand, L.A., Geeves, M.A., Ruppel, K.M. and Spudich, J.A. (2015). Contractility Parameters of Human β-cardiac Myosin with the Hypertrophic Cardiomyopathy Mutation R403Q Show Loss of Motor Function. Sci Adv 1(9):e1500511. doi: 10.1126/sciadv.1500511. PMID: 26601291.

Hariadi, R.F., Sommese, R.F., Adhikari, A.S., Taylor, R.E., Sutton, S., Spudich, J.A. and S. Sivaramakrishnan, S. (2015).  Mechanical Coordination in Motor Ensembles Revealed Using Engineered Artificial Myosin Filaments. Nature Nanotechnology 10:696-700. doi: 10.1038/nnano.2015.132.  Epub 2015 Jul 6.  PMID: 26149240.

Aksel, T., Choe Yu, E., Sutton,S., Ruppel, K.M. and Spudich, J.A. (2015).  Ensemble Force Changes that Result from Human Cardiac Myosin Mutations and a Small-Molecule Effector.  Cell Reports 11:910-920. doi: 10.1016/j.celrep.2015.04.006. Epub 2015 Apr 30. PMID: 25937279.

Spudich, J.A. (2015).  The Myosin Mesa and a Possible Unifying Hypothesis for the Molecular Basis of Human Hypertrophic Cardiomyopathy.  Biochem Soc Trans43:64-72. doi: 10.1042/BST20140324. PMID: 25619247.

Gupte, T.M., Hague, F., Gangadharan, B., Sunitha, M.S., Mukherjee, S., Anandhan, S., Rani, D.S., Mukundan, N., Jambekar, A., Thangaraj, K., Sowdhamini, R., Sommese, R.F., Nag, S., Spudich, J.A. and Mercer, J.A. (2015).  Mechanistic Heterogeneity in Contractile Properties of a-Tropomyosin (TPM1) Mutants Associated with Inherited Cardiomyopathies.  J Biol Chem 290:7003-7015.

Spudich, J.A. (2014). Hypertrophic and Dilated Cardiomyopathy: Four Decades of Basic Research on Muscle Lead to Potential Therapeutic Approaches to These Devastating Genetic Diseases.  Biophys J106:1236-1249.

Sommese, R.F., Nag, S., Sutton, S., Miller, S.M., Spudich, J.A., and Ruppel, K.M. (2013). Effects of Troponin T Cardiomyopathy Mutations on the Calcium Sensitivity of the Regulated Thin Filament and the Actomyosin Cross-bridge Kinetics of Human b-cardiac Myosin.  PLoS One. Dec 18;8(12):e83403. doi: 10.1371/journal.pone.0083403.

Sommese, R.F., Sung, J., Nag, S., Sutton, S., Deacon, J.C., Choe, E., Leinwand, L.A., Ruppel, K., and Spudich, J.A. (2013). Molecular Consequences of the R453C Hypertrophic Cardiomyopathy Mutation on Human beta-cardiac Myosin Motor Function.  Proc Natl Acad Sci USA110:12607-12612.